COLUMBIA LIBRARIES OFFSITE 
 
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 HX641 34253 
 C681 .N79 Studies in cardiac p 
 
 RECAP 
 
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 intftcCitpofJ^etD^orb 
 
 COLLEGE OF PHYSICIANS 
 AND SURGEONS 
 
 Reference Library 
 
 Given by 
 
STUDIES 
 
 Cardiac Pathology 
 
 GEORGE WILLIAM NORRIS, A.B., M.D. 
 
 ASSOCIATE IN MEDICINE AT THE UNIVERSITY OF PENNSYLVANIA 
 
 VISITING PHYSICIAN TO THE EPISCOPAL HOSPITAL OF PHILADELPHIA 
 
 ASSISTANT VISITING PHYSICIAN TO THE UNIVERSITY AND TO THE PHILADELPHIA GENERAL HOSPITALS 
 
 PHYSICIAN TO THE MEDICAL OUT-PATIENT DEPARTMENT OF THE PENNSYLVANIA HOSPITAL 
 
 FELLOW OF THE COLLEGE OF PHYSICIANS OF PHILADELPHIA. ETC. 
 
 WITH 8s ORIGINAL ILLUSTRATIONS 
 
 PHILADELPHIA AND LONDON 
 
 W. B. SAUNDERS COMPANY 
 
 1911 
 
Copyright, 1911, by W. B. Saunders Company 
 
 PRINTED IN AMERICA 
 
TO 
 
 THE MEMORY OF MY GRANDFATHER 
 
 GEORGE W. NORRIS 
 
 CLINICAL PROFESSOR OF SURGERY AT THE UNIVERSITY OF PENNSYLVANIA 
 AND OF MY FATHER 
 
 WILLIAM FISHER NORRIS 
 
 PROFESSOR OF OPHTHALMOLOGY AT THE UNIVERSITY OF PENNSYLVANIA 
 
Digitized by the Internet Archive 
 
 in 2010 with funding from 
 
 Open Knowledge Commons 
 
 http://www.archive.org/details/studiesincardiacOOnorr 
 
PREFACE 
 
 The opportunity of photographing specimens in the museums 
 of five of the most important hospitals of Philadelphia having been 
 afforded the author through the courtesy of the respective patholo- 
 gists of those institutions,* it has seemed worth while to reproduce 
 the same in order to secure for these interesting examples of cardiac 
 pathology a more enduring permanence and a more widespread 
 field of usefulness. In order to enhance the value of the exhibit 
 considerable data bearing on the pathology of cardiac lesions 
 have been added. No attempt has been made to publish a com- 
 plete work on the pathology of the heart, the text being mainh' in 
 the form of an explanation and an elucidation of the illustrations, 
 and but little space has been devoted to the microscopic tissue 
 changes. The result is perhaps open to criticism as being too 
 statistical in nature, and the same set of statistics can, as we know, 
 only too often, be manipulated to prove opposing hypotheses. On 
 the other hand, it cannot be denied that statistic compilation has 
 done considerable for the advance of medical science, and there is 
 much truth in Kant's dictum that the amount of pure science which 
 any given study contains is in direct proportion to the quantity of 
 mathematics it includes. 
 
 The author has endeavored to give due credit to all concerned, 
 
 * The author desires to express his indebtedness to the following gentlemen for their 
 courtesy in placing the pathologic material of the various institutions with which they are con- 
 nected at his disposal: Professor Allen J. Smith of the University of Pennsylvania, Dr. A. O. J. 
 Kelly of the German Hospital, Dr. W. T. Longcope of the Pennsylvania Hospital, Dr. R. C. 
 Rosenberger of the Philadelphia General Hospital, Dr. C. Y. White of the Protestant Epis- 
 copal Hospital, Dr. George Fetterolf and Dr. Alfred R. Allen of the University of Pennsyl- 
 vania, and Dr. George McClellan of the College of Physicians of Philadelphia. 
 
not only in the matter of specimens but also in regard to the 
 sources of information. This has added very greatly to the time 
 consumed in the preparation of the work and it is hoped that the 
 attempt has been sufficiently successful to do justice to the authori- 
 ties quoted and to assist such readers as may be desirous of more 
 detailed information. 
 
 George W. Norris. 
 
 1530 Locust Street, 
 
 Philadelphia, March, 1911. 
 
CONTENTS 
 
 PAGE 
 
 Acute Endocarditis 1 
 
 Chronic Infective Endocarditis 30 
 
 Chronic Endocarditis 39 
 
 Diseases of the Aortic Orifice 50 
 
 Aortic Obstruction 50 
 
 Aortic Insufficiency 55 
 
 Diseases of the Mitral Orifice 64 
 
 Mitral Obstruction 64 
 
 Mitral Insufficiency 80 
 
 Diseases of the Tricuspid Orifice 86 
 
 Tricuspid Obstruction 87 
 
 Tricuspid Insufficiency 92 
 
 Diseases of the Pulmonary Orifice 96 
 
 Pulmonary Obstruction 96 
 
 Pulmonary Insufficiency 98 
 
 Acute Pericarditis 100 
 
 Chronic Pericarditis 124 
 
 Cardiac Hypertrophy 136 
 
 Cardiac Dilatation ' 162 
 
 Coronary Arteriosclerosis 180 
 
 Cardiac Aneurism 188 
 
 Cardiac Thrombosis 192 
 
 Tumors of the Heart 198 
 
 Cardiac Syphilis 200 
 
 Congenital Lesions 206 
 
 Imperforate Ventricular Septum 206 
 
 Transposition of the Great Vessels 212 
 
 Patulous Ductus Arteriosus 212 
 
 Patulous Foramen Ovale 214 
 
 Anomalies of the Semilunar Valves 219 
 
 Double Mitral or Tricuspid Orifices 219 
 
 Index of Illustrations 229 
 
 Index of Subjects 231 
 
STUDIES IN 
 CARDIAC PATHOLOGY 
 
 I. ACUTE ENDOCARDITIS 
 
 Experimental evidence indicates that for the production of 
 an acute endocarditis two factors are necessary. First, a pre- 
 disposition or preparation on the part of the endocardium, which 
 may be produced by mechanical, chemical, or toxic action; and, 
 second, the presence of pathogenic micro-organisms. There has 
 been much debate as to whether toxemia alone can ever produce 
 verrucose lesions. Di Vecchi ^ has done considerable work on 
 this question, and believes that he has been able to produce 
 endocarditis by the injection of bacterial toxins together with 
 mechanically and chemically irritant substances, such as coal- 
 dust and argentic nitrate. Fulci, who has repeated the last- 
 mentioned experiments, was unable to produce lesions which were 
 not also found in the control animals, unless living organisms 
 were also injected.- He found, however, that toxins and me- 
 chanical irritants distinctly helped in preparing the endocardium 
 for the inflammatory process. These last findings are quite 
 in accord with those of other capable investigators. The mere 
 fact that we are not always able to demonstrate organisms in 
 the valvular lesions of endocarditis is to be explained, first, by 
 their occasional disappearance after the lesions have been pro- 
 duced; second, by inadequacy of our methods of investigation; 
 and, third, by the fact that in some instances we are doubtless 
 
 'Arch, di Anat. Putholog. c .Sfiierizf, 190.5, and ]iullet. dolhi ScicnzR med. di Bologna, 
 Jan., 1908. 
 
 2 Fulci: Bcitr. ■/.. pa1.li. Anat,. u. ■/,. allg. Patli., I9(1S, ]). :M9. 
 1 I 
 
2 STUDIES IN CARDIAC PATHOLOGY 
 
 dealing with the effects of as j'et undiscovered organisms, such as 
 those responsible for scarlatina, measles, chorea, etc. 
 
 We are forced to conclude, therefore, that all cases of acute 
 verrucose and ulcerative processes on the endocardium are in- 
 fectious in origin. This, of course, does not include purely sclerotic 
 processes, which are probablj- brought about in a similar manner 
 to arteriosclerosis elsewhere. 
 
 Recent advances in bacteriology have tended to simplify 
 greatly the subject of infective endocarditis. Much more accurate 
 results are obtained by means of intra-vitam blood-cultures than 
 by cultures from the heart's blood at autopsy, in which there is 
 always a tendency for terminal infection to play a role. This 
 fact probably explains the complex and hardly identifiable micro- 
 organisms described by some early observers. 
 
 Fig. 1, — Acute Ulcerative Mitral Endocarditis. 
 
 Female, white, aged forty years. (Pennsylvania Hospital. Autop.sy 408. Pathologist: 
 Dr. Longcope. Ph3fsician: Dr. M. J. Lewis.) 
 
 Clinical History; Denies previous diseases. Well until two weeks ago, since which 
 time she has had pain in the left side and a harassing nocturnal cough, without expectoration . 
 Night-sweats, dyspnea, and edema of the legs, also slight palpitation, were present. 
 
 Physical Examination: A loud vibratory systolic murmur is heard over the body of the 
 heart, which is transmitted to the left scapula, and can be heard over the whole chest and 
 abdomen. A soft systolic murmur is noted at the aortic area. 
 
 Pathologic Diagnosis: Acute ulcerative mitral endocarditis. Thrombosis of a small 
 branch of the pulmonary artery. Acute bronchopneumonia. Anemic infarction of the spleen 
 and kidneys. 
 
 Heart: The heart weighs 410 grams. The vessels are injected and a few punctate 
 hemorrhages are noted below the serous surface. The cavities contain postmortem clots. 
 The right ventricle is somewhat dilated. The endocardium is thickened. The mitral valve is 
 the seat of a most extensive vegetative growth, situated above the junction of the anterior and posterior 
 leaflets. Beneath it the valve is extensively ulcerated, and several chordce lendinece swing loose,, 
 being attached only to the vegetations. The vegetative inass is lobulated and nearly the size of a 
 walnut; it extends to the auricular surface for 2.5 to 3 cm., and when the heart is held in the up- 
 right position, "practically fills the auriculo-ventricular orifice. The vegetations are delicate, gray, 
 soft, friable, and lobulated. Numerous soft, gray, pinhead-size vegetations cover the posterior 
 leaflet and part of the auricular wall. The aortic valves are thickened and somewhat calcified 
 at the bases, but show neither retraction nor vegetation. The muscle is soft, brownish-gray, 
 and fragments easily. The coronary arteries show an extensive grade of sclerosis, and in 
 places are converted into rigid tubes. The aorta immediately above the valves, shows a diffuse 
 dilatation, measuring 9 cm. in circumference. Its wall is fairly smooth. 
 
 Microscopic Diagnosis: The pericardium is normal. Muscle-fibers are rather granular 
 and have partially lost their cross-strise. Between them some connective-tissue formation is 
 noted. The valvular vegetations showed diplococci, slightly lanceolate in form, Gram-positive. 
 Cultures showed numerous very small pin-point colonies, barely visible to the naked eye. 
 
Fk;. 1. 
 
4 STUDIES IN CARDIAC PATHOLOGY 
 
 Classification. — A satisfactoiy classification of acute infectious 
 endocarditis is at present impossible. No distinctions can be 
 made which will alwaj^s hold good. A division into simple and 
 infective is fallacious, since ]3robabl}^ all cases are infectious in 
 origin. Benign and malignant is equally unsatisfactor}-, inasmuch 
 as there are no "benign" cases, the endocardial changes instituted 
 being always sooner or later serious. A bacteriologic classifica- 
 tion is also objectionable, because although certain micro-organisms 
 tend on the whole to produce certain tjqDes of changes, yet there 
 are so many exceptions and uncertainties as to make this basis 
 infeasible. Finally, a classification into simple, ulcerative, ver- 
 rucose, etc., based upon anatomic appearances is useless, since 
 these are not radical differences, but largely accidental charac- 
 teristics, which merge more or less insensiblj^ into each other. 
 On the other hand, there are clinical types of the disease which 
 are quite distinct from each other, in the onset, course, and termina- 
 tion, so that some sort of differentiation must be attempted. Osier 
 
 Fig. 2. — Malignant Endocarditis, Aortic and Mitral. 
 
 J. M., male, white, aged thirty-three years. (Philadelphia Hospital. Autopsy: Vol. 
 xxii, p. 32. Phj'sician: Dr. J. Tyson. Pathologist: Dr. Foster.) 
 
 Clinical Notes': Laborer, hard worker. Alcohol to excess. Tobacco moderate; de- 
 nies sj'philis. Malaria in Philippines. Rheumatism three years ago. Epigastric pain, cough, 
 hemoptysis, vertigo, diplopia. Corrigan pulse; radial sclerosis. Heart enlarged to right and 
 left. First sound only fair. Pulmonic second accentuated. Apex-beat: sixth interspace, 
 1 in. outside midclavicular line. Systolic murmur at third left costal cartilage. 
 
 Pathologic Diagnosis: Malignant endocarditis — aortic and mitral; aortic insufficiency; 
 parenchymatous degeneration of heart; hemorrhagic infarcts of kidnej', spleen; fatty de- 
 generation of liver; chronic parenchymatous nephritis, with beginning interstitial changes; 
 healed bilateral pulmonary tuberculosis, etc. 
 
 Pericardium: Contains 60 c.c. of blood-tinged fluid. Serous surface smooth and glis- 
 tening. 
 
 Heart: Weighs 470 grams; is large and flabby; pale in color. Absence of epicardial 
 fat. Vessels prominent and engorged. Aortic valves incompeLenl to water lest. Heart 
 muscle soft, brownish-red, and granular. Papillary muscles pale. Aortic orifice, 8; mitral, 11; 
 tricuspid, 14; pulmonary, 7 cm. in circumference. 
 
 On the anterior and left -posterior aortic leaflets there are rough, reddish-yellow vegetations 
 about 1 cm. in diameter. On the ventricular surface of the mitral leaflet there is a large, irregidar, 
 cauliflower-like mass, ii xS x 1 .5 cm. Inflammatory changes incident to this massive vegetation 
 have occurred on the auricular surface of this leaflet, and consist of three circumscribed areas 
 of roughening covered with plastic lymph. The other valves are uninvolved. The base of 
 the aorta shows beginning atheromatous change about the coronary orifices. 
 
6 STUDIES IN CARDIAC PATHOLOGY 
 
 has suggested the following division: (1) malignant; (2) simple 
 acute; (3) chronic. 
 
 The virulence of the causative organism is often more im- 
 portant than the species. Organisms of low virulence may produce 
 severe subacute attacks without the production of any bactericidal 
 reaction on the part of the host. The main difference between 
 these types is in the amount of endocardial inflammation and 
 tissue necrosis. In malignant endocarditis emboli are more fre- 
 quent and more septic, right-sided involvement more common, 
 and micro-organisms are oftener found in the blood, in the emboli, 
 and on the valves. These cases are nearly always secondary 
 and generally fatal. Infants and children seem to be almost 
 exempt from this form of the disease.^ 
 
 Morbid Anatomy. — The earliest visible manifestation of acute 
 endocarditis consists in an opaque or slightly rough area upon 
 the valves or endocardium. If the process continues, bead-like, 
 nodular elevations appear which eventually develop into distinct 
 verrucse. The amount of fibrin which exudes is verj^ variable, 
 and upon this factor the appearance of the inflammatory products 
 largely depends. Where free outpouring occurs, large fleshy 
 vegetations are seen. When veiy little occurs, necrotic changes 
 in the endocardium producing various degrees of ulceration may 
 predominate in the picture. Even small vegetations entail 
 destruction of the endocardium. Larger growths have a deeper 
 origin and cause relatively greater destruction of tissue. A 
 combination of fungating and ulcerating lesions is the rule in 
 the severe forms. The latter may produce valvular perfora- 
 tion, and even destruction of the underlying myocardium. (See 
 Fig. 6.) Occasionally, necrotic areas without ulceration or foci 
 of suppuration occur. The vegetations vary greatly in appear- 
 ance; at times soft, friable, gelatinous, white, reddish or yellow 
 masses with adhering blood-clots; again, the well-known cauli- 
 flower growths are seen. In cases in which friction has been 
 
 ' Sicard (32 cases, Presbyterian Hospital, New York): Amer. Jour. Med. Sci., Nov., 1904. 
 
Fig. 3. — Acute Infective Mitral and Muhal Endocarditis. 
 The mitral valve is covered with large vegetations. Several of the chorda.- tendineaj 
 have been destroyed by ulceration, only short unattached stumps remaining. Vegetations 
 are also seen on the mural endocardium. (Specimen from the Pennsylvania Hospital.) 
 
5 STUDIES IN CARDIAC PATHOLOGY 
 
 marked, long pendulous thrombi maj^ occur. (See Fig. 12.) 
 Osier states that fibrous changes, and even calcification, may 
 occur even in acute cases. In such cases the condition might be 
 confused with the necrotic changes seen in arteriosclerosis without 
 micro-organismal infection.^ 
 
 Thrombosis in the auricular appendages, especially if associated 
 with necrosis, may also at times simulate mycotic endocarditis. 
 Severe cases may perforate septum or heart itself. 
 
 Simple endocarditis occurs especially at the line of valvular 
 contact; the endocardium becomes swollen, translucent, and 
 somewhat beaded. As the distended endothelial cells are detached 
 the blood-plaques agglutinate into small masses, which in time, 
 by the addition of leukocytes, develop into good-sized warty 
 growths. 
 
 In severe cases the chordae tendinese and the papillary muscles 
 are involved in infiltration and inflammation. The mural en- 
 docardium is less often involved than that of the valves, owing 
 to lessened functional activit}'. 
 
 Malignant endocarditis may be primary or secondary; the 
 right-sided valves are attacked oftener than in the simple variety. 
 The vegetations tend to be more exuberant and friable, and 
 mural involvement is commoner. Valvular rupture (chiefly 
 mitral and aortic) is sometimes preceded by aneurismal dilatation 
 of the same, extending in the direction of greatest pressure. An 
 aneurism of the mitral valve generally involves the anterior flap. 
 (See Fig. 14.) Rupture of the valves or chordae tendinese, es- 
 pecially when the process is acute, is usually preceded by old 
 valvular disease. Myocarditis maj^ occur by extension of the 
 inflammatory process. 
 
 The infarcts of malignant endocarditis perhaps so rarely lead 
 to suppuration on account of the low virulence of the organisms 
 to which many cases owe their existence. Embolic manifestations 
 vary greatly in different cases. Sometimes they are very extensive, 
 
 ' Brit. Med. Jour., Mar. 7, 1885, p. 438. 
 
Fig. 4. — Acute Infective Endocakuitis. 
 Specimen showing large thrombi formed on the ulcerated areas of the aortic leaflets. 
 .VlsD verj' small verruca in the sinu.s of Valsalva, and some small mural thrombi between the 
 eolumna; oarneic of the left ventricle. 
 
10 STUDIES IN CARDIAC PATHOLOGY 
 
 as in Hoper's case of mitral stenosis, in which both femorals, 
 the right internal iliac, the right renal, the superior mesenteric, 
 and the left brachial arteries were occluded by emboli.^ 
 
 The verrucose vegetations of endocarditis, which, as Hirsch- 
 f elder has pointed out, maj^ form within a few hours after damage 
 to a valve, are in part the result of the action of the blood-stream 
 upon the fibrinous exudation. In long-standing cases contraction 
 of organizing fibrin doubtless plays a part in the production of 
 wartlike vegetations. 
 
 Predisposition. — The more frequent involvement of the left 
 side of the heart has been explained by the fact that after birth 
 blood-pressure is higher and oxygenation greater than on the right. 
 The former, as the result of stress and trauma, favors the localiza- 
 tion of micro-organisms, the latter favoring both localization and 
 growth. - 
 
 In 237 cases of congenital endocarditis Rauchf uss found the lesions right-sided 
 in 192. The relative frequency of right-sided lesions in fetal life was ascribed by 
 Rokitansky to the effect of congenital malformations, a belief which subsequent 
 investigation has corroborated. Yet despite the fact that this predisposition 
 exists, the engrafting of an acute endocarditis upon a congenital lesion is not 
 common, owing to the fact that malignant endocarditis is a disease of middle 
 life, an age which the subjects of developmental heart lesions do not, as a rule, 
 attain.' G. C. Robinson^ has collected 17 cases of endocarditis and congenital 
 malformation, adding two cases thereto, and omitting those in whicli the mal- 
 formation was limited to the valves. In 11 cases there was deficiency of the 
 interventricular septum, and in 6 of these pulmonary valvular obstruction. 
 Fig. 76 was from one of the cases published by Robinson. Fig. 77 also illustrates 
 the coincidence of infectious endocarditis and congenital defect. 
 
 Embolic manifestations in the lung, spleen, kidneys, etc., are much more 
 frequent in malignant or "infective" endocarditis than in the simple type. 
 Among 64 cases of the former, Glynn found 44 instances ; among 64 of the latter, 
 only 18.'' 
 
 iHoper: Lancet, Aug. 18, 1906. 
 
 - Wadsworth: Jour. Infect. Dis., 1909, p. 279. 
 
 ' Malignant endocarditis is rare in childhood. The statistics of StefTen, Von Dusoh, 
 Hochsinger, and Weil show that 62 per cent, are of the simple variety, and involve the mitral 
 valve. Endocarditis is rare in infants. Holt failed to find any instance in 1000 autopsies 
 on children under three years; Steffen, in 45 cases, found only .5 in the first year of life; Hoch- 
 singer, in .53 cases, only one in the first year of life; v. Dusch, in 45 cases, 5 between eight 
 months and three years; Sutiagin, in 108 cases, 11 in the first year of life. 
 
 ■* G. C. Robinson: Bull. Ayer Clinical Laboratory, Pennsylvania Hospital, 1905. 
 
 5 Lancet, April 18, 1903, p. 1073. 
 
Fig. .5. — iSuBACuxE Infective Endocarditis. 
 Showing large thrombotic mas.ses almost completely occluding the aortic orifice. There 
 i.s marked left ventricular hypertrophy, and sclerotic patches are seen on the aorta above the 
 sinus of Valsalva. 
 
12 STUDIES IN CARDIAC PATHOLOGY 
 
 Pathogenesis. — Anj^ infectious disease may be accompanied 
 or followed by an endocarditis, which may be homologous, heter- 
 ologous, or due to a mixed infection. A predisposition to it is 
 to be found in the minute endothelial lesions, which are naturally 
 commonest where pressure or friction is greatest — on the mitral 
 valve. When this valve is insufficient, the right heart may be 
 more likely to develop acute endocarditis, as in a case described 
 by Marini.^ The youthful endocardium is much more suscep- 
 tible to infection than that of advanced years, as Church's statistics 
 of 700 cases show:'- 
 
 1 to 10 years 80 per cent. 
 
 10 " 20 " 69 
 
 20 " 30 " 62 
 
 .30 " 40 " .?0 
 
 40 " .50 " 21 
 
 Further corroboration is to be found in the well-known fact that 
 in the rheumatic fever of childhood the heart rareh^ escapes involve- 
 ment, whereas in adults this is by no means so unusual an occur- 
 rence. 
 
 Dunii'^ in 300 cases of rheumatic arthritis at the Children's Hospital in 
 Boston found evidences of endocarditis in 140, and of pericarditis in 58. Two 
 hundred and eighty-one at some time in the attack showed evidences of endo- 
 carditis, so that only 19 in all escaped entirely. Mitral insufficiency was noted 
 70 times, a double mitral lesion 56 times. The 140 cases were admitted as 
 "endocarditis," there being other evidences of disease at that time. Thus 60 
 per cent, of the cases showed distinct evidences of endocarditis at a time when 
 there were no arthritic manifestations. 
 
 The tendency of certain organisms to attack the endocardium is well exem- 
 plified by Lenhartz's results: In a study of 226 cases of general sepsis, there were 
 38 cases of malignant endocarditis. In 149 cases of sepsis due to the strepto- 
 coccus pyogenes there were but 6 cases of endocarditis. In other words, the 
 .streptococcus is the most common cause of sepsis, in scarlatina, the puerperium, 
 etc. ; yet, proportionately, endocarditis was much more common in the cases due 
 to the other organisms. On the other hand, 95 per cent, of the staphylococcus 
 cases showed endocarditis.* (His investigations revealed: staphylococcus 10, 
 pneumococcus 10, streptococcu? 16, gonococcus 1.) 
 
 ' Marini: Gazz. degli ospedaU, 1907, No. 24. -St. Bart. Hosp. Report, -\xiii. 
 
 ' Dunn: ,Jour. Amer. Med. Assoc, 1907, p. 49:^. 
 
 ■' Lenhartz, quoted by Reye: Jahrb. d. Hamburger Staatskrank. Anst., 190.5, p. 224. 
 (The valvular involvement in these cases was as follows: Mitral, 18: aortic, 11; both, 2. 
 Tricuspid, 4; puhnonic, 2; aortic and jjulmonic, 1.) 
 
ACUTE ENDOCARDITIS 13 
 
 The researches of Prudden/ Rosenbach,'^ Wyssokowitch/* and 
 Rosenow "* have demonstrated the fact that endocarditis is more 
 apt to develop on an endocardium which has been previously 
 injured or diseased than on a normal one. Goodhart '" found ap- 
 parently antecedent valvular thickening in 61 out of 69 cases. 
 A large number of different organisms have from time to time been 
 described as the causative factor of endocarditis. "The colon, 
 Friedlander, typhoid, diphtheria, influenza organisms, the meningo- 
 coccus, the tubercle bacillus, the bacillus pyocyaneus, unrecognized 
 species, others little known but described as the bacillus endo- 
 carditis griseus, the micrococcus rugatus, the micrococcus cap- 
 sulatus of Weichselbaum, the bacillus pyocyaneus fetidus (Fasset), 
 the diplococcus tenuis (Klemperer) — these and other organisms 
 have been credited with producing the condition" (Wadsworth "). 
 At present there seems to be a tendency to regard many of these 
 diverse and little known organisms as atypical forms of well- 
 known varieties, such as the streptococcus. The pneumococcus, 
 the staphylococcus, the streptococcus, and the gonococcus are 
 undoubtedlj^ the most freciuent causes of malignant endocarditis. 
 "Bacterial species comparatively benign in other parts of the body 
 prove serious and fatal in endocarchal lesions" (Wadsworth). 
 
 Among 50 cases of pneumococcus endocarditis, 25 per cent, 
 showed old lesions upon which the recent infection had become 
 engrafted (Preble). 
 
 Although the difference between simple and malignant endo- 
 carditis is nearly always only one of degree, yet certain infections 
 have a marked tendency to cause definite types. Thus rheumatic 
 fever and chorea, so frequently the cause of simple endocarditis, 
 rarely cause the malignant variety; whereas with pneumonia 
 and puerperal sepsis the reverse is the case. The mere fact that 
 
 ' Prudden: Am. Jour. Med. Sci., 1887. 
 
 * Roscnbach: Arch. f. exper. Path., 1878. 
 
 ' Wyssokowitch : Virchow's Arch., 1886, p. 301. 
 
 ■• Rosenow: Jour. Infect. Dis., vi, 1909, p. 245. 
 
 'Goodhart: Tran.s. London Patli. Soc, xxxiii, p. 52. 
 
 " Wadsworth: .Med. Record, Dec. 28, 1907. 
 
14 STUDIES IN CARDIAC PATHOLOGY 
 
 endocarditis complicates a disease is, of course, no indication that 
 this is not due to a secondarj^ infection with some other species 
 of organism. For example, the pyogenic cocci are generally the 
 cause of endocarditis in diphtheria and tuberculosis, although 
 both the Klebs-Loffler and the tubercle bacillus have been 
 shown, both clinically and experimentally, to possess the faculty 
 of producing endocardial inflammation. However, we must not 
 forget that "the organism isolated from an ulcerative case may 
 experimentally in one case animal give rise to an ulcerative form 
 of endocarditis, while in another animal of the same species 
 simple endocarditis may result."' 
 
 Sometimes the experimental injury of valves in animals has 
 been followed by lesions similar to those of malignant endocarditis; 
 although not the ulcerative type, which appears to occur only 
 when infection is also present. It is conceivable, therefore, that 
 valvular rupture might give a similar picture in man. Practically, 
 however, malignant endocarditis means a severe type of infection, 
 localized either by means of the general blood-stream or the 
 coronary arteries. Slight local injur j^, such as the application 
 of nitrate of silver, is enough to determine the focus of the infection 
 on the endocardium (Prudden) . The mycotic origin of practically 
 all cases of verrucose endocarditis is generally admitted. Articles 
 bearing on this subject are very numerous. Thus Bartel- studied 
 23 cases and concluded that all cases of verrucose endocarditis 
 have such an origin; the extent of the lesion varying with the 
 duration and virulence of the infection, and with the amount of 
 individual tissue resistance. 
 
 Rheumatic fever is by far the most prohfic source of "simple" 
 endocarditis, from 80 to 90 per cent, of this variety being due to 
 this cause. Rheumatic fever is now universally regarded as an 
 infection, and although the exact micro-organism which causes 
 it has not yet been definitely determined, the majority of cases 
 
 ' Beattie and Dickson: Special Pathology, 1909, p. 12. 
 = Bartel: Wien. klin. Woch., Oct. 10, 1901. 
 
Fig. 6. — Acute Infective Endocarditis. 
 Showing extensive ulceration of the aortic valves. About the center of the aortic orifice 
 a match-stick projecting from a thrombotic mass indicates the course of the perforation in the 
 aortic leaflet. fSpecimen from the Philadelphia Hospital.) 
 
16 STUDIES IN CARDIAC PATHOLOGY 
 
 owe their origin to various organisms of the streptococcus group. 
 A diplococcus described by Wasscrmann, and later by Poynton 
 and Paine, Longcope, and otliers, seems to be responsible for a 
 considerable number of the cases. According to Beattie and 
 Dickson, the diplococcus rheumaticus, which is a common in- 
 habitant of the mouth and intestines, may, under certain condi- 
 tions of increased virulence on the part of the germ, or decreased 
 resistance on the part of the host, produce the infection. They 
 suggest that some of the cases of endocarditis occurring in rheu- 
 matic fever, Bright's chsease, scarlatina, and chorea may thus 
 arise.-' 
 
 Sibson in 325 cases of rheumatic fever found endocarditis in 130, both 
 endocarditis and pericarditis in 54, and the latter alone in 9. Seventy-nine per 
 cent, of the cases with previous endocardial lesions developed an acute infection, 
 whereas of those with no antecedent disease only 56 per cent, were afflicted. 
 Among 270 cases of rheumatic fever studied by McCrae, 85, or 32 per cent., had 
 undoubted organic endocardial disease — mitral, 95 per cent.; aortic, 23 per 
 cent. ; both valves, 18 per cent. Of the 85 cases of mitral involvement, 54 were 
 insufficiency, 3 obstruction, and 8 a double lesion. At St. Thomas' Hospital 
 among 535 cases of rheumatic fever the mitral valve was involved in 97 per cent., 
 the aortic in 12 per cent., the aortic alone in 3 per cent. There were apparently 
 no cases of malignant endocarditis in McCrae's series. He found in addition to 
 the above mentioned cases 78 (28 per cent.) in which organic disease was doubt- 
 ful; of these, 60 were discharged with murmurs of uncertain cause. In 136 cases 
 of rheumatic fever reported by Latham, 90 showed cardiac involvement — 63 
 endocarditis, 7 pericarditis, 11 both, 9 doubtful cases. Among 150 cases of 
 infective endocarditis at St. Bartholomew's Hospital, Horder found that 72 gave 
 a history of acute or subacute rheumatic fever or chorea, 10 of scarlatina, 7 of 
 gonorrhea, 4 of typhoid fever, 4 of malaria, 2 of syphilis, 2 of influenza, 1 of 
 exophthalmic goiter, 1 of dysentery, 1 of pneumonia. In 53, no history of pre- 
 ceding disease could be obtained. Phillips in 210 cases of acute rheumatic fever 
 found 63 cases of undoubted endocarditis — mitral 56, aortic 13, both 11. Among 
 288 cases of rheumatic arthritis in Christiania there were heart comphcations in 
 33 per cent. ; and of 242 cases of heart disease there was a history of rheumatic 
 fever in 46.5 per cent., of syphihs in 9.2 per cent., influenza in 2.5 per cent. Of 
 the chorea cases 31 per cent, showed cardiac lesions.- Among 30,000 patients, 
 Litten found 400 cases of endocarditis. In 35 per cent, of these the cardiac 
 
 ' Details regarding the bacteriology may be found in Bulloch's article, "Rheumatic Fever," 
 vol. ii, part 9, of the new edition of Allbutt and Rolleston's System of Medicine, 1906, vol. ii, 
 part i, p. 594. 
 
 ' Thiis: Norsk Mag. f. Laegevedenskaben, Oct., 1909, Ixx. 
 
ACUTE ENDOCARDITIS 17 
 
 lesion was certainly due to rheumatic fever. In 30 per cent, other definite 
 causes could be as.signed, and in the remaining 30 per cent, no etiologic factor 
 was demonstrable.' Forssner- found that 45 out of 74 cases of acquired heart 
 disease in children, and 32 among 60 in adults, resulted from rheumatic fever. 
 Romberg in 670 cases of valvular disease at the Leipzig chnic found that 
 58.9 per cent, were rheumatic in origin. Among 258 cases of acute endo- 
 carditis in children Perroud^ found it associated with different infectious 
 processes as follows: rheumatic fever, 150; chorea, 39; tuberculosis, 15; 
 scarlatina, 12; pneumonia, 7; measles, 7; cUphtheria, 7; typhoid fever, 4 ; dys- 
 entery, 3; erythema nodosum, 2; undetermined, 12. 
 
 In a study of 1,369 clinical reports of scarlatina cases, Rochely found no 
 acute endocarditis, nor did Reimer among 48 autopsies. The endocarditis of 
 scarlatina and variola is said to be generally of the simple variety. In 550 cases 
 of scarlatina, Beatty"" found 7 cases of endocarditis. It has also been reported 
 following vaccination. Barbier in 45 diphtheria autopsies found 23 cases of 
 cardiac thrombosis (chiefly right auricular) ; these cases were considered as 
 resulting from mural endocarditis due to the "diplococcus hemophilus per- 
 lucidus." Cohn^ has reported a fatal case of endocarditis following chancroid, 
 both lesions culturally exhibiting the staphylococcus pyogenes aureus. 
 
 Pneumonia heads the list of all diseases complicated by severe 
 endocarditis (Osier). Acute endocarditis has been attributed to 
 pneumonia as follows: 
 
 Harbitz 
 
 Traux 
 
 Kanthack and Tickell 14 
 
 Lenhartz 
 
 Jackson 
 
 Waller 
 
 Weichselbaum 
 
 O-sler 54 
 
 2 out of 
 
 9 cases 
 
 8 " " 
 
 22 
 
 
 14 " " 
 
 34 ' 
 
 
 9 " " 
 
 43 ' 
 
 
 1 " " 
 
 6 ' 
 
 
 14 " " 
 
 84 ' 
 
 
 5 " " 
 
 38 ' 
 
 
 1 " " 
 
 5 • 
 
 
 1 " " 
 
 21 ' 
 
 
 6 " " 
 
 33 ' 
 
 
 54 " " 
 
 209 ' 
 
 ' (Ulcerative) 
 
 Total 115 out of .504 cases (22 per cent.) 
 
 Preble,*^ basing his statement on collected statistics, states 
 that the pneumococcus is something over twice as apt to involve 
 the aortic valves as other bacteria, and about one-third as apt 
 
 1 Deut. mod. Woch., May 22, 1902. 
 
 2 Nordiskt Med. Arkiv., 1909, xli, No. 3. 
 
 ' Perroud : Weill's Traits clinique des mal. du cocur chcz les enfants. 
 * Dublin Jour. Med. Sci., 1907. 
 'Cohn: Jour. Amer. Med. A.ssoc, 1909, 47, p. 1106. 
 
 'Preble; " Pneiiiiiotiia and Pneumococcic Infections," Chicago, lOO.'), p. 133. 
 2 
 
18 STUDIES IN CARDIAC PATHOLOGY 
 
 to involve the mitral, while it attacks the tricuspid twenty times 
 as often. The last fact is probably influenced by the special 
 physical conditions which result from pulmonary consolidation. 
 Pneumococcus endocarditis is twice as common in women as in 
 men, and about three-fourths of the cases are ulcerative in char- 
 acter, while lesions of the right heart are more common than 
 in other varieties of endocarditis. The aortic and pulmonary 
 valves are involved more frequently than in other forms of the 
 disease. Among 32,894 cases of pneumonia collected from the 
 literature, 149 cases of acute endocarditis were reported, and 
 among 2,722 pneumonia autopsies acute endocarditis occurred 
 158 times. ^ The pneumococcus generally produces large, isolated, 
 friable, pedunculated vegetations, which on being detached leave 
 but a small ulcerated surface. The streptococcus, on the other 
 hand, often causes extensive ulceration covered by small verrucose 
 excrescences, at times hemorrhagic and necrotic. Billings,' in 
 a study of 14 cases of chronic infectious endocarditis, found 11 
 due to the pneumococcus, 3 to the streptococcus. Culturally the 
 former organism showed distinct differences from the type which 
 ordinarily causes pneumonia. The origin of infection was as 
 follows: Pneumonia 1, tonsillitis 2, alveolar abscess 2, influenza 1, 
 no discoverable cause 8 . We are thus gradually coming to realize 
 the fact that relativelj' unimportant infections of the nares, naso- 
 pharynx, ears, mouth, gums, etc., may be the portal of entrance 
 for the most severe t.ype of endocardial inflammation. 
 
 As has been intimated, pneumococcus endocarditis is apt to 
 be rapidlj^ fatal. Acute cases do not usually last over three 
 months, although Frankel has reported a case of pneumococcus 
 endocarditis lasting six months.^ In Rosenow's experiments 
 the lesions were generally progressive, though healing did occur. 
 He states that "a close relationship exists between the biologic 
 characters of the bacteria and their abihty to produce endo- 
 
 ' Statistics collected by the author. 
 
 '- Billings; Arch. Int. Med., 1909, iv, No. 5. ' Frankel: Deut. med. Woch., 1900. 
 
Fio. 7. — Acute Infective Endocarditis. 
 The aortic leaflets are thickened, shriveled, perforated, and show extensive ulcerative 
 tissue destruction with little thrombosis. Beneath the aortic leaflets the ulceration is begin- 
 ning to extend downward toward the mitral valve. 
 
20 STUDIES IN CARDIAC PATHOLOGY 
 
 carditis in the class of cases observed." " The bacteria isolated, 
 while having little or no pathogenic power to animals, and 
 being susceptible to phagocytosis, present definite evidence of 
 being immunized against the antibodies of the individual host, 
 thereby perhaps overcoming the resistance of the latter." 
 
 In a series of cases of pneumococcus endocarditis studied by 
 Rosenow^ the mitral and tricuspid valves were mostly diseased, 
 a state of affairs which he attributes to the presence of capillaries 
 in these valves favoring embolism. 
 
 The exact distribution in Preble's cases of endocarditis in 
 pneumonia was as follows: 
 
 Per Cent. 
 
 Aortic only 56 39.7 
 
 Mitral only 40 28.3 
 
 Aortic and mitral 20 14.1 
 
 Tricuspid only 12 8.5 
 
 Pulmonary only 5 3.5 
 
 Aortic, mitral, and tricuspid 5 3.5 
 
 Mitral and tricuspid 2 1.4 
 
 Aortic and tricuspid 1 0.7 
 
 In Jurgensen's collection we find: 
 
 Peh Cent. 
 
 Aortic only 18.7 
 
 Mitral only G6.3 
 
 Aortic and mitral 9.2 
 
 Tricuspid only 0.4 
 
 Pulmonary only 2.3 
 
 Aortic, mitral, and tricuspid 1.0 
 
 Mitral and tricuspid 1.8 
 
 Aufrecht gives the following data regarding the distribution 
 in relation to age, as well as the distribution of pneumonia itself: 
 
 Pneumococcus 
 Number Endocarditis. Pneumonia. 
 
 Decade. of Cases. Per Cent. Per Cent. 
 
 First 2 1.4 1 6.8 1 
 
 Second 8. . . . 5.7 i 11.9 22.2 j- 58 
 
 Third 15 ... . lO.S J 29.0 J 
 
 Fourth •. 42. . . ..30.4 \ 17.0 ] 
 
 Fifth 27. . . .19.5 [70.9 13.0 1-35.5 
 
 Sixth 29. . . .21.0 J 5.5 J 
 
 Seventh and over 15 ... . 10. S 6.0 
 
 Chorea, another disease which has lately been added to the 
 list of infections, is a common cause of endocarditis. Thayer^ 
 
 ' Rocenow; Jour. Infect. Dis., 1909, p. 245. - Thayer: Jour. Am. Med. Assoc, 1906, p. 1352. 
 
ACUTE ENDOCARDITIS 21 
 
 in 689 cases of chorea found cardiac murmurs in 235 (40.5 
 per cent.); cardiac involvement was more frequent during second 
 attacl'vis and in those cases which had had rheumatic fever. 
 Forssner^ was able to trace the subsequent history of 28 chorea 
 cases for periods of from fifteen to twenty-two years, and found 
 that 5 showed pronounced heart disease, while 7 had died of it. 
 Among 35 cases of rheumatic fever thus followed, 17 developed 
 heart disease and 7 had died as a result. 
 
 The importance of the gonococcus as a cause of acute endocard- 
 itis has been justly much emphasized since the cultural demon- 
 stration of the organism in the blood during life, bj^ Thayer and 
 Blumer in 1895. Before that time the organism had been found 
 on the valves bj^ v. Ley den, and even as far back as the time of 
 Ricord and Brandes the association of endocarditis and urethritis 
 had been noted. In 1903 Kuelbs- collected from the literature 
 49 cases of endocarditis due to the gonococcus, in 28 of which the 
 aortic valve was affected, the mitral in 8, the pulmonary in 6, 
 and the tricuspid in 1. Gonococcus endocarditis is often very 
 severe, producing large vegetations, deep and extensive ulceration, 
 and at times myocardial involvement. Emboli appear to be 
 infrequent. It more freciuently complicates gonorrhea in the 
 male than in the female. Although disease of the mj'ocardium 
 and endocardium may be caused by this organism, endocardial 
 disease is more commonly the result of this infection. Sometimes, 
 however, mild attacks do occur, and in these the mitral valve is 
 more often involved. The severe form is usually associated with 
 other metastatic manifestations, such as arthritis, etc. At autopsy 
 grayish-red, easily detachable vegetations are usually found near 
 the margins of the valves, which occasionally extend to the en- 
 docardium beyond. The gonococcus is sometimes tinctorially, 
 less often culturally, demonstrable. Mixed and secondary in- 
 fections occasionally occur. Valvular involvement is generally 
 
 ' Forssru'r: .l.'iiiilj. f. J<inilcrlii'ill<., Jan., 1910, Ixxi. 
 - Kudb.s: Wicn, kliii. WoiJ]., l!l()7, .\x. 
 
22 STUDIES IN CARDIAC PATHOLOGY 
 
 not multiple. A lethal outcome is the rule, although some cases 
 recover. Irons^ states that there are now on record some 120 
 cases of gonorrheal endocarditis, in several of which pericarditis 
 was also found. The infarcts rarely suppurate and petechise 
 are infrequent. 
 
 Although the occurrence of endocarditis and tuberculosis 
 coincidently is by no means as exceptional as was once supposed, 
 and although verrucose endocarditis has been experimentally 
 produced by the tubercle bacillus,- yet true tuberculous endo- 
 carditis is distinctly rare. MarshalP makes five classifications 
 to cover the relationship of the two conditions. (1) Miliarj^ 
 tuberculosis; (2) true tuberculous endocarditis; (3) tuberculous 
 cardiac thrombosis; (4) tuberculous endocarditis secondarj^ to 
 mj^ocarditis; (5) toxic tuberculous endocarditis. 
 
 Unfortunately the majority of available statistics, including 
 my own,'' which deal with the occurrence of recent endocarditis 
 in pulmonaiy tuberculosis, give no information regarding the 
 microscopic findings or bacteriologic examinations. The frequency 
 with which this condition has been encountered is shown in the 
 appended tabulation : 
 
 Tuberculous Recent 
 
 Endocarditis. Per Cent. 
 
 Teissier 100 32 32.0 
 
 Schultze 6,937 67 0.966 
 
 Osier 216 12 ', r, 
 
 Kidd 500 6 1.2 
 
 Norris 1,764 16 0.9 
 
 Fenwick 1,560 13 0.7 
 
 Otto 185 4 3.1 
 
 Dittrich 403 1 0.24 
 
 11,665 151 1.2 
 
 Doubtless in the majority of the above cases the acute endocarditis was due 
 to other causes than the tubercle bacillus. In one of Osier's cases fresh tubercles 
 were found upon the mitral leaflet, but no tubercle bacilli could be demonstrated 
 in the sections. Kidd and Councilman also failed to find them. Even when 
 the bacilli can be demonstrated, it is perfectly possible that their presence is 
 
 1 Irons: Arch. Int. Med., 1910, p. 601. 
 
 - Michaelis and Blum: Deut. med. Woch., 1895. 
 
 ' Marshall: Johns Hopkins Hospital Bull, 1905, p. 303. 
 
 ■* Norris: .4m. Jour. Med. Sci., Oct., 1904. 
 
ACUTE ENDOCARDITIS 23 
 
 simply accidental, as a roughened endocardium would present a favorable 
 ground for the lodgment of micro-organisms carried thence by the blood-stream. 
 
 Slight degrees of simple sclerotic endocarditis are met with very commonly 
 in pulmonary tuberculosis, aiid are presumably due to the toxemia which is 
 present in the chronic variety of this disease. The researches of Auclair ^ have 
 shown that the metabolic products of the tubercle bacillus possess sclerogenetic 
 as well as necrogenetic properties, which would readily account for the endo- 
 cardial thickening. Boinet and Romary's - experiments indicate that bacterial 
 toxin, even in the absence of bacteria themselves, and without the addition of 
 trauma, are capable of producing changes in the endocardium and aorta. 
 
 "Ectasine," the vasodilatory substance which Bouchard has shown to be a 
 constituent of the tuberculous toxin, by producing vascular relaxation would 
 favor diapedesis of the leukocytes, thus paving the way for sclerogenous pro- 
 cesses. 
 
 Teissier has enunciated the behef that mitral stenosis is frequently produced 
 by the prolonged action of the tuberculous toxin upon the endocardium, which 
 in time results in a narrowing of the valvular orifice, and states that this form of 
 valvular lesion exerts an inhibitory effect upon the pulmonary disease. If such 
 an inhibition exists, it is more probably due to the increased resistance which the 
 bodily tissues have acquired through the prolonged presence of the toxin in the 
 system than to the mechanical action of the stenosis. Chartier ^ remarks that 
 this sclerogenous tendency is not tuberculosis, but the index of immunity versus 
 tuberculosis. 
 
 A tuberculous process may of course be engrafted upon a pre-existing val- 
 vulitis of different etiology, or the condition may be reversed. An interesting 
 case has been reported by Debove;* an incUvidual aged thirtj^-four years died 
 in a cachectic condition, and at autopsy tubercle bacilli were found in the blood 
 and in the mitral vegetations, no tuberculous lesions being encountered else- 
 where. 
 
 Heller, Cornil, and Kundrat were among the first to describe tuberculous 
 endocarditis, but the credit of the first definite and accurate report of this condi- 
 tion belongs to Tripier, who, in a case of miliary tuberculosis, found a small 
 nodule on the anterior leaflet of the mitral valve which showed the characteristic 
 cellular changes upon microscopic examination, as well as the tubercle bacillus 
 itself. Some time afterward v. Leyden reported four similar cases, in one of 
 which the condition was diagno.sticated ante mortem. Lion, and Londe and Petit 
 demonstrated tubercle bacilli in the valvular endocardium, but derived negative 
 re.sults from inoculation experiments. Similar results were obtained by Etienne, 
 de Thiry, Benda, Poncet and Dor, Ferrand and Rathery. Michaelis and Blum 
 were the first to succeed with inoculation by producing tuberculous endocarditis 
 in rabbits; and, finally, Braillon and Jousset demonstrated tubercle bacilli in 
 
 ' Auclair: Arch. mcd. cxpor., 1900, p. 189. 
 2 Boinet and Romary: Ibid., 1S57, p. 902. 
 ' Charlior: Rev. do la Tubcrculosc, Feb., 1904. 
 ' Debovo: Oa/„ deis Hopilaiix, 190.'i. 
 
24 STUDIES IN CARDIAC PATHOLOGY 
 
 the blood of a man dying of primary tuberculous endocarditis, the only other 
 evidences of this infection having been a few pleural adhesions. Tuberculous 
 endocarchtis usually assumes a verrucose, but sometimes an ulcerative form. 
 According to Benda, the majority of the cases have their origin in a miliary in- 
 fection, which happens to become localized upon the valves, being in this respect 
 analogous to the condition described by this author as tuberculous endangeitis. 
 In searching through the records of the Philadelphia Hospital among 1,606 
 tuberculosis autopsies two cases were found which were designated as "tuber- 
 culous endocarditis"; small tubercles had been found upon the valves, but ap- 
 parently no microscopic examination had been made.^ 
 
 The bacillus typhosus is one of the rarer causes of endocarditis. 
 When endocarditis occurs in typhoid fever, it generally results 
 from mixed infections. Experimentally endocardial lesions have 
 been produced by the typhoid toxin by Di Vecchi. As a rule, 
 however, the mj'ocardium suffers more in typhoid fever than the 
 endocardium, just as it does in diphtheria and in influenza. 
 
 Acute endocarditis in malaria is extremely rare. The mis- 
 conception regarding this fact has been due to the fact that the 
 chills and fever of malignant endocarditis have been mistaken 
 for plasmodial infection. 
 
 Subacute, insidious endocarditis occurs frequently in the 
 subjects of arteriosclerosis, chronic valvular, renal, or hepatic 
 disease, also in mild cases of rheumatic fever or of tonsillitis. A low 
 grade of endocardial inflammation continues for a long time, doing 
 more and more valvular damage, until finally attention is called 
 to the seriousness of the case by increasing fever, anemia, or an 
 attack of broken compensation. Blood-cultures in these cases 
 often yield streptococci of low virulence or of atypical appearance. 
 Slight degrees of fever of prolonged duration may be constantly 
 or intermittently present. - 
 
 Chronic Infective Endocarditis. — Osier has described a series 
 of ten cases, in one of which the process lasted thirteen months. 
 Of course, it is hard to differentiate between subacute and chronic 
 
 ' For further bibliographj' of tuberculous endocarditis see article by the author in Am. 
 Jour. Med. Sci., Oct., 1904. 
 
 - See "901 cases of Chronic Endocarditis with Especial Reference to Fever," J. S. Thacher, 
 Am. Jour. Med. Sci., ,Tan., 1906. 
 
Fig. 8. — Acute Infective Endocarditis. 
 
 Clixic^i. Notes: Case of a man aged twenty-one years, with the physical signs of aortic 
 and mitral insufficiency with nephritis. 
 
 Pathologic Notes: Acute infective endocarditis with hypertrophy and dilatation of the 
 heart. Passive oonKcstion of the lungs, hver, etc. 
 
 The heart weighs G70 gm. The aortic leaflets are covered with large vegetations of recent 
 origin. Similar although smaller vegetations are also found on the left ventricular wall and upon 
 the mitral valve. (Philadelphia Ho.spital, vol. xxi, p. 2.56. Physician: Dr. J. Sailor. Patholo- 
 gist: Dr. D. J. Wilson.) 
 
26 STUDIES IN CARDIAC PATHOLOCxY 
 
 cases. No exact dividing-line can be drawn between the point 
 at which a subacute infection ends and chronicity begins. In 
 the above mentioned cases, which were all fatal, embolic mani- 
 festations occurred in four, blood-cultures were sterile in three, 
 showed streptococci in two, and staphylococci in one instance. 
 
 Cultures made in 66 cases from the vegetations and heart's 
 blood in 107 cases of acute endocarditis at the Pennsjdvania 
 Hospital showed the following micro-organisms: 
 
 Diploeoccus lanceolatus 10 
 
 Staphylococcus pyogenes aureus 10 
 
 Bacillus coli communis 9 
 
 Streptococcus pyogenes 10 
 
 Pneumococcus 3 
 
 Bacillus typhosus 2 
 
 Micrococcus citreus 1 
 
 More than one species 6 
 
 Gonococcus 1 
 
 Meningococcus 1 
 
 Bacillus proteus vulgaris 1 
 
 A chromogenic bacillus 1 
 
 Atypical streptococcus 1 
 
 Unidentified species 1 
 
 Sterile cultures 7 
 
 Contamination 2 
 
 (In 41 no cultures were made.) 
 
 As compared with the diphtheria and the tubercle bacillus, the staphylo- 
 coccus pyogenes aureus shows much greater coagulogenetic power. ^ 
 
 These 107 cases occurred among 1,300 general autopsies. Valvular involve- 
 ment was as follows: aortic, 25; mitral, 47; both, 23; aortic, mitral, and tri- 
 cuspid, 2; mitral and tricuspid, 4; tricuspid, 3; pulmonic, 1 (gonococcus); all 
 valves, 2. Sixty-five of these cases showed also a chronic endocarditis, resulting 
 from previous infection (60 per cent.). In nearly every instance the acute in- 
 fection localized itself upon a valve which had already been diseased. 
 
 At the Philadelphia General Hospital among 8,640 autopsies, acute endo- 
 carditis occurred as follows: aortic, 164; mitral, 143; tricuspid, 15; pulmonic, 
 7; mural ulcerative, 6; vegetative, 5. 
 
 At St. Bartholomew's Hospital- among 19,904 medical in-patients there 
 were 115 cases of infective endocarditis. Valvular involvement was as follows: 
 Mitral only, 38; aortic only, 22; both, 63; mitral, aortic, and tricuspid, 14; 
 mitral, aortic, and pulmonic, 7; mural endocarditis — auricular 43, ventricular 8. 
 
 ^ Thorel: Lubarsch and Ostertag's Ergebnisse d. allg. Path., 1907, p. 483. 
 = Horder: Quart. Jour. Med., 1908, ii, 289, 324. 
 
ACUTE ENDOCARDITIS 27 
 
 Most of the cases occurred between the ages of twenty and forty years, the dis- 
 tribution between the sexes being about equal. 
 
 The cause of death in the last-named cases was as follows: Circulatory 
 failure, 66; coma, 23; sudden death from embolism or changes in the heart 
 itself, — rupture of aneurismal valves, septal perforation, rupture of the heart, — 
 19; uremia, 18; exhaustion, 8; dehrium, 5. 
 
 Embolism in endocarditis was unrecognized previous to Vir- 
 chow's description; since that time it has been considered one of 
 the most direful consequences of endocarditis. Emboh are clas- 
 sified, first, according to their origin as endogenous and exogenous, 
 and, second, according to their nature as simple or infective. In 
 a study of 250 cases of embolism occurring in heart disease at 
 the medical clinic at Zurich, Ginsburg^ found 110 cases (44 per 
 cent.) in men, 56 per cent, in women, the age distribution being as 
 follows : 
 
 10 to 20 years 8 cases, 3.2 per cent. 
 
 21 to 30 " 33 " 13.2 
 
 31 to 40 " 21 " 8.4 
 
 41 to 50 " 44 " 17.6 
 
 51 to 60 " : 59 " 23.6 
 
 61 to 70 " ' 59 " 23.6 
 
 Over 70 " 26 " 10.6 " 
 
 One hundred and ninety-eight occurred in cases of endocarditis, 30 in 
 cardiac hypertrophy and dilatation, 17 in myocarditis, 5 in simple "cardiac 
 insufficiency. " Among the first-named class the mitral valve was diseased in 
 100 cases (50.8 per cent.), the aortic in 19 (9.6 per cent.), the mitral and aortic in 
 43 (21.7 per cent.), the mitral and tricuspid in 14 (7 per cent.), the mitral, aortic, 
 and tricuspid in 17 (8.6 per cent.), the aortic and tricuspid in 1, and all valves in 
 2 instances. It will be noted that the left heart was the source of emboli in 79, 
 and the right in 13 cases. The distribution of the emboli was as follows: Kid- 
 neys, 62; spleen, 23; brain, 15; lungs, 14; mucosa of the intestines, 3. Sper- 
 ling's statistics based on 300 cases of endocarditis are much the same. In all, 
 embolism was noted in 84 cases ; in 76 cases left-sided lesions were the cause, the 
 distribution being as follows: Kidney, 57; spleen, 39; brain, 15; digestive 
 tract, 5; skin, 4. 
 
 Clinical Considerations. — While some of the severer cases of 
 acute endocarditis, with hectic fever, tachycardia, cardiac murmurs, 
 and local evidences of infarction are easily diagnosticated, the 
 le.ss fulminating cases are too easily and too often overlooked. 
 
 ' (liii.shuri;: Drul. .\rcli. f. kliii. Med., lOOl, l.\ix, 006. 
 
28 STUDIES IN CARDIAC PATHOLOGY 
 
 Recent investigations have shown that subacute bacteremia 
 with progressive endocardial inflammation may go on for weeks 
 and months while the patients are still up and about. From one 
 to five months may elapse between the onset of acute endocarditis 
 and the symptoms pointing to valvular lesions.^ All autopsy 
 statistics demonstrate the frequencj^ with which acute endocarditis 
 is diagnosticated as typhoid fever, uremia, chronic endocarditis, 
 pneumonia, malaria, influenza, tuberculosis, etc. In the hospital 
 
 ' Four cases with three autopsies, reported by Leclero, Lessieur, and Mouriquand, Lyon 
 Medic, 1906, No. 5L 
 
 Fig. 9. — Acute Mural Endocarditis. 
 
 F. F., female, aged eleven years. (Philadelphia Hospital. Physician: Dr. S. S. Cohen. 
 Pathologist: Dr. Funke.) 
 
 Clinical Notes: Previous diseases, measles, diphtheria, typhoid fever. 
 
 Physical Examination: Cyanosis, dyspnea, cervical pulsation, marked precordial 
 bulging, with a tremendous heavinp: pulsation. Apex-beat in the seventh interspace in the 
 anterior axillary hne. A prondumcil diastolic thrill is felt in the second and third interspaces. 
 Marked enlargement of the cardiac dulhicss to both right and left. Two murmurs are heard, 
 the diastolic being loudest at the pulmonic area. It is very high-pitched and transmitted 
 down the sternum. A loud, somewhat musical murmur is heard at the apex and transmitted 
 to the axilla, which does not quite replace the first sound. At the aortic area a faint tone is 
 heard suggestive of a friction sound. A loud systolic, probably tricuspid murmur is noted at 
 theensiform cartilage. The liver is enlarged, but does not pulsate. Hemoglobin, 4.5 per cent.; 
 erythrocytes, 2, .500,000. The urine contains albumin and hyalin and granular casts. Death 
 occurred gradually after a considerable hemoptysis, and with increasing failure of compensation. 
 
 Pathologic Diagnosis. — Acute ulcerative endocarditis of the mitral leaflets and of the 
 posterior wall of the left auricle. Perforation of the pulmonary leaflet. Adhesion of the aortic 
 leaflets. Hypertrophy and dilatation of right ventricle and of the left auricle. Atheroma of 
 the aorta. 
 
 Heart: Weighs 480 gm. The right auricle is distended with black blood-clots and its 
 cavity is large. Its wall measures O.o cm. at its thickest portion and its muscle is firm. 
 The endocardium is opaque and presents reddish discolorations in some areas. The mitral 
 orifice measures 3 cm. in diameter. The right ventricle has a separate apex and seems large; 
 its wall measures 1 cm., its color is bright red, and its endocardium is smooth and glistening. 
 The tricuspid leaflets show slight thickening along the hne of contact. The pulmonary valves 
 are incompetent owing to a perforation in the posterior leaflet. The left auricle is very large; 
 its muscle, which is firm and pale, measures 5 mm. Beginning at the mitral orifice and extend- 
 ing along the posterior wall of the auricle is an area 4 x 6 cm., of closely set, irregidar, pinkish 
 vegetations, many of which measure 3 mm. in height, and which have somewhat the appearance 
 of necrotic bone. The left ventricle is also large, has a distinct apex, and measures 16 mm. in 
 thickness. On the anterior surface of the ventricular endocardium are two irregular circular 
 areas, one measuring 6 mm., the other 3 mm. in diameter, consisting of elevated granular, 
 pinkish vegetations. The smaller of these is superficial; the larger extends almost to the 
 pericardial surface. The auricular aspect of the mitral valve presents an appearance similar 
 to that of the posterior wall of the left auricle. The edges of the leaflet are comparatively 
 smooth, although vegetations are occasionally noted. At the junction of the posterior and 
 internal leaflets a perforation is seen. 
 
 (Photograph by Dr. A. R. Allen.) 
 
30 STUDIES IN CARDIAC PATHOLOGY 
 
 statistics this point is certainly underestimated, because of the 
 greater facilities for laboratory methods at the command of the 
 clinicians in a modern hospital. Blood-cultures when carefully 
 and repeatedly made are of the greatest assistance in arriving 
 at correct conclusions. 
 
 Among 107 cases of acute endocarditis autopsied at the Penn- 
 sylvania Hospital the endocarditis was correctly diagnosticated 
 in 24 instances. In many cases the true condition was completely 
 overshadowed by other conditions. The following diagnoses 
 were recorded: typhoid fever, 12; pneumonia, 9; chronic en- 
 docarditis, 14; septicemia, 3; chronic nephritis, 4; acute peri- 
 carditis, 3; miliary tuberculosis, 1; congenital heart disease, 1; 
 rheumatic fever, 1; renal calculus, 1; asthma, 3; etc. Nine 
 cases were admitted in a moribund condition, and no diagnosis 
 established. These figures cast no reproach upon the physicians 
 of the hospital, who, as is well known, stand in the foremost 
 rank of the Philadelphia medical world. They merely illustrate 
 the insidious nature of the pathologic process which we have been 
 discussing. It should also be borne in mind that in the vast 
 majority of these cases the diagnoses made were correct. The 
 endocarditis was simply a complication of other diseases, which 
 did not manifest itself b}^ prominent sj^mptoms or physical signs. 
 
 CHRONIC INFECTIVE ENDOCARDITIS 
 
 Bacteriology. — Horder,"^ who has been more fortunate than 
 most other investigators, states that with careful technic, positive 
 blood-cultures can be obtained intra vitam sooner or later in 
 90 per cent, of all cases of infective endocarditis. He has published 
 analyses of 40 cases, in 27 of which the bacteriologic findings were 
 substantiated at autopsy as follows: Streptococcus, 26; bacillus 
 
 'Details of Herder's technic, Practitioner, Nov., 190.5. "Treatment with Vaccines" 
 (Horder), Practitioner, 1908, p. 714. Positive blood-cultures in 28 consecutive cases: Strep- 
 tococcus, IS; bacillus influenzie, 5; pneumococcus, 3; gonococcus, 1; staphylococcus, 1. 
 Hence the streptococcus type caused 65 per cent., or, if including pneumococcus, 77 per cent., 
 of all cases. See also Libman and Celler (43 cases) : Trans. Assoc. Amer. Phys., May, 1910. 
 
ACUTE KNDOCARDITIS 31 
 
 influenzae, 5; pneumococcus, 5; gonococcus, 2; staphylococcus 
 albus, 1; unidentified, 1. 
 
 It will be observed that the genus streptococcus causes 77 
 per cent, of the cases (some 6 cases in which bacillus influenzae 
 was successfully cultivated from blood are now on record). He 
 quotes 100 postmortem cultures from the heart's blood as corrob- 
 orating his intra- vitam findings. 
 
 Following surgical infections the staphylococcus aureus is 
 more frequent. These infections, which are seen in osteomyelitis, 
 etc., are often rapidly fatal. Differentiation of the varieties 
 of streptococci based upon certain metabolic reactions seems to 
 show that the streptococcus generally found in endocarditis is 
 not the same species which is found in acute suppurative conditions. 
 
 Border's investigations indicate that infective endocarditis 
 is generally due to streptococci of low virulence, such as those 
 normally found in the saliva and the intestinal tract, a fact which 
 explains the jDrotracted insidious character of this so frequently 
 overlooked process. "It may be that the very lowness of the 
 virulence of these habitual saprophytes of the alimentary canal 
 accounts for the lack of efficient resistance on the part of the 
 patient, there being no adequate stimulus to call forth the de- 
 fensive mechanisms necessary for the destruction of the cocci" 
 (Horder) . 
 
 Horder suggests the following classification : 
 I. Latent infective — a terminal condition, in old valvular 
 cases, etc. 
 
 II. Fulminating infective. 
 
 III. Acute infective — the clinical picture is that of pneumonia, 
 it is often due to pneumococcus. 
 
 IV. Subacute infective — the commonest variety associated 
 with a gradual development of dyspnea, weakness, arthritis or 
 chorea, etc., lasting from two to six months. 
 
 V. Chronic infective: Insidious — ambulant cases — organisms 
 of low virulence — streptococcus fecalis often found. 
 
32 STUDIES IN CARDIAC PATHOLOGY 
 
 The valvular form of syphilitic endocarditis, except when it 
 follows aortitis, is generally secondary to syphilitic myocarditis as 
 the result of direct extension. Parietal lesions are more frequent 
 than valvular alterations. Macroscopically they often show no 
 sclerotic changes. Occasionally, however, as in a case reported 
 by Duckworth/ minute gummata occur. The seat of predilection 
 
 ' Duckworth: Lancet, 1895. 
 
 Fig. 10. — Acute Ulcerative Mitral and Aortic Endocarditi.s. 
 
 Negro. (Pennsylvania Hospital. Autopsy No. 328. Pathologist: Dr. Longcope. 
 Physician: Dr. A. Stengel.) 
 
 Clinical Notes: Twenty-three years old. Denies venereal disease. Has never been 
 ill before, except with pneumonia six months ago. For the last four days has had dyspnea, 
 chills, and vomiting. 
 
 Heart dullness much enlarged. Apex-beat forcible and diffuse. Systolic thrill near apex. 
 Pulmonic second sound accentuated. A loud, long, diastolic murmur over the heart, and 
 through both sides of the chest. 
 
 Pathologic Notes: Acute ulcerative mitral and aortic endocarditis. Acute myocarditis; 
 acute hemorrhagic pericarditis, etc. 
 
 Heart: is much enlarged; feels like thick-walled cyst, and is rather rounded in shape. 
 It collapses about the hand when held at the apex. Epicardium: irregular areas of opaque, 
 white thickening over surface of left ventricle. Sometimes these follow the vessels, which 
 are otherwise not very prominent. Beneath the endocardium, heart has mottled yellow 
 appearance, and shows numerous ecchymotic hemorrhages at the vascular terminations. 
 Tricuspid and pulmonary valves normal; the orifices measure respectively 13 and 7.5 cm. in 
 circumference. Right ventricle, 4 mm., left ventricle distended by clot. Left auricle slightly 
 dilated. Mitral valve is seat of extensive ulcerative endocarditis; the vegetations, situated especially 
 on,' the auricular surface, are yellowish, soft, and friable. They frequently measure 1 cm. in diam- 
 eter, and project high above the valve surface. Smaller vegetations on the surface of the auricle. 
 From the free border of the aortic valves two large pendulous thrombi hang into the ventricle, 
 measuring 2 cm. in length, the valve being much ulcerated at their point of attachment, the 
 thrombi covering the ulceration. On the endocardium of the ventricle there is a patch 2 cm. in 
 diameter below the insertion of the aortic valves, covered with small yellowish accumulations. 
 Aortic valves thickened and ulcerated along their free margins. Heart-muscle soft and friable, 
 pale brownish-gray. Sprinkled through the section are minute yellow points; one or two large 
 ones (1 to 2 cm. in diameter). Papillary muscles and columnce carnece of both ventricles much 
 fliUened. Left ventricle 1 cm. Definite cardiac contractions are elicited by pinching muscle 
 with forceps; especially is this true of the papillary muscles (one and three-fourths hours after 
 d3ath). 
 
 Microscopic Examination: Muscular strise poorly marked. Nuclei: large, pale, in- 
 dsSnite, and in some places surrounded by clear spaces. Muscle-cells show moderate frag- 
 mentation; many are filled with large vacuoles. Slight hemorrhages are scattered through 
 the SBction, beneath the endocardium and pericardium. They are fairly extensive. The 
 vacuole-like degeneration is most marked near the hemorrhages, and everywhere occurs in 
 patches. At one point a mass of polymorphonuclear leukocytes is seen in the myocardium; 
 surrounding it there are some hemorrhages and much degeneration of muscle-cells. In the 
 mass of muscle degeneration the muscle-nuclei have entirely disappeared. 
 
 Acute parenchymatous degeneration of the myocardium. 
 
 The pneumococcus was obtained from the heart's blood and the vegetations. 
 
34 STUDIES IN CARDIAC PATHOLOGY 
 
 seems to be the left ventricle. When the valves are attacked, 
 the lesions are often limited to a valve or part of a valve. Sclerotic 
 changes — retraction, etc. — ultimately result. Taneff^ collected 
 95 cases of syphilitic endocarditis, in 10 of which, however, the 
 etiologic factor was questionable.- (Compare chapters on aortic 
 endocarditis and cardiac syphilis.) 
 
 Trauma may produce valvular lesions in two ways: Either 
 (a) by rupture of a papillary muscle or chorda tendinese, or 
 (6) by rupture of the endocardium, with the production of thrombi 
 or subendothelial hemorrhages. Injuries which produce such 
 valvular damage generally consist of crushing forces or violent 
 blows. It is verj^ doubtful whether mere sudden increase in 
 vascular tension as a result of heavy lifting, etc., is capable of 
 rupturing an}" part of a healthy heart. Such cases are reported, 
 but are presumably the result of localized weakening through 
 antecedent pathologic processes. Blows inflicted in the precordial 
 
 ' Inaug. Dissert., Berlin, 1896. 
 
 -Complete literature by Herxheimer: Lubarsch and Ostertag's Ergebnisse der allg. 
 Path., i, 1906. 
 
 Fig. 11. — Acute Vegetative and Chronic Endocarditis. 
 
 W. R., male, aged forty-six years. (Pennsylvania Hospital. Autopsy 1165. Physician: 
 Dr. J. A. Scott. Pathologist: Dr. Krumbhaar.) 
 
 Clinical Notes: The patient, who is an alcoholic, has been ill for two days with cough 
 and chills. Lungs: full of rales. An apparent pulmonary consolidation at the left base. 
 Cyanosis, tremors. Heart negative. Death two days later, suddenly, apparently from acute 
 cardiac dilatation. 
 
 Pathologic Diagnosis. Lobar pneumonia. Acute vegetative and chronic endocarditis. 
 Pulmonary congestion and edema. 
 
 Pericardium: Contains 30 c.c. of turbid yellow fluid, with a few fibrinous flakes. 
 
 Heart: The heart is much enlarged (490 grams), especially to the right. It is greatly 
 distended with currant-jelly and pinkish chicken-fat clots. Except for a patch of thickening 
 on the posterior surface, the epioardium is negative. The mitral orifice admits three fingers. 
 Tlieh-fl nnlrirtc is enlarged, and measures from 1 ', In IS mm.: it is somewhat pale and friable. 
 The iniliiiMrdium is smooth. All three aorlir i-iisp.': .ilmir mnrkedly a vegetative growth. The 
 cusp opposite the right coronary artery shows tlic :;iiiiillisl rvijcldlton, which is limited to the cardiac 
 side of the valve. The growth is yellomsh, irregular, nodular, and in some places calcareous, the 
 greater part, however, being semitransparent, soft, and friable. The vegetations on the other valves 
 are soft and gray. They are irregularly nodular with a finely granular surface. One of them, 
 measures 1 cm., the other 2.5 cm. in length. The large vegetation has a base about 1 cm. in breadth, 
 so that it is freely movable in the left ventricular cavity. The mitral valve shows slight thickening. 
 The aortic cusp at the highest point of its attachment shows a similar thickening. The coronary 
 arteries are large, thin, and patent. The valvular orifices measure as follows: Tricuspid, 12 cm.; 
 mitral, 12 cm.; pulmonary, S cm.; aortic, 8.5 cm. 
 
36 STUDIES IN CARDIAC PATHOLOGY 
 
 region may produce endocardial, pericardial, or myocardial lesions, 
 even when the skin and thorax remain uninjured. Among 34 
 animals experimentally studied by Kuelbs^ the following lesions 
 were produced: valvular damage, 21; distributed — mitral 12, 
 aortic 7, tricuspid 5, pulmonic 4. All of these lesions were hem- 
 orrhagic. Actual valvular rupture occurred once. In no instance 
 were any of the chordse tendinese torn. Mj^ocardial damage 
 followed in 15 cases and consisted chiefly of hemorrhages or tears 
 in the septum. In one case there was cardiac rupture. The 
 pericardial lesions were eleven in number, mainly hemorrhagic in 
 character. None of the cases showed loss of compensation, and 
 onl}^ rarely were murmurs present. Experimental valvular lesions 
 in animals show a very marked tendenc}' to rapid healing with 
 simple scar tissue formations.^ If there is a chance for infection, 
 
 ' Kuelbs: Mitt. a. d. Grenz. der Med. u. Chir., 1909, p. 679. 
 
 - For trauma as a cause of endocarditis, etc., see : Stern, Ueber die traumatische Entstehung 
 innerer Krankheiten, vol. i; Thorel, Lubarsch and Ostertag's Ergebnisse, 1907, ii, 434; Drey- 
 fuss, These de Paris, 1896; Heimann, Dissert. Berlin, 1896; Sinnuber, Deut. med. Woch., 
 1904, No. 32; Frankel, Miinch. med. Woch., 1905, No. 15; Marcus, ibid., No. 47; Herzfeld, 
 Jour. Am. Med. Assoc, 1906, p. 855. 
 
 Fig. 12. — Ulcer.\tive Aortic Endocarditis. 
 
 I. S., male, white, aged forty-eight years. (Pennsylvania Hospital. No. 320 (1902). 
 Autopsy 189. Pathologist: Dr. Longoope.) 
 
 Pathologic Diagnosis: Ulcerative aortic endocarditis. Globular throinbus attached to 
 aortic value. Extensive multiple thrombosis of arteries and veins. Acute bronchopneumonia. 
 Chronic pulmonary tuberculosis, etc. 
 
 Heart: The heart is quite small, weighs 250 grams. The epicardium contains a moderate 
 amount of fat and two milk patches. The tricuspid, pulmonary, and mitral valves are normal. 
 The left ventricle is very small, measuring only 7 cm. from the aortic valve to the tip; it is 15 
 mm. in thickness. On the mitral cusp of the aortic valve is a large globular thrombus which meas- 
 ures 2 cm,, in diameter, being firmly attached to the outer portion of the valve. It projects into the 
 aortic orifice, forming as it were a complete plug for it, when the valves are in normal position. 
 It is mixed red and gray in color, somewhat tabulated and firm. The sinus of Valsalva of the 
 valve is filled with a recent thrombus of similar character which projects about 8 mm. above the velum 
 of the valve. The two globidar thrombi are joined by a fibrinous band. The portions of the leaflet 
 which are uninvolved are thin and delicate, as is also the velum. The other two valve cusps 
 are a trifle thickened, but still delicate and evidently competent. The heart muscle is brown 
 and firm; and the endocardium is slightly flecked with yellow. The aorta is small. The 
 coronaries are patent. 
 
 Microscopically the thrombi consist largely of erythrocytes and fibrin: 
 
 Bacteriologic Diagnosis: Heart's blood: Sterile after forty-eight hours at 36.5° C. 
 Thrombi on aortic valve : Streptococcus pyogenes. Lung: Micrococcus lanceolatus. Throm- 
 bus from vena cava; Bacillus coli. 
 
38 STUDIES IN CARDIAC PATHOLOGY 
 
 however, as when the animals are kept in dirty kennels, these 
 injured valves not infrequently become the seat of an acute 
 endocarditis. 
 
 A considerable number of instances of traumatic valvular 
 disease have been recorded, as, for instance, a case of Schmidt's^ 
 of an aged patient falling out of a second-story window and rup- 
 turing the aortic and mitral valves. 
 
 The danger of trauma, then, in relation to endocarditis is 
 twofold. It may reactivate a quiescent lesion, or it may prepare 
 the soil of a previously healthy endocardium for subsequent in- 
 fection. Its action may be direct, through the force of a blow, 
 or indirect, as the result of suddenly increased blood-pressure. 
 
 The endocardial changes following infectious endocarditis are 
 in some respects different from those due to purely mechanical 
 causes, as in chronic valvular disease. Thus, for instance, in 
 the latter case the line of valvular closure of the leaflets shows the 
 principal changes; in the former, the free margins are involved. 
 
 ' Schmidt: Miinoh. med. Wooh., Sept. 23, 1902. Claisse and Socquet report the case of a 
 healthy man of forty-eight years who was crushed on the chest by a heavy stone which he was 
 trying to lift into place. The injury was followed by sudden pain and dyspnea. At autopsy 
 five months later a ruptured papillary muscle was found. (Bull, et Mem. Soc. M6d. des Hop. 
 de Paris, 1908, p. 769.) Another case was reported by Marcus. (Mlinch. med. Woch., 1905, 
 p. 228). 
 
11. CHRONIC ENDOCARDITIS 
 
 The term "chronic endocarditis" as currently applied is 
 ambiguous. It should, of course, be limited to those cases in 
 which an acute endocarditis has become established as a continuous 
 progressive process; but often it is employed to designate an 
 old endocardial lesion, even of the arteriosclerotic type, the course 
 of which may have been completely arrested. On the other hand, 
 we must bear in mind that in many apparently quiescent cases 
 active inflammation due to organisms of low virulence or the 
 fibrogenic activities of an antecedent inflammation may still be 
 operative. 
 
 The term chronic endocarditis is generally applied to a fibrotic 
 process which follows an acute infection. About one-half of the 
 cases of valvular heart disease arise in this manner, the remainder, 
 with negligible exceptions, resulting from the arteriosclerotic 
 changes of advancing life. As in other parts of the body, destruc- 
 tion of tissue is followed by the formation of scars, which on the 
 endocardium produce deformities of the valves and their orifices 
 by contraction, induration, puckering, and adhesion, and ulti- 
 mately in some cases calcification. In this manner valvular 
 obstruction and insufficiency may be developed. 
 
 In the mitral area the occurrence of adhesions tends to fuse 
 together the valvular curtains, and if the chordse tendinese are also 
 involved, a funnel-shaped orifice results. Skrinking and fibrosis 
 continue, thus bringing about more and more induration, shorten- 
 ing, and stiffening. If only partial union of the free lateral valve 
 margins occurs, a sfit-like opening is left — the "buttonhole mitral." 
 The anterior flap of the mitral is most frequently and extensively 
 involved, especially in the region nearest to the aortic valve, 
 where the greatest strain occurs owing to the auriculo-ventricular 
 and the vontriculo-aortic blood-stream. Organic mitral disease 
 
40 STUDIES IN CARDIAC PATHOLOGY 
 
 generally follows infectious endocarditis, while, excepting syphilis, 
 aortic lesions are more often the result of arteriosclerosis. Mitral 
 stenosis also is verj^ commonly a sequel of endocarditis; pure 
 insufficiency is less often. Contraction and induration result 
 from the organization of granulation tissue, and in this process 
 the chordse tendinese and the papillary muscles often share. 
 Calcification which results from the deposition of lime salts in the 
 diseased areas produces roughness and inflexibility. In this process 
 the aortic valves, especially about the corpora Arantii and along 
 the free margins, are chiefly affected. In all cases of valvular 
 damage the amount of calcium ions in the blood plays an important 
 part in the degree and extent of the lesions produced. This 
 process of calcification is nature's method of repairing weak spots 
 and leaks, and in robust plethoric individuals she often overplays 
 her part. As Sir James Barr puts it in speaking of the calcium 
 ions in relation to mitral stenosis: "They raise blood-pressure, 
 increase the force of the cardiac contractions, give rise to hyper- 
 trophy of the papillary muscles, cause violent collision of the 
 mitral cusps, increase the formation of fibrous tissue, and gradually 
 cement and unite the edges of the cusps together." 
 
 In sclerotic endocarditis not only the valvular leaflets, but 
 also the chordse tendinese and papillary muscles are affected. 
 
 Fig. 13. — Acute Vegetative and Ulcerative Aortic and Mitral Endocarditis. 
 
 W. G., male, aged fifty-six years. (Philadelphia Hospital, vol. xviii, p. 142. Physician: 
 Dr. R. G. Curtin. Pathologist: Dr. Guthrie McConnell.) 
 
 Clinical Notes: A paroxysmal drunkard; was admitted with cough, edema, and dysp- 
 nea. 
 
 Physical Examination. — Heart is enlarged to right and left. A systolic murmur is 
 heard at the apex and transmitted to the axilla. A doubtful systolic murmur is heard at the 
 aortic area. The second sounds at the base are indistinct. The patient developed uremic 
 symptoms and died suddenly during an attack of coughing associated with marked cyanosis. 
 
 Pathologic Diagnosis: Acute vegetative and xdcerativc aortic and mitral endocarditis. 
 Cardiac hypertrophy, hydrothorax, ascites, chronic parenchymatous nephritis, etc. 
 
 Heart: Weighs 620 gm. The middle leaflet of the aortic valve shows a vegetation 13 x 10x3 
 mm., soft in consistence, reddish-yellow in color. Smaller vegetations are seen on the other leaflets 
 and on the mitral valve, the anterior curtain of which shoxvs a circular ulcerated area, 10 mm. in 
 diameter, the central portion of which has completely perforated the leaflet. The auricular surface 
 is covered by a large irregular vegetation. The chorda; tendinece show many pinhead-sized 
 vegetations. The pulmonary valves are normal. The tricuspid orifice is dilated. 
 
42 STUDIES IN CARDIAC PATHOLOGY 
 
 Lowenstein^ in a study of the fibrosis of the latter was led to con- 
 clude that these fibroid changes are secondary to previous muscular 
 degeneration, a process to which this part of the cardiac muscula- 
 ture seems to be especially susceptible. Actual bone formation 
 in the valves and even the heart itself has been described. 
 
 Frequency. — The frequency of valvular disease and the type 
 vary considerably in different statistics, at different ages, in the 
 two sexes, and according to the etiologic factor. Thus, under 
 forty years of age, especially in women and in children, and as 
 the result of rheumatic endocarditis, mitral lesions are in pre- 
 ponderance. After forty years of age, and in men (especially 
 syphilitics and arteriosclerotics), aortic lesions assume the pre- 
 dominating role. Andrew among 1,474 cases of heart disease 
 found 887 (60.1 per cent.) in men, and 587 (39.8 per cent.) in 
 women. Endocardial lesions — acute and chronic — formed 87 
 per cent, of the total number of cardiac ailments (pericardial 
 5.4 per cent., myocardial 5.5 per cent.). The greatest number of 
 chronic mitral cases occurred between twenty and thirty years, 
 of aortic disease between forty and fifty years, and degenerative 
 myocardial changes after fifty years.- The statistics of Bollinger 
 and of Eulenburg show that well-marked disease of the cardiac 
 valves or orifices occurs in from 5 to 10 per cent, of all autopsies. 
 
 From a morphologic standpoint Dewitsky^ has formulated the 
 five following types of chronic valvular lesions: 
 
 I. Diffuse infiltration of the leaflets: an extension from the 
 endocardium, inflammatory in character, the terminal phase of 
 an acute endocarditis. 
 
 II. Lesions on the valvular edges: resulting from hyper- 
 trophy of the subendothehal layer, caused by relative insufficiency 
 of the valves affected. 
 
 III. Lesions at the base of the leaflets: a quasi-physiologic 
 process found with increasing frequency as life advances. 
 
 ^ Lowenstein: Centralb. f. allg. Path. u. path. Anat., 1907, p. 385. 
 
 ^Andrew: "Age Incidence, Sex and Comparative Frequence of Disease," London, 1909. 
 
 ' Dewitsliy: These du Mo.scow, 1908. (See also Virchow's Archiv, 1910, excix.) 
 
CHRONIC ENDOCARDITIS 
 
 43 
 
 IV. Lesions found only on semilunar valves: arteriosclerotic 
 
 in nature and extending from the vascular wall to the leaflets. 
 V. Lesions on the free border of the aortic valve: resulting 
 
 from thrombotic changes initiated by an acute endocarditis 
 
 (infectious). 
 
 (These types, though distinct, are often mixed.) 
 
 From a clinical standpoint the relative involvement of different 
 
 valves has been reported as follows : 
 
 Ashton (Med. News, June .30, 
 
 1894) 
 
 Crook (N. Y. Med. Jour., 1897, 
 
 821). 
 
 Satterthwaite (Dis. of Heart and 
 
 Aorta) 
 
 Chambers (Med. Times and 
 
 Gazette, 1852) 
 
 Bamberger (Virchow's Arch., ix, 
 
 p. 524) 
 
 Schnitt (Dissert. Jena., 189-3) . . 
 Leuch (Dissert. Zurich, 1889) . . 
 Hirsch, (Mitt. a. d. Med. Khnik, 
 
 Wurtzb , vol. ii, p. 305) . . . 
 Koster (Dissert. Gottingem, 
 
 1883) 
 
 Leuch 67 
 
 Guttmann (Dissert. Breslau 
 
 1891) 13961 
 
 SperHng (quoted Gibson) i 300 
 
 Middleton (Lancet, 1889) . 
 
 Sansom \ 300 
 
 Lambert (J. A. M. A., 1908) . . . . i 283 
 
 Olsen 
 
 Pennsylvania Hospital (autop- 1 
 
 sies) ! 274 
 
 1024 
 
 478 
 
 65 
 
 367 
 
 211 
 210 
 241 
 
 203 
 
 116i 
 
 63 
 
 7 
 
 13 
 
 13 
 
 934 
 
 283 
 
 1.57i 40 
 
 801 20 
 
 255! 129 
 
 2.32 124 
 
 29 1 26 
 
 84 
 
 114 
 
 3226 
 
 1315 
 
 gf^ 
 
 4 12 5S 
 116 68 691 
 
 A valvular aneurism consists of a "circumscribed pouching 
 (jf onf of the valve segments." Two varieties are met with: 
 
 (a) In which the whole thickness of the leaf is pouched. 
 
 (b) In which as the result of ulcerative endocarditis the lamellae 
 of tlic valves have become dissected apart. 
 
44 STUDIES IN CARDIAC PATHOLOGY 
 
 Valvular aneurisms vary in size from a small lentil to a small 
 pigeon's egg, and are occasionally multiple. The mitral valve 
 is most frequently attacked and shows the largest aneurisms, 
 although rupture occurs more frequently when the aortic valves 
 are involved. In some chronic cases, instead of rupture, thrombosis 
 of the sac occurs. (See Fig. 14.) 
 
 Clinical Considerations. — Given a case of valvular heart 
 disease, the practitioner is called upon to determine a number of 
 questions: The site of the lesion, whether it is obstructive, or 
 regurgitant, or combined; whether more than one valve is in- 
 volved. What is the severity of the lesion as regards actual 
 mechanical effects? What is the cause of the lesion — infectious, 
 arteriosclerotic, or merely functional? Is it apt to be progressive? 
 and if so, how rapidly? Is the actual infection still continuing? 
 The importance of the last question cannot be overestimated, 
 and it is bj' no means easily answered. As has already been 
 stated, the infection often goes on insidiously for months. Thacher 
 has called attention to the persistence of fever in many of these 
 cases, and Coleman has pointed out how exactly the fever curves 
 may simulate different tjqoes of malarial infection.^ With the 
 possible exception of the last question the following is the most 
 important of all: What is the state of the mj'ocardium, — how 
 much actual damage has it sustained, either from the infection 
 or from the degenerative changes of age, syphilis, tobacco, etc.? 
 The French have an axiom which well emphasizes this : "A disease 
 of the valves is not a disease of the heart." 
 
 As to the duration of life, this of course varies greatl.y. In 
 Romberg's clinic one patient was known to have lived thirty-eight 
 years with a valvular lesion. Sir Andrew Clark in a study of 
 700 cases found that often there was practically no shortening 
 of life. The emergencies of life and infectious processes are less 
 well withstood. 
 
 When cardiac failure does occur, it is hj no means rarely due 
 
 ' Amer. ,Jour. Mod. Sci., March, 190.5. 
 
Fig. 14, — Large Aneurism of the Mitral Valve with Fenestration. 
 
 Bulging into the auricular cavity. (Specimen from tlie University of Pennsylvania 
 
 Museum.) 
 
46 STUDIES IN CARDIAC PATHOLOGY 
 
 to chronic infection, at least this is Stein's^ conclusion, and this is 
 borne out by the results of artificially produced valvular lesions 
 in animals. 
 
 While combined valvular lesions are often doubly disad- 
 vantageous, they may to a certain extent be beneficial and com- 
 pensating. Thus an aortic obstruction added to an insufficiency 
 may to some extent prevent left ventricular dilatation; the 
 mitral insufficiency which is sometimes engrafted upon an ob- 
 struction represents a certain grade of healing (Krehl) . 
 
 Heredity. — A hereditary tendency to certain forms of heart 
 disease seems to exist. Perhaps the best known type is that 
 described by Huchard as "aortism," by which is meant the well- 
 known plethoric, hypertensive, ultimately arteriosclerotic type 
 of man who dies suddenly of apoplexy, and in whose family this 
 history is very common. 
 
 The term "myocardism" has been suggested by Galli for 
 the type of individual in whose familj^, although demonstrable 
 arteriosclerosis is not a prominent feature, there is a tendency 
 toward myocardial weakness and degeneration.'- Virchow and 
 Beneke pointed out that a small arterial system predisposed to in- 
 fectious endocarditis. 
 
 The term "mitralism" has also been suggested as descriptive 
 of a tendency to lesions, more especially stenosis of this orifice. 
 
 STATISTICAL DATA FROM THE PENNSYLVANIA AND THE PHILADELPHIA 
 
 GENERAL HOSPITALS 
 I. Endocardium. 
 
 -_. , T- T Pennsylvania Philadelphia 
 
 Mitral Valve. Hospital. Hospital. 
 
 Acute simple endocarditis of mitral alone 
 
 Acute vegetative endocarditis of mitral alone : \ 47 
 
 58 
 
 Acute ulcerative endocarditis of mitral alone J J 
 
 Acute mitral and aortic endocarditis 23 33 
 
 Acute mitral and tricuspid endocarditis 2 4 
 
 Acute mitral, tricuspid, and aortic endocarditis 2 
 
 Aneurism of mitral valve (with rupture) 1 
 
 Anomaly of mitral valve (1 fenestration, 1 pouching, 1 su- 
 pernumerary leaflets) 3 
 
 [Table continued on p. 48.) 
 
 ' Stein: Nordschr, Med. Arch., 190.5, xlii. ■ Galli: Berlin, klin. Woch., 1907, p. 372. 
 
Fig. 15. — Chronic Mitral .\nd Thictjspid Endocarditis. 
 
 B. S., female, negro, aged twenty-one years. (Philadelphia Hospital. Autopsy vol. xviii, 
 p. 1.54. Physician: Dr. Hughes. Pathologist: Dr. McConnell.) 
 
 Clinical Notes: Acute rhewnatic fever ionr years a.go, and again two years ago. Severe 
 leukorrhea for last four years. Denies syphilis, but shows what are apparently luetic scars. 
 Alcohol moderately. Four years ago began to have vertigo and d3'spnea, which have grad- 
 ually increased in frequency and intensity, and were generally induced by exertion. For last 
 few months has also had cough, gastric symptoms, and muscae volitantes. 
 
 Heart dullness enlarged. Presystolic thrill within the apex, at which area a double mitral 
 murmur is heard. Both second sounds are accentuated, especially the pulmonic. Pulse 110. 
 Death occurred gradually from pulmonary congestion. 
 
 Pathologic Diagnosis: Chronic mitral and tricuspid endocarditis; chronic pleuritis; 
 right-sided hydrothorax; congestion and edema of right lung; bilateral pulmonary infarction; 
 diffuse nephritis. 
 
 The pericardium contains a small amount of fluid. 
 
 Heart: weighs 340 gm. Aortic leaflets, thin and transparent. Mitral orifice barely 
 tulmils lip of index-finger; its leaflets are much thickened. The lips of the papillary muscles show 
 marked fibrosis. Pulmonary leaflets normal. Tricuspid orifice (the lowermost on plate) i.s 
 small; leaflets thickened, and on free edges are numerous vegetations. On one leaflet there is a 
 vegetation one inch in height, which extends directly into the opening. 
 
48 
 
 STUDIES IN CARDIAC PATHOLOGY 
 
 Statistical Data from the Pennsylvania and the Philadelphia General Hospi- 
 tals — {Continued) 
 
 I. Endocardium. Mitral Valve— (Continued). "^'hosJitYl'"" ^ HotpfT™''* 
 
 Hematoma of mitral valve 1 1 
 
 Calcification of mitral valve 112 
 
 Stenosis of mitral valve 72 
 
 Rupture of mitral valve 1 
 
 Aortic Valve. 
 
 Acute vegetative endocarditis of aortic alone \ o- -sn 
 
 Acute ulcerative endocarditis of aortic alone J 
 
 Acute aortic and tricuspid endocarditis 
 
 Acute aortic and pulmonary endocarditis 3 
 
 Aortic stenosis 6 42 
 
 Aortic fenestration 2 43 
 
 Aortic calcification (ossification) 1 1 
 
 Aortic anomaly (bicuspid valve) 2 3 
 
 Aortic valvular aneurism (with rupture) 1 
 
 Acute endocarditis of all valves 2 16 
 
 Subendocardial hemorrhage 13 
 
 Subendocardial cyst 1 1 
 
 Tricuspid Valve. 
 
 Acute vegetative endocarditis of tricuspid alone \ „ ^_ 
 
 Acute ulcerative endocarditis of tricuspid alone > 
 
 Subacute endocarditis of tricuspid 2 
 
 Anomaly (pouching) 1 
 
 Supernumerary leaflets 1 
 
 Fenestration 1 
 
 Pulmonary Valve. 
 Acute vegetative endocarditis of pulmonary valve alone . . . "1 ^ 
 Acute ulcerative endocarditis of pulmonary valve alone . . . I 
 
 Chronic pulmonary endocarditis — sclerosis 1 44 
 
 Congenital malformation of 1 4 
 
 Fenestration 17 
 
 Supernumerary leaflets 1 9 
 
 Acute Mural Endocarditis. 
 
 (a) Vegetative \ r, 5 
 
 (b) Ulcerative ^ " 6 
 
 Auricular thrombosis \ ^^ '^^ 
 
 Ventricular thrombosis > 
 
 Tuberculous endocarditis 2 
 
 II. Myocardium. 
 
 Rupture of left ventricle 1 
 
 Rupture of left auricle 2 
 
 Rupture of right ventricle 1 
 
 Rupture of 'papillary muscle, or chordse tendinete 1 1 
 
 Hemorrhage into myocardium 4 
 
 Acute hemorrhagic myocarditis 2 
 
 Acute suppurative myocarditis 1 5 
 
 Sarcoma of myocardium 1 4 
 
 Carcinoma of myocardium 4 
 
CHRONIC ENDOCARDITIS 49 
 
 Statistical Data from the Pennsylvania and the Philadelphia General Hospi- 
 tals — (Continued) 
 
 nTLjr , , ( ri f j\ Pennsylvania Philadelphia 
 
 . Myocardium— (Conimued). Hospital. Hospital. 
 
 Tuberculosis of myocardium 1 4 
 
 Gumma ot myocardium 2 1 
 
 Cardiac aneurism 6 3 
 
 Calcification of myocardium 2 
 
 Infarction of myocardium 2 6 
 
 Parietal thrombus left ventricle 7 
 
 Parietal thrombus right ventricle 7 
 
 Tuberculosis of aorta ,1 
 
 Intenentrictilar Septum. 
 
 Ulceration of interventricular septum 1 
 
 Perforation of interventricular septum 2 3 
 
 Aneurism of interventricular septum 1 
 
 Rupture of interventricular septum 1 
 
 Patulous interventricular septum 4 1 
 
 Patent ductus arteriosus 1 9 
 
 Pennsylvania Hospital 1300 autopsies 
 
 Philadelphia Hospital S640 autopsies 
 
 The foregoing statistics were collected from the autopsy 
 records of the two above named hospitals. The discrepancy of 
 some of the figures when the two sources of data are compared is 
 largely due to the fact that at the Pennsylvania Hospital only 
 acute cases are admitted, whereas the Philadelphia Hospital, 
 being connected with the almshouse and the insane asylum, is 
 filled mainly with people advanced in life. 
 
III. DISEASES OF THE AORTIC ORIFICE 
 
 Chronic aortic endocarditis may be divided into two classes: 
 (a) cases secondary to infectious endocarditis, and (b) cases due 
 to arteriosclerotic processes. Calcareous change, which is nature's 
 method of repairing weak structures, may occur in either, but is 
 much more marked in the latter and in those cases in which the 
 valvular disease has extended downward from the aorta. There 
 is, however, another type of the sclerotic variety which is met 
 with in middle life, which is secondary to syphilitic aortitis, is 
 productive of valvular insufficiency, and is less prone to calcareous 
 changes. 
 
 Fisher^ calls attention to two distinct types of aortic disease: 
 one of fatty degeneration with subsequent deposition of calcium 
 salts, and one in which areas of grayish instead of yellowish 
 thickening are found, the summits of which may be streaked with 
 white or yellow, and which are localized to certain parts of the 
 arterial wall. 
 
 AORTIC OBSTRUCTION 
 
 Occurrence and Pathogenesis. — Aortic obstruction is some- 
 times a congenital lesion, but generally it results from infective 
 endocarditis. It may also be caused by arteriosclerotic processes. 
 In its pure form it is a distinctly rare variety of valvular lesion. 
 Syphilis, so often the cause of aortic insufficiency, causes obstruc- 
 tion less often, since the aortitis which this disease produces is 
 generally most marked about 13^ inches above the valves, and 
 hence is more apt to produce dilatation and contractive shortening 
 than actual obstruction. (See Fig. 71.) When aortic obstruction 
 results from rheumatic fever, the mitral valve is generally involved 
 also. The fact that this combination is so much commoner in 
 men than in women would indicate that there is some other factor, 
 
 1 Fisher: Hospital, Mar. 9, 1907, p. 406. 
 50 
 
DISEASES OF THE AORTIC ORIFICE 51 
 
 possibly strain, concerned. AUbutt states that the combined 
 lesion is commoner in women who have had laborious occupations. 
 Chorea as a cause of aortic obstruction is not frequent. Gowers ^ 
 in 250 cases of chorea reported only three cases of aortic disease, 
 only one of which was obstruction. 
 
 Morbid Anatomy. — The morbid anatomy of this condition 
 varies considerably. Vegetations, fusion of the leaflets, infiltra- 
 tion, and stiffening or actual calcification may occur. At other 
 times the cause of the obstruction is found in a mediastinal neoplasm 
 or aneurism. Although at first sight the character of this lesion 
 would seem to be one of exceptional severity, yet as a matter 
 of fact its subjects often live a long time. AUbutt- states that 
 under favorable circumstances life may continue until the aortic 
 orifice — which measures 20 mm. at birth, 60 mm. in adult hfe, 
 and 68 to 70 mm. in advanced years — is reduced to the size of a 
 crow-quill or less. He quotes Bradbury's case, in which "the 
 chink by which the blood found access to the aorta was only dis- 
 covered on the closest search after death." Inasmuch as many 
 cases are prolonged in duration and progressive in character, 
 great hypertrophy of the ventricle is often found. It is in this 
 variet}^ of valvular lesion that the so-called "concentric hyper- 
 trophy" is most nearly approximated. Practically, however, 
 some degree of dilatation is always associated. 
 
 Rarely a double obstruction is found, one at the aortic ring 
 itself, and one beneath it, due to sclerosis of the tissue between 
 the septum and the anterior mitral leaflet. 
 
 Coarction of the aorta consists of a narrowing of the vessel at 
 that portion which extends from the subclavian artery to the 
 ductus arteriosus. This part of the aorta carries before birth 
 only part of its full quota of blood, and is hence small. After 
 birth, when the side-track path of the ductus arteriosus is occluded, 
 it assumes its full function and enlarges. Two types of coarction 
 
 ' (jowcr.s: IJi.sf.'ascis of tho Nervouw System, IS9'2, p. 'MS. 
 2 AUbutt: System of Medicine, 1898, vol. vi, p. 908. 
 
52 STUDIES IN CARDIAC PATHOLOGY 
 
 have been described : (a) Infantile, consisting of a diffuse narrowing 
 of the isthmus, developmental in origin. These cases die early. 
 (6) Adult, consisting of an abrupt cord-like obstruction near the 
 end of the ductus arteriosus. (See Fig. 83.) 
 
 Pathologic Physiology. — Owing to the obstruction to ventric- 
 ular outflow blood-pressure is very greatly increased in the left 
 ventricle, and this chamber empties itself much more slowly 
 and gradually than normal. Left ventricular systole may con- 
 sume from 5 to 50 per cent, more than the normal time, and blood- 
 pressure in this chamber may even rise to twice the normal. Such 
 
 Fig. 16. — Mitral Stenosis. 
 
 L. F., male, white, aged thirty-five years. (Philadelphia Hosjjital. vol. xxiii, p. 1. 
 Physician: Dr. F. P. Henry. Pathologist: Dr. Karsner.) 
 
 Clinical Notes: At one time chorea; some time after, while lifting a heavy weight, he 
 felt something give way in the chest, and has been unable to work since. He is an intelligent 
 mechanic, who has been under observation in this hospital for several years. Symptoms: 
 Cyanosis, dyspnea, edema, arrhythmia (extrasystolic), tachycardia, pulsating liver, jugular 
 veins, etc. Signs of double mitral and tricuspid lesion. Died gradually with symptoms of 
 pneumonia. 
 
 Pathologic Diagnosis: Cloudy swelling of heart, with double-sized dilatation. Mitral 
 stenosis; tricuspid insufficiency. Chronic congestion of lungs; hypostatic pneumonia of 
 right; beginning gangrene of left. Cyanotic induration of kidneys; arteriosclerosis; chronic 
 congestion with fatty degeneration of liver, also slight perilobular fibrosis, etc. 
 
 Pericardium: sniooth and glistening, contains 150 c.c. of serous fluid. 
 
 Heart: is large, soft and flabby; weighs 580 gm. Epicardium shows a few areas of 
 thickening about the apex. The muscle cuts with ease, and shows a light brown, slightly 
 striated, bleeding, and friable surface. Left ventricular wall measures 11 mm. Aortic orifice, 
 6.5 cm., and shows moderate general thickening of the valve leaflets, and slight sclerosis of 
 the sinus of Valsalva. Mitral orifice ivas not incised; its leaflets are enormously thickened and 
 contracted, showing at the right junction slight calcification; the whole ■presenting the appearance 
 of the funnel-shaped buttonhole mitral. The chordae tendinece are enormously thickened, retracted 
 and adherent, and are attached to papillary muscles which are much elongated and have sclerotic 
 tips. The fibrosis of the anterior mitral leaflet extends forward along the septum, beloiv the bases 
 of the aortic valves, producing a thickening which extends transversely through the bundle of His. 
 The ventricular cavity is enlarged, contains chicken-fat clot, and well shows flattening of the col- 
 umnae earner. Right ventricular wall, 4 mm. Auriculo-ventricular orifice measures 15 cm.; 
 shows leaflets which are moderately thickened along the free edge. Chordae tendineae thick- 
 ened and retracted. Pulmonary orifice 9 cm.; shows general thickening of the valves and 
 sclerosis of the sinuses. Pulmonary artery shows slight plaque-like sclerosis. Endocardium 
 generally normal. Coronary artery moderately sclerosed. 
 
 (For several years previous to this patient's death the author had from time to time oppor- 
 tunities of studying the heart by means of the cardiosphygmograph. Very marked arrhythmia 
 was always present and consisted of the type which Mackenzie describes as "nodal rhythm," 
 the "pulsus irregularis perpetuus" of Hering, but which, according to more recent investiga- 
 tions, is probably due to auricular fibrillation. This -is of especial interest in view of the 
 extensive fibrons in the region of the auriculo-ventricular bundle.) 
 
54 STUDIES IN CARDIAC PATHOLOGY 
 
 a state of affairs naturally causes a stasis and an increased pres- 
 sure in the left auricle and in the pulmonary circulation, so that 
 hypertrophy of the left ventricle and auricle, and in time of the 
 right heart, occurs. 
 
 Up to a certain point the tendency of the left ventricle to 
 hypertrophy is prevented by the prolongation of the presphygmic 
 period,^ a fact which gives the ventricle a longer time in which 
 to empty itself. But since this prolongation of the presphygmic 
 period s only limited, sooner or later hypertrophy must occur, 
 owing to the increased demand for work. When dilatation of 
 the left ventricle appears, a relative mitral insufficiency is estab- 
 lished, which in turn and in time leads to pulmonary congestion, 
 and to dilatation of the right heart. 
 
 Clinical Considerations. — The frequency' with which this lesion 
 is tabulated in some statistics is due to the fact that they were 
 taken from clinical and not from autopsy records. A systolic 
 murmur over the aortic area, especially in advanced years, is 
 very common, and results, as a rule, from calcification, stiffening, 
 slight roughening of the orifice, or dilatation of the aorta. Such 
 conditions should, of course, not be considered an "obstruction." 
 (See Fig 5.) At the Philadelphia General Hospital among 8,640 
 autopsies there were 42 cases of aortic obstruction (0.47 per cent.). 
 Among 100 autopsies in Boston, Jackson- found 5 cases, one well 
 marked. Aortic obstruction occurred in 5 per cent, of 1,781 cases 
 of heart disease at the Johns Hopkins Hospital, ■■* and in 2.73 per 
 cent, of Romberg's cases. 
 
 When any considerable degree of obstruction exists, it is usual!}' 
 associated with insufficiency. Aortic disease occurs with especial 
 frequency in the American negroes, a fact which is doubtless due 
 to the prevalence of syphilis among them. 
 
 ^ Gad and Luederitz: Zeitschrift f. klin. Medizin, xx, p. 374. 
 
 - Jackson: Boston Med. and Surg. Jour., 1896, p. 12-1. 
 
 ' Hirschfelder: Diseases of the Heart and Aorta, 1910, p. 382. 
 
DISEASES OF THE AORTIC ORIFICE 55 
 
 AORTIC INSUFFICIENCY 
 
 Pathologic Anatomy and Occurrence. — Incompetence of the 
 aortic valves generally results from disease of the leaflets, although 
 leakage from dilatation of the aorta is occasionally accountable 
 for the condition. Fibrosis, which generally acts by thickening, 
 stiffening, retraction, or uneven contraction of the cusps, is gener- 
 ally responsible for the lesion. Such changes are often associated 
 with disease of the root of the aorta, and hence the coronary 
 arteries. With advancing years the aortic leaflets increasingly show 
 the signs of wear and tear by a thickening, and curling, so that 
 the margins fail to overlap. Endocarditic vegetations, ulcerations, 
 and perforations of variable shape, size, and consistency are also 
 responsible for a certain number of instances, but when such is 
 the case the incompetency is apt to be associated with obstruction. 
 Pure isolated aortic insufficiency is generally sj^philitic or arterio- 
 sclerotic in origin. It is rare in children, and relatively freciuent 
 in men of laborious occupations, especially after forty years of 
 age, and among syphilitics. It more commonly follows pneumo- 
 coccus and gonococcus endocarditis than that which occurs in 
 rheumatic fever and chorea. Occasionally aortic insufficiency is 
 produced very early in certain cases of severe infective endocarditis 
 in which there has been a rapid ulcerative destruction of the 
 leaflets, but generally its production occurs slowly and insidiously. 
 Among the rarer causes of aortic insufficiency valvular rupture 
 resulting from strain or trauma, and congenital malformation of 
 the cusps, may be mentioned. 
 
 In addition to the foregoing changes the following are generally 
 seen: Thickening or atrophy of the endocardium; thickening 
 of the free margins of the valves; atrophy of the trabecular 
 muscles with connective-tissue infiltration; hypertrophy and dila- 
 tation of the ventricular muscle; also minute warty vegetations, 
 the result of recent infection. The thickening of the free valvular 
 margins is constant in aortic insufficiency, at times cylindrical, at 
 
56 STUDIES IN CAHDIAC PATHOLOGY 
 
 others irregular in shape. One, two, or all of the leaflets may 
 be involved. The right cusp suffers most frequently and exten- 
 sively. The valve flaps may be normal in size or even larger. 
 Trabecular atrophy is most marked in the left wall of the ventricle 
 near the apex. Wasting and flattening of the medial papillary 
 muscle is common, as is also localized fibrosis of the subendo- 
 cardial muscle, chiefly in the outer wall. 
 
 Zahn^ has described as anatomically diagnostic of aortic in- 
 sufficiency, (a) localized thickening of the interventricular septum, 
 and (b) parallel, bow-shaped lines of varying thickness, composed 
 of connective tissue, running at right angles to the cardiac axis 
 and parallel to the aortic leaflets, on the endocardium of the ven- 
 tricular septum. He attributes their formation to the constant 
 downward pressure of the regurgitating blood, although he admits 
 that the elasticity and contraction of the heart muscle might play 
 an etiologically contributing role. 
 
 Lately Schminke^ has reported an exaggeration of this process 
 in which the redundant endocardial folds both on the septum and 
 on the ventricular wall form small pockets — actual sacculations 
 which are reproductions in miniature of the valves themselves. 
 He believes that these pockets indicate a functionally compensating 
 action on the part of the endocardium, through the agency of 
 which the regurgitation of blood is diminished. He attributes 
 their genesis to a process similar to that by means of which the 
 semilunar valves develop in the fetal heart. 
 
 (Before the truncus arteriosus divides, four folds of gelatinous 
 tissue covered by endocardium are formed, two of which, on di- 
 vision of the truncus arteriosus into the aorta and the pulmonary 
 artery, are cut in half, so that each vessel gets three folds which 
 subsequently take on the form of pockets, a metamorphosis in 
 which the mechanical action of the blood-stream jDrobably plays 
 a role.) 
 
 1 Zahn: Verhandlung. d. Kongr. f. inn. Med., 189.5, p. 351. 
 - Schminke: Virchow's Archives, 1908, cxcii, p. 50. 
 
Fig. 17. — Sclerotic Endocarditis. 
 
 L. B., male, Italian, aged seventy-seven years. (Philadelphia Hospital vol. xxiv, p. 97. 
 Physician: Dr. A. A. Eshner. Pathologist: Dr. H. T. Karsner.) 
 
 Clinical Notes: Patient was admitted in a delirious condition. The heart is enlarged 
 and its sounds are weak. No distinct murmurs are heard. The urine is albuminous. Hem- 
 oglobin, 68 per cent.; erythrocytes, 5,200,000. Death occurred gradually, preceded bj' an 
 extensive and a generalized purpuric cutaneous erruption. 
 
 Pathologic Diagnosis: Emphysema, hypostatic pneumonia, chronic interstitial myo- 
 carditis, sclerotic endocarditis of all the valves, chronic interstitial nephritis, etc. 
 
 Heart: Weighs 360 gm. The left ventricle mea.9ures 13 mm. The mitral orifice 11 cm. 
 Its leaflets and chordae tendineae show slight general thickening and rd r:icl ion. The i)aiiillary 
 muscles are fibrosed. The aortic orifice measures 7.5 cm. Its IcoJIcIk mr llilrl.iiir,! <tiiil nl Iheir 
 bases slightly calcified. The sinus of Valsalva is sclerotic, this changr innilvimj llif coromirij ori- 
 fices. The right ventricular wall measures 6 mm., and the tricuspid orifice 9 cm., its leaflets 
 being thickened. The pulmonic orifice measures 8.5 cm.; its leaflets are thickened, as is also 
 the ventricular endocardium. The coronary arteries are sHghtly sclerotic. 
 
 This .specimen illustrates the type of case in which the disease of the aortic leaflets is the 
 primary and the main lesion, the aorta itself being relatively uninvolved. (Compare with 
 F'igs, 52 and 53.) 
 
58 STUDIES IN CARDIAC PATHOLOGY 
 
 Experimental section of the aortic valves is followed almost at 
 once by a fall of the diastolic pressure, by dilatation of the left 
 ventricle, and sooner or later by the establishment of a mitral 
 insufficienc3^ In man the occurrence of the latter has been 
 regarded as beneficial, on the assumption that the leak acts as 
 a safety-valve, just as does tricuspid dilatation in the right heart 
 during muscular strain.^ 
 
 Some unusual and curious aortic cases have been recorded. 
 Thus, Tegeler' reported a case in which a revolver bullet was 
 
 1 Taylor: Brit. Med. Jour., June 23, 1906. 
 
 ^Tegeler: Mtlnch. med. Woch., 1909, No. 34, p. 1740. 
 
 Fig. 18. — Chronic Mural and Aortic Endocarditis. 
 
 O. G., male, white. (Pennsylvania [Hospital. Autopsy: 1133. Physician: Dr. New- 
 lin. Pathologist: Dr. Krumbhaar.) 
 
 Clinical Notes: Denies syphilis. Gonorrhea fifteen years ago, followed three months 
 later by severe arthritis. Complains: Abdominal pain, constipation, headache, cough with 
 slight expectoration, pain after food, eructations, orthopnea, edema. 
 
 Heart: Second space 3.5 cm. to right of mid-sternal line; fifth space 12. .5 cm. to left of 
 mid-sternal line. Action is regular. Sounds weak and soft. Distinct double apical murmur 
 transmitted to axilla and base, loud at the aortic area. Water-hammer pulse. Blood-pressure : 
 135 mm.; diastohc 82 mm. (Stanton). Urine: Albumin and casts. Death: Gradual with 
 delirium and coma. 
 
 Pathologic Diagnosis: Chronic mural and aortic endocarditis with incompetency. Gen- 
 eral arteriosclerosis, cardiac hypertrophy and dilatation. Chronic diffuse nephritis, etc. 
 
 Pericardium: Contains 50 c.c. slightly turbid fluid containing flakes. 
 
 Heart: Enormously dilated (15 x 14 x 9 cm.). Weighs 600 gm. Large milk spot on 
 anterior surface of right ventricle, and a few small ones posteriorly. Over the auricular sur- 
 face numerous minute reddish points. Muscle of the left ventricle hght red streaked with 
 yellow, but the right ventricle is pale and yellow. Currant-jelly clot in right side of heart and 
 in auricular appendage. Right auriculo-ventricular valves normal. Muscle 6 to 8 mm. 
 Left auricle and ventricle also currant-jelly clots. Mitral valve is not much thickened, but is 
 shrunken and apparently incompetent. Aortic valves are diffusely thickened, and the aorta shows 
 general sclerosis. The endocardium, especially of the septum, shows peculiar raised white streaks 
 of an irregular padding which measure 2 mm. in diameter and project from the surface 2 mm. 
 Just below the aortic valves there is a diffuse thickening of the endocardium, which extends into the 
 aortic valve for some distance, and also into the mitral leaflets. Left ventricular muscle 14 to IS mm.; 
 normal in color and firm. Its cavity shows some dilatation. The coronary arteries are scler- 
 otic near their origin, but the small branches are thin and delicate. Valves: Tricuspid 12; 
 pulmonary 8; aortic 9; mitral 11 cm. in circumference. 
 
 Microscopic Examination: Immediately beneath the endocardium the muscle-fibers are 
 much swollen, granulated and vacuolated, with ragged edges. They have lost their striae. 
 Nuclei are large, and in the longitudinally cut fibers vacuoUzation is found to be most marked 
 about the nuclei. This process is well marked in the papillary muscles, their endocardial 
 covering being thickened. There is a slight diffuse increase of delicate fibrous tissue. In 
 some places this is sufficiently marked to produce atrophy and degeneration of the muscle- 
 fibers. 
 
60 STUDIES IN CARDIAC PATHOLOGY 
 
 unexpectedly found encysted in an aortic cusp, in a man who was 
 accidentally killed by other causes. In Jacobi's case,^ which 
 appeared to be traumatic in origin, the heart murmurs could be 
 heard across the room. The question of foreign bodies in the 
 heart has been studied b.y Zesas,- who collected 118 cases. 
 
 Pathologic Physiology. — Owing to the increased amount of 
 blood which the left ventricle is called upon to handle, hyper- 
 trophy and dilatation occur. In favorable cases when the nutrient 
 supply of the ventricle is sufficient, this process goes on for a 
 long time. In such events the enormous cor bovis is produced, an 
 enlargement greater than is seen in any other form of valvular 
 disease. When the hj^pertrophic growth exceeds the nutritive 
 supply, however, as is sooner or later bound to occur, degenerative 
 changes followed by dilatation and signs of insufficiency occur. 
 Or it may be that before these changes are brought about, the mitral 
 valve, owing to constant overstrain, by virtue of either actual 
 damage to its leaflets or dilatation of its sphincter, becomes 
 markedly insufficient, and thus a pulmonary congestion is brought 
 about. The marks of wear and tear upon the left-sided valves, 
 and upon the whole arterial system, in this form of valvular 
 disease are very pronounced. The incessant pounding of the 
 hypertrophic ventricle, the high systolic and low diastolic pressure, 
 produce a very intermittent blood-supply, which of course affects 
 the coronary arteries as well as those of the whole arterial system. 
 If one-third or one-fourth of the systolic output regurgitates, 
 marked hypertrophy and dilatation will of course occur; but if 
 the aortic lesion is slight, so that only a few cubic centimeters of 
 blood flow backward, although a diastohc murmur may be heard, 
 yet enlargement of the heart may not be sufficient to be clinically 
 demonstrable (Krehl). 
 
 The experiments of Henderson, Stewart/ and Moritz indicate 
 that much less blood regurgitates in aortic insufficiency than has 
 
 ' Jacobi: New York Med. Jour., Aug. 9, 1902. 
 
 - Zesas: Fortschritte in. d. Medizin, 1910, xxviii, p. 649. 
 
 ' Henderson: Archives of Internal Medicine, Jan., 1908. 
 
I''ir;. 10, — Aortic f>B.sTuucTiox, Seen from Above. 
 
 The leaflfits are fused together, thickened, and indurated. Tliey are covered witli small 
 
 vegetations. 
 
62 STUDIES IN CARDIAC PATHOLOGY 
 
 hitherto been supposed. This is owing to an increased tonicity 
 which the left ventricle assumes. The marked fluctuations of 
 blood-pressure which occur in these cases seem to be due to a reflex 
 lowering of the diastolic pressure. This is borne out by the well- 
 known clinical fact that diastolic pressure often ranges between 
 40 and 60 mm. Hg, even where compensation is fairly well main- 
 tained, while the systolic pressure is often as high as 180 mm. 
 The amount of regurgitation depends upon the severity of the 
 lesion and the efficiency of compensation in the myocardium, 
 especially of the left ventricle and of the left auricle. 
 
 Until quite recently it was generally believed that aortic 
 insufficiency was due to the same causes as those which produce 
 an obstruction or sclerotic change. Although this is no doubt 
 true, yet recent investigations point very strongly toward the 
 fact that a large number, if not the majority, of cases of isolated 
 aortic insufficiency are the result of syphilis. The association 
 of this lesion with locomotor ataxia has long been noted, ^ and 
 recently it has been shown that a very large proportion of cases 
 of aortic insufficiency give a positive Wassermann reaction,^ 
 while mitral cases do so only exceptionally. The spirocheta 
 pallida has been demonstrated in these lesions.^ 
 
 The possibilit}^ of a relative or functional aortic insufficiency 
 has been much discussed, and seems to have been definitely 
 established by having been experimentally produced by Thayer 
 and MacCallum.* But certainly the vast majority of cases of 
 this lesion seen in practice result from actual valvular damage — 
 thickening, shrinking, perforation, stiffening, roughening, or 
 calcification of the aortic cusps. It can be easil)^ understood 
 that where such changes as those just mentioned are present, 
 
 ' Babinski: Soc. Med. des Hopit., Paris, 1901, Nov. 14 and 21. Strlimpell: Deut. med. 
 Woch., 1907, No. 47. Schiitze: Deut. Zeit. f. Chir., 1908, 1-5, etc. 
 
 - Danielopolu: Bull. Soc. Biolog., Paris, May 30, 1908. Collins and Sachs; Amer. 
 Jour. Med. Sci., Sept. 1909. Debove and Tremolieres: Jour. Med. Franijais, April, 1910. 
 Longcope: Jour. Am. Med. Assoc, 1909. Pasaschivescu: These de Bucarest, 1910. 
 
 ^Wright and Richardson: Bo.ston Med. and Surg. Jour., April 29, 1909. 
 
 * Thayer and MacCallum: Amer. Jour. Med. Sci., Feb., 1907. 
 
DISEASES OF THE AORTIC ORIFICE 63 
 
 both obstruction and insufficiency are apt to result, and such is 
 generally the case — a pure insufficiency or obstruction being the 
 exception. 
 
 Clinical Considerations. — Aortic insufficiency may exist with- 
 out an audible murmur, and even when such is present it is apt 
 to be low-pitched and difficult to hear. Jackson found that this 
 was the most frequently overlooked valvular lesion in 100 autopsies. 
 Animal experimentation has further corroborated the foregoing 
 statements. In advanced life relative aortic insufficiency is 
 favored by the fact that both the diameter and the length of the 
 aorta increase with time, while its elasticity diminishes.^ 
 
 'Scheel: Virchow's Arcliiv, cxci, 1908. 
 
IV. DISEASES OF THE MITRAL ORIFICE 
 MITRAL OBSTRUCTION 
 
 Varieties. — From an etiologic standpoint there are three varieties 
 of this lesion: (a) infectious; (b) arteriosclerotic; (c) congenital; 
 the first-named being probably the commonest. Hensen has 
 reported mitral stenosis as the result of pressure from a thoracic 
 aneurism. Morgagni reported one due to the pressure of a calcified 
 pericardium. A functional form of mitral stenosis, supposedly 
 due to nervous influences, occurring chiefly in neuropaths and 
 chlorotics, as the result of orificial constriction or retroversion of 
 the leaflets from the regurgitating blood of an aortic insufficiency, 
 has been described especially in the French literature.^ Its 
 existence rests upon purely hypothetic grounds, and is very 
 questionable. 
 
 From the anatomic standpoint four varieties are recognized: 
 (a) buttonhole; (6) funnel-shaped; (c) vegetative; (d) cystic 
 (due to valvular aneurism). - 
 
 The mitral orifice in men averages 110.37 mm., in women 
 92.68 mm. in circumference. The mitral and tricuspid valves 
 show the greatest difference in size when the sexes are compared, 
 a fact which probably has some bearing on the preponderance of 
 stenosis of these orifices in women. 
 
 It has been shown that the large, freely movable anterior 
 mitral leaflet has a somewhat different function from the small, 
 relatively fixed, posterior leaflet, in that the former, in addition 
 to preventing regurgitation into the auricle during ventricular 
 systole, actually forms, together with the interventricular septum, 
 a channel which helps to conduct the ventricular contents into 
 
 'Bard; Semaine M6d., 1906, No. 20. Lepine: Provence Medic, xx, No. 2. Cecone: 
 Riforma Medic, July 27, 1908. 
 
 = Cruveilhier: Anat. Path., ii, 1852. 
 
66 STUDIES IN CARDIAC PATHOLOGY 
 
 the aorta ^ (the "Stromrinne" [flume] of Oesterreich -). It has 
 thus a double function, and pathologic alterations in its structure 
 have a double result. In this connection Beitzler ■' considers the 
 white spots frequently to be found on the ventricular surface 
 of the anterior mitral leaflet as mechanical and not inflammatory 
 in origin, due to conditions similar to those which are active in 
 the production of aortic sclerosis. Looked at, then, from the 
 standpoint of physiology, this surface of the anterior leaflet is 
 really a part of the aorta. The fact that this leaflet is so much 
 oftener diseased than the others has also been explained as due 
 to greater tension when closed (Sibson), a smaller line of contact 
 during closure, greater tendinous traction, greater vascularit.y, — 
 favoring embolic processes. It should also be borne in mind that 
 the anatomic relationship of the mitral, tricuspid, and aortic 
 valves is a very intimate one. (See Figs. 7 and 8.) 
 
 Pathologic Anatomy. — IMitral stenosis* may or may not begin 
 as an insufficiencj', which, through gradual adhesion of the leaflets 
 and contraction of the surrounding tissues, ends as a combined 
 lesion, sometimes passing through a stage of firm obstruction. 
 When the free edges of the leaflets are chiefly involved, the well- 
 known funnel-shaped oriflce, which is generally seen in early life, 
 results. (See Figs. 16 and 22.) When mechanical pressure factors 
 have existed, as in the cases occurring in chronic nephritis, the 
 leaflets are less affected, and the lesion consists more of a 
 thickening, hardening, shortening, and sometimes a calcification of 
 the papillary muscles and chordae tendinese. "The insertions of the 
 chordae tendinese are spread out over the greater part of the lower 
 surface of the leaflets, and when there is long-continued, high, intra- 
 cardiac pressure, the whole valve becomes very much thickened, 
 and there is a great increase in the fibrous tissue, which eventu- 
 ally leads to the puckering or contraction of the segments, and the 
 
 ■ Arch. f. exp. Path. u. Pharm., 1907, Ivii, .57. 
 
 - Virchow's Arch., Ixi, pp. 180, 196. 
 
 ' Virchow's Arch., 1901, Ixi, 343. 
 
 * Heitz and Sezary: Arch, de Mai. du Coeur, Dec. 1, 1908. 
 
DISEASES OF THE MITRAL ORIFICE 67 
 
 diaphragmatic or buttonhole variety is produced."^ (See Fig. 24.) 
 Some writers — Haj^den, Sanson,- Hilton, and Fagge — have held 
 that the funnel shape is almost exclusively that of youth, and the 
 buttonhole form that of adult life. Barr suggests that it is largely 
 a question of the duration of the lesion, and that long-standing 
 cases, with marked infiltration, sclerosis, and contraction (and 
 these are the conditions which obtain later in life), develop the 
 buttonhole shape. 
 
 " In some cases the mitral cusps are so thickened and contracted 
 that they mereh' form a transverse septum with a narrow slit 
 between auricle and ventricle. In such cases the chordae tendinese 
 are frequently thickened and matted together, and the papillary 
 muscles in such a fibroid condition that it would seem impossible 
 for a first sound to be generated by the mitral valve." 
 
 A congenital form is frequently discussed, especially in the 
 French literature. It is described as often of the funnel-shaped 
 type, produced by fusion of the leafiets, which are said to resemble 
 other congenital lesions n that they present no signs of inflamma- 
 tory changes — thickening, contraction, etc. It is sometimes asso- 
 ciated with other developmental anomalies, such as hare-lip. 
 Occasionally it occurs together with infantilism, myxedema, etc.^ 
 Other observers consider that these lesions result from a fetal 
 endocarditis. The symptoms in these cases appear between the 
 seventh and fourteenth years, the period in which, despite rapid 
 bodily growth, the heart remains almost at a standstill. 
 
 According to Bizot and Beneke, the heart, which is perfectly formed by the 
 seventh week after conception, doubles its size between the time of birth and the 
 age of twenty-four months, and again between three and seven years. It re- 
 mains almost stationary from seven to fifteen years, and again increases one- 
 third of its size between fifteen and twenty years, at which time normal growth 
 practically ends.'' 
 
 ' .J. Barr: Lancot, Doc. 19, 1908, p. 17S9. 
 
 'San.son CAllbutt's System;: In children one "buttonhole" is seen to eight funnels, where- 
 a.s in adults there is one funnel to twenty-five "buttonholes." 
 ' K'ippel and Chabrol: Rev. de M6d., 1910, p. 1.53. 
 'Quoted Pawlinow: "Kongcnitale Mitral Stenose," Berlin, 1909, p. (5. 
 
68 STUDIES IN CARDIAC PATHOLOGY 
 
 Quenus '■ states that the mitral valves are developed in the second and third 
 months of fetal life, existing at first as muscle-fibers which at the beginning of the 
 fourth month are transformed into connective tissue. It is in this stage of 
 embryonic life that congenital lesions would be produced. 
 
 Pawlinow states that in congenital mitral stenosis neither the right ventricle 
 nor left auricle hypertrophy, owing presumably to nutritional defect. The 
 leaflets themselves are thinner, weaker, more delicate, and are more easily torn 
 than normal ones. He believes that the cases of mitral stenosis which Pitt ~ 
 describes as so frequently associated with chronic nephritis are cases of congenital 
 mitral stenosis, and that this congenital form predisposes to infections. The 
 heart is smaller, but the patient's life longer, than in the acquired lesions, for 
 despite the fact that many cases develop pulmonary tuberculosis, the latter 
 tends to run a prolonged course. This association of mitral stenosis and pul- 
 monary tuberculosis was explained by Potain as due to toxemia. 
 
 The belief that mitral stenosis is often a result of acquired 
 or hereditar}^ pulmonary tuberculosis, was first enunciated by 
 Tripier,'' and notabi}' elaborated by Potain * and Teissier. ° A full 
 discussion of this hypothesis would lead too far. Suffice it to say 
 that this view that mitral stenosis may be caused by the toxin 
 of the tubercle bacillus is not generally accepted. Hereditary 
 syphilis has also been described as a cause.'' 
 
 The normal auricular capacity ranges between 40 and 70 cm. 
 (average 55 cm.). In mitral stenosis these figures may be 
 greatly increased. In one case reported by Briquet ' the enormous 
 proportions of 650 cm. were reached — practicallj' equal to the 
 size of a whole normal heart. Auricular hypertrophy is insignifi- 
 cant compared to what ma.y occur in the ventricle, nevertheless 
 an increase to the thickness of 3 cm. has been observed.^ Atrophy 
 
 ' Quenus: These de Paris, 18S3, p. 42. 
 
 - Pitt, at Guy's Hospital, found that mitral stenosis occurred three times as often in 
 association with renal sclerosis as in other diseases, and that two-thirds of the cases occur in 
 women. 
 
 'Tripier: Arch, de MM. Exper., ISSS. 
 
 * Potain: Jour, de Med. et de Chir. Prat., 1891. 
 
 5 Teissier: These de Paris, 1894. Sears (St. Paul Med. Jour., March, 1907) found well- 
 marked tuberculosis in 11 or 22 per cent, of the Boston City Hospital cases. A number 
 of other cases showed chronic pleuritis, which, if counted as tuberculous lesions, would raise 
 the percentage to 40. Crawford in 112 autopsies found pleuritis 48 times, but definite tuber- 
 culosis only twice. 
 
 * Labadie, Lagrave, and Deguy: Jour, des Prat., July, 1899. 
 ' Briquet: These de Paris, 1890, case xix. 
 
 « Bourdcl: Soc. Anat. Paris, 1880. Samways: These de Paris, 1896. 
 
Fifi. 21. — Chroxic Aortk- and Mitral ENDorARiuTis, with Hypertrophy and Dila- 
 tation OF THE Left Ventricle. 
 
 The aortic valves are thickened and retracted. The aorta above them shows well-marked 
 sclerotic changes involving the mouth of the right coronary artery. The mitral valve is 
 thickened, retracted, and sclerotic. The predominant lesion in each instance is insufficiency. 
 (Specimen from the German Hospital, Philadelphia.) 
 
70 STUDIES IN CARDIAC PATHOLOGY 
 
 of the auricular muscle is by no means rare, and may be of such 
 extreme degree that the muscular tissue may completely disappear, 
 leaving only a fibrous sac.^ When the auricle is thus greatly 
 distended, its functional capacity ceases, as is shown b)^ the dis- 
 appearance of the auricular wave in the jugular (Mackenzie), 
 in the esophogram (Joachim), and in the volume curve (Hirsch- 
 f elder). . Occasionally enormous dilatation is met with, as in 
 Mliller's case, in which the left auricle was larger than a child's 
 head, and the heart weighed 620 gm., the patient's bodily weight 
 being onlj^ 65 Kg. (normal relations: heart, 297 gm. to body of 
 60 or 70 Kg.). 
 
 According to Witwicki,- the left auricle is the most distensible 
 of all the heart chambers, and Samuelson'' has stated that occlu- 
 sion of the left coronary artery produces a flaccid dilatation of the 
 left auricular wall. Although these facts may be correct, the left 
 auricle is, owing to its anatomic relations, much less likely than 
 the right to expand, since such an occurrence can take place in 
 but one direction, viz., upward. Owen and Fenton have reported 
 a left auricle with a capacity of 900 c.c.,* and Minkowski' has 
 recorded a dilated heart which contained 4 liters of blood, 
 nearly three of which were found in the left auricle. In such 
 cases the auricular wall exists as a mere membranous sack, no 
 thicker than a visiting card (Sansom), and resembles a greatly 
 distended bladder. Such distention by dilation of, and upward 
 pressure on, the left pulmonary artery may cause left recurrent 
 laryngeal paralysis by compression of this nerve between the last 
 named vessel and the aortic arch. Ten such cases with autopsy 
 reports and a considerably larger number of clinical observations 
 are now on record. In some of these cases direct pressure of the 
 
 ' Mtiller: Zeit. f. klin. Med., 190.5, hi, p. 520. 
 
 -' Witwicki: Zeit. f. kl. Med., xxvii, 1895, p. 321. 
 
 ' Samuelson: Ibid., vol. ii. 
 
 ■• Fetterolf and Norris: "The Anatomic Explanation of Paralysis of the Recurrent Laryn- 
 geal Nerve Found in Certain Cases of Mitral Stenosis." Trans. Coll. Phj-sicians of Phila- 
 delphia, 1911, Am. Jour. Med. So., 1911. 
 
 5 Owen and Fenton: Trans. Clin. Soc. London, M;iy 24, 1901. 
 
DISEASES OF THE MITRAL ORIFICE 71 
 
 left auricle upon the aorta has been described, but as has been 
 shown by Fetterolf and myself such a state of affairs is an- 
 atomically impossible.^ Right recurrent paralysis has also been 
 described, it being assumed in explanation, and without post- 
 mortem substantiation, that the brachiocephalic and the sub- 
 clavian arteries had undergone displacement. 
 
 It was formerly taught that mitral stenosis is practically always associated 
 with insufficiency. This has been vigorously contradicted, and much discussion 
 has been aroused. Romberg found only two cases of pure stenosis among 670 
 heart cases. Krehl considers it very rare, and some chnicians deny its existence 
 altogether. Hampeln,^ on the other hand, finds pure obstruction in from 10 to 
 20 per cent, of all his mitral cases, and Schabert^ states that at least half of all 
 the mitral lesions at the Stadtkrankenhaus at Riga are pure stenosis. There 
 can be no question that in a good many cases the stenotic is the serious and 
 evident, and the insufficiency the slight and inconsequential lesion. Personally, 
 although I have seen quite a number of cases of isolated obstruction, yet it is my 
 belief that the lesion is much more commonly a mixed one. 
 
 Etiology. — The great majority of cases of mitral stenosis, 
 especially those of early life, owe their existence to an antecedent 
 rheumatic infection. Following this in frequency come chorea, 
 arteriosclerosis, and infectious processes of different kinds, including 
 syphilis. Chronic interstitial nephritis is also not infrequently 
 associated with mitral stenosis. 
 
 Goodhart in 192 cases of this form of renal disease found the last-named 
 valvular lesion in about 25 per cent., and Pitt states that mitral stenosis is three 
 times as common in patients with Bright's disease as in those not so afflicted. 
 Although these facts are doubtless correct, it must not be forgotten that in these 
 cases the valvular disease is simply a part of a general arteriosclerosis, in which 
 such extreme degrees of mitral disease as are seen as the result of inflammatory 
 lesions are distinctly the exception. They occur in individuals more advanced 
 in life, present quite a different clinical picture, and play much less important a 
 role in the production of death. 
 
 Occurrence. — Among 4,791 autopsies at Guy's Hospital, 
 Samways ^ found 196 cases of mitral disease in which the orifice 
 
 ' Minkowski: Munch, med. Woch., Ivi, igo."), p. 1S2. 
 ^ Hampcln: Dcut. med. Woch., 1908, p. 1.301. 
 'Schubert: Deut. Arch. f. klin. Med., 1909, p. 117. 
 
 * Sarnways: Hrit. Med. Jour., 1S98, p. 364. (AmonK 8,040 autopsies at (he I'hil;i,ili'l|)hia 
 Hospital there were 1 Id well-marked enses of milral stenosLs.) 
 
72 STUDIES IN CARDIAC PATHOLOGY 
 
 measured less than 3J^ inches (admitted two fingers or less). 
 Minor grades of stenosis were therefore excluded. In 108 cases 
 the orifice measured 234 inches (admitted one finger) or over, 
 and in 85 cases measured less than 23^ inches, three cases being 
 doubtful; 107 cases were in females, 89 in males. The average 
 age at the time of death among the former was 33.6 years; among 
 the latter, 43.6 years. In 32 cases tricuspid obstruction was 
 also present; generally this occurred in the severe cases. In a 
 large proportion of cases the aortic valve was also thickened, 
 •but actual stenosis was seldom encountered. Left auricular 
 hypertrophy occurred in 44 of 77 severe cases, and in 21 of 96 
 moderate cases (in the first class in more than half, in the second 
 in less than one-quarter). Left auricular dilatation was marked 
 in 14 of 77 severe, slight in 6, the data being incomplete in 18 
 cases. Right ventricular hypertrophy appeared in 41 of 77 severe, 
 and 25 of 96 moderate cases. Right ventricular dilatation was 
 present in 40 out of 77 severe, and 27 of 96 moderate cases. The 
 left ventricle was generally normal or small, rarely enlarged. 
 Among 23 cases dying "surgical deaths," only 4 had dilated left 
 auricles. Pericarditis was present in nearly one-third of the cases, 
 and sudden death occurred in 7. Sixty per cent, of the cases 
 gave a history of rheumatic infection. Nineteen cases were ad- 
 vanced in life and gave no such history, showing that this lesion 
 TCiSLy have a sclerotic as well as an infectious origin. Nearly all 
 statistics show that mitral obstruction, especially the form which 
 occurs in early life and results from an infectious valvulitis, is 
 very much more common in the female sex. Various explanations 
 have been offered, such as, for instance, that prolonged subacute 
 infections are more frequent in women, also that, owing to 
 lessened cardiac activity and intracardiac pressure, the mitral 
 valve makes less extensive excursions, and is hence more prone 
 to adhesive changes. Congenital structural differences have also 
 been suggested. It must be admitted, however, that none of 
 these explanations are satisfactory. Among 50 autopsies of 
 
Fig. 22. — Mitral Stenosis. 
 8|jccimen .showing mitral stenosis viewed from the ventricular side. The valvular end<i- 
 cardium is thickened and has lost much of its flexibility; the chorda; tendinea; are thickened, 
 indurated, contracted, and more or less fused together. Small verrucose vegetations are seen 
 on the ventricular endocardium just to the left of the mitral valve. 
 
74 STUDIES IN CARDIAC PATHOLOGY 
 
 mitral stenosis cases Sears found in 25 a mitral lesion only (19 
 admitted only one finger). In 7 other cases the mitral lesion was 
 the principal one (2 fibrous pericarditis, 5 aortic disease). So 
 that in 27 cases there was mitral disease alone, in 17 mitral and 
 aortic, in 1 mitral and tricuspid, in 5 mitral, aortic, and tricuspid, 
 in 4 fibrous pericarditis. 
 
 Pathologic Physiology. — The presence of mitral stenosis at 
 first tends to produce left auricular hypertrophy, owing to obstruc- 
 tion to outflow offered by the constricted orifice. Hirschfelder ^ 
 and Wolfsohn have shown that the first effect of mitral stenosis 
 as indicated by the volume curve is to slow the inflow into the 
 ventricles. "As the result of this the left auricle is more than 
 usually full at the time of its systole, and forces an unusually 
 large quantity of blood into the ventricle." The capability of 
 the auricle to hypertrophy is limited, however, and great thickening 
 of its walls is rarely seen. With continued overwork the chamber 
 elongates, becomes cone-shaped, and, as nutrition fails, dilates. 
 That this dilatation is not a conservative phenomenon, but an 
 evidence of failing compensation, has been pointed out by Samways, 
 who in 36 severe cases of mitral stenosis found hypertrophy in 26, 
 whereas dilatation occurred in only 14, in 11 of which it was asso- 
 ciated with hypertrophy. This process of dilatation manifests 
 itself first in the auricular appendix, owing to the relatively 
 unyielding structures by which the auricle proper is surrounded 
 (the aorta, vertebrae, and esophagus behind, the other heart cham- 
 bers in front, the diaphragm and liver below, and the aortic arch 
 and pulmonary artery above). (See Figs. 45, 46, and 47.) 
 
 Thrombosis, either ante mortem or post mortem, of either of 
 these chambers occurs frequently, owing to circulatory stagnation 
 and roughening of the endocardium bj^ vegetations. (See Fig. 9.) 
 Such a state of affairs is a prolific source of emboli, and adds much 
 to the weakness of the heart which is manifest during intercurrent 
 infections, such as influenza, and which is often attributed to 
 
 ' Hii'schfelder and Wolfsohn: Johns Hopkhis Hosp. Bulletin, xix, 190S. 
 
:;- — to 
 
76 STUDIES IN CARDIAC PATHOLOGY 
 
 myocarditis (Huchard). Increased pressure leads to endocardial 
 thickening in the auricle, and as compensation fails, to thickening 
 and dilatation of the pulmonary arter3^ In time the right ven- 
 tricle hypertrophies as the result of pulmonary stasis, and assumes 
 a somewhat rectangular shape from enlargement of the conus. 
 When this chamber dilates under continuous overstrain, tricuspid 
 insufficiency occurs, which in turn leads to overdistention of the 
 right auricle. This chamber in extreme cases becomes greatly 
 thinned, stretched, and ceases to contract, becoming eventually a 
 mere distended reservoir at the orifices of the venae cavse. 
 
 The question as to whether mitral stenosis can produce left 
 ventricular hypertrophy has provoked much discussion, a good 
 deal of which may be found in Dunbar's ^ article. He himself 
 found hypertrophy and dilatation in cases with good compensa- 
 tion. Some observers state that atrophy is the corhmonest 
 lesion, and attribute its existence to a lessened amount of blood 
 which this chamber is called upon to handle. The existence of 
 left ventricular hypertrophy, when present, has been explained 
 as resulting from back pressure in the venous system, making- 
 it more difficult for the blood to pass from the arteries into the 
 veins, and thus necessitating increased ventricular effort. An in- 
 creased systemic venous pressure has been found by some observers, 
 but is denied bj^ others. Another reason for hj^pertrophy has 
 been offered by Giuffre, namely, that diastolic filling is interfered 
 with as a result of the mitral narrowing, and since diastole is now 
 generally regarded as in part, at least, an active muscular action, 
 an obstacle to it would lead to enlargement. A verj^ excellent 
 study of this subject has been made by Hirsch, who examined the 
 hearts in ten cases by the Miillerian method, and found hyper- 
 trophy only when insufficiency of the mitral was the chief lesion. 
 Schabert also found either an actual atrophy of the ventricle or 
 at least no increase in pure obstruction. There seems to be little 
 doubt that left ventricular hypertrophy, when present, can generally 
 be accounted for by other lesions, either within or without the heart. 
 
 ' Dunbar; Dcut. Arch. f. klin. Med., 1S92, p. 283. 
 
DISEASES OF THE MITRAL ORIFICE 77 
 
 Mitral obstruction may be produced experimentally either 
 by introducing a distensible balloon through the auricular appen- 
 dage, or by passing a suture or clamp around the auriculo-ventric- 
 ular ring.^ 
 
 "The immediate result is the lowering of the general arterial pressure and 
 the great elevation of the pressure in the pulmonary arteries, the pulmonary 
 veins, and the left auricle. The pressure in the systemic veins is little if at all 
 elevated, unless there arises an insufficiency of the right ventricle, or with it a 
 relative insufficiency of the tricuspid valve. The essential feature of the process, 
 as indeed of all changes of blood-pressure due to any obstruction of the blood- 
 stream from alterations of the heart, lies in the fact that the amount of blood 
 in actual circulation is diminished, while the rest of the blood stagnates behind 
 the obstruction." 
 
 In the human being the constrictive process occurs gradually, 
 and thus a better chance for compensation is offered. The fall 
 in the systemic pressure is counterbalanced by an increased arterial 
 constriction, so that arterial tension is maintained at practically 
 a normal level. 
 
 Clinical Considerations. — Owing to the serious and progressive 
 character of mitral stenosis, and the fact that so manj' cases wreck 
 individual existences early in life. Sir Lauder Brunton suggested 
 some years ago that at some future time this lesion might be 
 treated by surgical means. At present this is, of course, out of 
 the question, but recent experience shows that this is by no means 
 as chimerical a suggestion as it at first appeared to be. The 
 heart is no longer surrounded by an invincible noli me tangere. 
 Bernheim's experiments have shown that it is a good deal easier 
 to convert a mitral obstruction into an insufficiency than to pro- 
 duce the former lesion.^ Wounds of the heart are treated on the 
 same principles as the wounds of other muscles, and with no small 
 degree of success. Of some 160 cases of cardiac wounds surgically 
 treated thus far, 69 were in the right ventricle, with 48 deaths 
 ''69.6 per cent.j; 74 in the left ventricle, with 45 deaths (60.8 
 
 ' Mlc.CMuu, :iw\ .VInClurc; 'J'lvuis. Assoc. Am. Phys., ]90(), p. 5. 
 ■' I5r-nilii-i,„: l;,il|..tin .lolms llcpkiiis Ilospiliil, April, HIOO. 
 
78 STUDIES IN CARDIAC PATHOLOGY 
 
 per cent.); 5 in the left auricle, with 2 deaths (33.3 per cent.).^ 
 Furthermore, Elsberg- has shown experimentally that the heart 
 in rabbits and dogs is capable of resisting an astonishing amount 
 of trauma, "even ligation of the entire left heart at the junction 
 of the lower and middle thirds of the ventricles, and amputation 
 through the ventricles below the ligature, may be followed by 
 recovery." 
 
 While mitral stenosis is generally and justly regarded as a 
 far more serious lesion than insufficiency, yet this question is 
 worthy of some little thought. Mitral stenosis is perhaps not so 
 rare a lesion as some of us think, ^ and the recent investigations 
 of Schabert are at least suggestive of the fact that some stenoses 
 may be the terminal stages of insufficiencies. The question as 
 to the preponderance of the lesion can to a certain extent be 
 determined by careful weighing of the fat- and blood-freed in- 
 dividual heart chambers, and by the water test; but, needless 
 to say, other conditions, such as the hypertension of nephritis, 
 must be carefully excluded before drawing definite conclusions. 
 
 The fact that mitral obstruction is not rarely associated with 
 congenital malformations naturally suggests a common cause, 
 such as syphilis, alcoholism, tuberculosis in the parents, etc. 
 Heitz and Lezary* have recently collected 15 cases in which, in 
 addition to mitral stenosis, such lesions as syndactjdia, ectopic 
 testicles, harelip, sternal malformations, imbecility, were observed. 
 It is quite possible, however, that such cases are coincidences, 
 or the result of an intrauterine infection, since the symptoms of 
 mitral stenosis rarely manifest themselves before the twelfth 
 year (Poynton). A "mitral heredity" has been dwelt upon by 
 Hirtz.'^ 
 
 ' Peck: Annals of Surgery, July, 1909. 
 ■- Elsberg: Jour. Exper. Med., 1899, p. 479. 
 
 ' Cabot states that 2.5 out of 48 cases discovered at. autopsy at the Massachusetts General 
 Hospital were overlooked clinically. 
 
 * Heitz and Lezary: Arch. d. Mai. du Cccur, 190S, i, p. 701. 
 ^Hirtz: Presse Med., Sept. 19, 1903. 
 
Tic. 24. — Stenosis of the Aortic, Mitral, and Tricuspid Valves. 
 
 The aortic leaflets are fused together and the orifice is greatly reduced in caliber. The 
 mitral orifice consists of a mere .slit, of crescentic outline — buttonhole type. The tricuspid 
 orifice is also contracted. (Specimen from the Philadelphia Hospital.) 
 
80 STUDIES IN CARDIAC PATHOLOGY 
 
 MITRAL INSUFFICIENCY 
 
 Pathogenesis. — The mitral valves may fail to prevent back- 
 ward leakage owing to organic disease or to atonicity of the mus- 
 cular sphincter, upon the integrity of which the proper functiona- 
 tion of the valve so largely depends. This atonicity of the sphinc- 
 ter in turn may result from muscular degeneration or from purely 
 functional causes. The conditions necessary to produce a func- 
 tional lesion are diminished muscular tonicity and an overworked 
 ventricle. When mitral insufficiency results from organic causes, 
 it is not infrequently associated with some obstruction. The 
 valves may be fused, retracted, puckered together with more or 
 less induration of the leaflets or the surrounding structures. 
 Insufficiency may also occur when the left ventricle enlarges to 
 such an extent as to draw on the papillary muscles before the 
 leaflets are in complete apposition. Actual ulcerations, perfora- 
 tions, or vegetations may also prevent sufficiency. In fact, 
 Schabert's recent studies indicate that such lesions are the com- 
 monest cause of pure organic mitral insufficiency. 
 
 Occurrence. — Mitral insufficiency is the commonest of all 
 valvular diseases, constituting about 25 per cent, of all such cases. 
 Among 1,024 cases of valvular disease in applicants for life in- 
 surance Ashton found mitral stenosis 32, insufficiency 557, aortic 
 obstruction 136 (?), insufficiency 47.^ At the Edinburgh Infirmary 
 out of 1,914 cases of valvular disease there were 585 cases of pure 
 insufficiency, and 463 combined mitral lesions, 231 of which were 
 mitral stenoses.^ Among the 8,640 autopsies at the Phila- 
 delphia General Hospital there were 1,253 cases of chronic mitral 
 endocarditis. Among these there was one aneurism (with rupture), 
 one hematoma, and one case of supernumerary leaflets. 
 
 The great discrepancy between the frequency of the diagnosis 
 of mitral insufficiency in clinical records, and in autopsy statistics, 
 is to be explained by the fact that, accepting the statement of 
 
 1 Ashton: Medical News, June .30, 1894. 
 
 ^ Gillespie: Edinburgh Hospital Reports, 1S9S, p. 31. 
 
DISEASES OF THE MITRAL ORIFICE 81 
 
 Virchow, it has been held to be impossible to test the functionation 
 of this valve by hydrostatic methods, in the way in which the 
 semilunar valves may be. Lately Schabert ^ has especially studied 
 this question and found that such a test can be made with com- 
 parative satisfaction, celerity, and accuracy, and as a result three 
 grades of insufficiency have been suggested. (The valves may 
 also be tested with an air-bellows.-) 
 
 The left auricle is cut up as far as the mitral insertion, and the flap reflected 
 for inspection. The aorta is occluded by pinching, and through a cut in the 
 ventricular wall a tube connected with running water is introduced into the 
 ventricle. A source of error is admitted for hearts of greatly relaxed muscula- 
 ture, — anemia, sepsis, postmortem decomposition, etc., — and also for cases in 
 which thrombi are lodged between the leaflets. Similar conclusions, though 
 based on a different technic, have been reached by Oesterreich and Bleicheroeder.^ 
 
 Notwithstanding these tests, however, functional and even 
 organic insufficiency is often overlooked at autopsy on account 
 of rigor mortis of the heart muscle which prevents relaxation, 
 and also on account of the redundancy of the valves. 
 
 Pathologic Anatomy. — The anatomic changes in mitral in- 
 sufficiencjf consist of sclerotic, ulcerative, or vegetative alterations 
 of the leaflets or chordae tendinese, with occasional perforation or 
 rupture, and frequently with induration and shortening. The 
 commonest sign of relative insufficiency consists of thickening of 
 the free valvular margin with more or less contraction, the former 
 being generally uniform. Inversion of the flaps is rare because 
 the chordae tendinese are so attached as to leave a considerable 
 margin between their insertions. When actual inversion does 
 occur, it is generally on the anterior leaflet. On the posterior 
 surface of the auricle, between the valve opening and the mouth 
 of the pulmonary veins, we sometimes find the endocardium 
 infiltrated and thickened, presenting an angular, ridgy, gelatinous 
 appearance, with the convexity toward the pulmonary veins 
 
 ' Schabert: Zontralb. f. Path. u. path. Anat., 1907, p. 3.3. 
 ' Hamilton: Tc.xt Hook of P.ath., 1889, p. 9. 
 
 ' Oostfrrcich aud HIcichcrocclcr: Virfhow's Arch,, vol. cli, p. 19.5, 1902, p. l.'J9. 
 6 
 
82 STUDIES IN CARDIAC PATHOLOGY 
 
 (Zahn). In the earlier stages the auricle is hypertrophied, and 
 in advanced cases atrophied. The valvular leaflets are thickened 
 and at times show aneurismal dilatation. (See Fig. 15.) The 
 auricular surface of the anterior leaflet generally shows the most 
 marked changes. The early evidences of rheumatic endocarditis 
 consist of small nodules on the leaflets, and are of little importance 
 of themselves. The later and serious changes result from extension 
 of the inflammatory process to the chordae tendinese, which become 
 thickened and shortened. "Rheumatic disease of the mitral 
 valve is mainly a disease of the chordae tendinese" (Fisher). 
 This process of contraction ultimately leads to stenosis and in- 
 sufficiency. 
 
 Pathologic Physiology. — "In every variety of uncompensated 
 valvular lesion, either an insufficiency or an obstruction, blood- 
 pressure and systolic output fall on the distal, and rise on the 
 proximal, side of the lesion. Compensation is brought about by 
 transferring backward to another heart chamber the increased 
 pressure. Compensation is brought about in the stenoses by 
 increased contractile tension, and in the insufficiencies by increased 
 systolic output. As a corollary, to compensate an obstruction 
 hypertrophy is required, but to compensate an insufficiencj'^, both 
 hypertrophy and dilatation must exist" (Moritz).^ As the 
 result of mitral insufficiencj'', pressure in the aorta falls, in the pul- 
 monary veins and in the arteries it rises, wherefore the amount of 
 blood in the greater circulation diminishes; in the lesser, increases. 
 The systolic output of the left ventricle increases, that of the 
 right decreases. Distinct dilatation of the right ventricle is not 
 the result of pure mitral insufficiency. Mitral insufficiency leads 
 to dilatation and hypertrophy of the left ventricle. With increase 
 of left ventricular systolic output, the aortic pressure may return 
 to normal and the pulmonic pressure diminish to normal; true 
 compensation is, therefore, possible. In mitral stenosis the work 
 of the left ventricle decreases. 
 
 1 Moritz: Deut. Arch. f. klin. Med., 1899, Ixvi, p. 349. 
 
Fig. 
 
 -Mitral Insufficie.ncy. 
 
 ShowinK vr-ry extensive tissue destruction. The chorda; tendineaj at the central part of 
 the valvular margin have been destroyed by ulceration, leaving only short shriveled stumps. 
 A few vorruco.se vegetations are seen. The ventricular wall is much thickened. (Specimen 
 from the Pennsylvania Hospital.) 
 
84 STUDIES IN CARDIAC PATHOLOGY 
 
 When mitral insufficiency is exj)erimentally produced — by 
 cutting the leaflets or chordee tendinese by means of a knife-hook 
 introduced through the left auricular appendage — arterial pressure 
 falls in proportion to the severity of the lesion. Pressure in the 
 pulmonary artery is not much altered; it falls somewhat, with 
 extreme insufficiency, and with slight lesions rises somewhat. 
 The systemic venous pressure too shows but little change. The 
 most striking alterations occur in the left auricle, in which pressure 
 rises, distention becomes marked, and the pulsation not only 
 violent, but systolic in time. The latter occurs because the 
 auricle now forms practically a continuous chamber with the 
 ventricle, and the powerful contraction of the latter far over- 
 shadows the feeble pulsation of the former. Mitral insufficiency 
 brings about hypertrophy and later dilatation of the left auricle. 
 The greater the leakage, the greater the dilatation. When 
 regurgitation is less extreme, there is apt to be more hypertrophy 
 (Gibson). 
 
 Hypertrophy of the left ventricle occurs on account of the 
 increased amount of blood which this chamber has to handle in 
 order to keep up anj'thing like a normal circulation. But since 
 this merel}^ means that a certain amount of blood is forced back 
 against the lower auricular pressure, it is more likely that the 
 ventricle actually does less and not more work than normal. 
 When marked hypertrophy is present, in such cases, it is often due 
 to other causes, such as arteriosclerosis, etc. Congestion of the 
 lungs generally occurs sooner or later, and this is followed bj^ a 
 train of changes similar to that described under mitral stenosis. 
 Thrombosis of the cavities is common in the later stages, both as 
 an antemortem and as a postmortem occurrence. Left ventricular 
 dilatation enables the ventricle to receive the increased amount 
 of blood which is furnished first by increased auricular activity, 
 and later by right ventricular hypertrophy. 
 
 The cause of the right ventricular hypertrophy has been much 
 discussed. The experiments of MacCallum and McClure have 
 
DISEASES OF THE MITRAL ORIFICE 85 
 
 shown that in so far as blood-pressure changes are an index, 
 the pulmonary capillaries may be regarded as a system of rigid 
 tubes, and inasmuch as the left ventricular contractions are trans- 
 mitted backward into the pulmonary artery with so little loss of 
 time, the contraction of the left ventricle is manifested in the right 
 ventricle during the systole of the latter. An additional cause for 
 right ventricular hypertrophy lies in the fact that when the left 
 auricle becomes dilated, as it early does, it compresses the upper 
 left pulmonary vein between the auricular appendix and the 
 bronchus; left ventricular enlargement tends to compress the 
 left lower pulmonary vein, while right auricular enlargement 
 encroaches upon the right pulmonary veins. Compression of 
 these veins at once produces congestion in the arterial and venous 
 radicles of the lungs and pleurae. (See Fig. 45.) 
 
 Right-sided cardiac hydrothorax or pulmonary congestion 
 often occurs without evidences of stasis in the greater circulation, 
 and, when present, the hydrothorax is generally confined to, or 
 most marked on, the right side. This right-sided localization, 
 which was formerly attributed to pressure by the dilated auricle 
 upon the vena azygos major, has been shown by Fetterolf and 
 Landis ^ to be the result of right auricular pressure upon the pul- 
 monarj^ veins, into which the vessels of the pleura empty. Pressure 
 on the vena azygos major by the dilated right auricle is anato- 
 micalh^ impossible. Marked dilatation of the left coronary sinus 
 has simulated an enormously dilated right auricle, seemingly 
 overlapping the left auricle from behind.- 
 
 "The greater frequency of hydrothorax on the right side is due to the fact 
 that dilatation of the right auricle is more common and more easy than a similar 
 condition on the left side, and such dilatation is the only factor needed to cause 
 damming back in the right pulmonary veins. On the left side in order to include 
 both uf)per and lower veins there is needed dilatation of the left auricular appen- 
 dix and the left ventricle, with possibly a retrodisplacement of the vertical 
 septum" f Fetterolf and Landis). 
 
 ' Fr;t,U;rolf and Landi.s: Am. .lour. Mod. Soi., Nov., 1909, p. 712. 
 Miollct: Wion. klin. VVndi., 1910, |,. 119, 
 
V. DISEASES OF THE TRICUSPID ORIFICE 
 
 Pathogenesis. — Valvular disease of the right heart is much 
 less common than of the left. This apparently bears some relation 
 to the much greater work which the left heart has to perform, 
 since during fetal life, when this difference does not exist, the 
 proportionate involvement of the two sides is about equal. Two 
 facts which recent investigations seem to have emphasized are 
 that tricuspid disease, while by no means common, is not so rare 
 as has hitherto been supposed, and that when present it is more 
 frequently the result of acquired disease than of a congenital 
 defect. This statement, of course, refers only to actual organic 
 disease of the valve, and not to simple atonic dilatation of the 
 orifice, which is very common. The functional efficiency of this 
 valve depends very largely upon the tone of the sphincter-like 
 muscular fibers surrounding the orifice. Both Harvej^ and Hunter 
 realized that the tricuspid valve is a much less perfect valvular 
 mechanism than the mitral. We are not surprised to find, there- 
 fore, that tricuspid stenosis is one of the rarest, and tricuspid 
 insufficiency one of the commonest, valvular lesions. 
 
 Griffith,' in an excellent study of 270 cases of tricuspid disease, in which 
 simple dilatation was excluded, has called attention to the foregoing facts. 
 Among 150 specimens of cardiac disease in the Pathological Museum of York- 
 shire College studied by him, there were no less than 26 instances of organic 
 tricuspid disease, all of which were apparently acquired after birth. Fenwick - 
 and Herrick ^ have arrived at similar conclusions. The latter among 154 cases of 
 tricuspid stenosis found an antecedent rheumatic history in 57, probable rheu- 
 matism in 4, chorea in 2. Among 28 there was no such history, and in the re- 
 mainder the etiologic factor could not be determined. Combining the statistics 
 of Leudet,'' Herrick, and Griffiths, there was a history of rheumatic fever or 
 
 1 T. W. Griffith; Edinburgh Med. Jour., 1903, Iv, 105. 
 -Fenwick: Transactions Pathological Society of London, ISSl. 
 ' Herrick: Boston Med. and Surg. Jour., 1S97, cxxxvi, 2-15. 
 "Leudet: Paris Thesis, 1881. 
 
DISEASES OF THE TRICUSPID ORIFICE 87 
 
 chorea in 34.9 per cent. Pitt's ^ series showed a percentage of 62, due to these 
 causes. 
 
 Tricuspid stenosis is nearly always associated with other valvular lesions, 
 especially mitral stenosis, as the collected statistics of Herrick show. 
 
 Tricuspid and mitral stenosis 102 
 
 Tricuspid stenosis alone 14 
 
 Tricuspid and pulmonary 1 
 
 Tricuspid, aortic, and pulmonary 2 
 
 Tricuspid and aortic 64 
 
 Tricuspid and mural 1 
 
 184 
 
 In only 6 of the last-named author's cases was there not also some mitral 
 involvement, and in only 4 cases were all the other valves normal. The Guy's 
 Hospital material collected by Pitt showed only 2 among 87 cases without coin- 
 cident mitral stenosis. These facts alone point very strongly toward an in- 
 flammatory origin, although they have been used in explaining the tricuspid 
 stenosis as the result of back pressure from mitral obstruction. But such a 
 result does not follow mitral insufficiency in which there is also back pressure, 
 and, furthermore, actual endocarditic vegetations are not infrequently found on 
 the tricuspid valve. However, some recent investigations have tended to 
 corroborate the back pressure theory. "In view of the work of Goodhart, Roy 
 and Adami, and Weber and Deguy, it is not unlikely that the overstrain of the 
 right ventricle leads to edema and hemorrhage into the tricuspid valve, and that 
 these processes usher in the fibrosis. In other words, the mitral lesion itself 
 becomes an etiologic factor in the tricuspid lesion, and the pathologic process 
 completed in the mitral is now transferred one step back in the circulation and 
 repeats itself in the tricuspid" (Hirschfelder). 
 
 TRICUSPID OBSTRUCTION 
 
 Occurrence. — At the Philadelphia General Hospital among 
 8,640 autopsies there were 162 cases of chronic tricuspid endocard- 
 itis. There were 58 instances of marked incompetence, 8 cases 
 of stenosis, 4 cases of marked calcification, and 1 case of super- 
 numerary leaflets. Tricuspid obstruction is much commoner 
 in women than in men (133 to 38) and between the second and 
 third decades (Herrick). 
 
 Occasionally tricuspid obstruction has a congenital origin. 
 Some cases show a nodular condition of the valves near their 
 margins. In the fetus the blood-vessels extend nearer to the free 
 
 ' Pitt: Allbutt's Sy.stom of Medicine, vol. i. 
 
85 STUDIES IN CARDIAC PATHOLOGY 
 
 margins than in the adult (Darier), and as thej^ retract small 
 areas may remain, which may cause hematomas. Rarely ob- 
 struction may be caused by tumors or ball thrombi (Gairdner). 
 Morbid Anatomy. — From what has just been said it will be 
 evident that the condition of the heart will vary according to 
 the time at which death occurred. During the first stage there 
 will be a hj'pertrophic enlargement of the auricular wall and of 
 the superior vena cava. During the second stage the caval 
 orifice is found greatly enlarged, so that the auricle and the veins 
 form a continuous sac. Thus, in one case a thrombus was found 
 which extended from the auricle directly backward into the cervical 
 vessels. The auricular myocardium in such cases undergoes 
 atrophy and may become almost a mere fibrous sac formed by 
 the endocardium and epicardium. Pericarditis, sometimes acute, 
 but more frequently the chronic adhesive variety, has been found 
 
 Fig. 26. — Acute and Chronic Endocarditis, Mitral Stenosis. 
 
 A. L., white, laborer, aged forty-two years. (Philadelphia Hospital, vol. xviii, p. 210. 
 Physician: Dr. S. S. Cohen. Pathologist: Dr. Funke.) 
 
 Clinical Notes: Was admitted complaining of cough, anasarca, and dyspnea. The 
 latter had existed for two years. 
 
 Physical Examination: Heart: The apex-beat extends from the fifth to the eighth 
 interspaces in the anterior axillary line. There is no thrill. The dullness extends from the 
 mid-sternal to the anterior axillary lines. A presystolic murmur is heard near the apex when 
 the heart beats strongly. The first sound is loud and booming, and followed by a soft systolic 
 murmur which is transmitted to the axilla, at which point it is loudest. The aortic second 
 sound is feeble, the pulmonic second accentuated, and the heart action tumultuous. A sys- 
 tolic murmur is also heard at the aortic and at the tricuspid area. 
 
 The patient improved under treatment until he was able to leave his bed for half an hour. 
 On the second day of his so doing he suddenly fell to the floor, greatly cyanosed, and died almost 
 at once. 
 
 Pathologic Di.^gnosis: Acute and chronic endocarditis, mitral stenosis, pulmonary in- 
 farction (anemic), renal congestio7i. 
 
 Heart: Weighs 500 gm. The right side is dilated, its muscle thin, bright red in color, 
 and its endocardium opaque. The foramen ovale is obliquely patulous. The tricuspid orifice 
 admits three fingers with ease. The right ventricular wall measures 0.5 cm.; it is quite firm, 
 and traversed by yellowish lines which commence in the subpericardial fat. The papillary 
 muscles are firm, and bright red in color. One of the mitral leaflets contains two fenestrations 
 along its line of contact. The pulmonary leaflets are normal. The left auricle is distended, 
 thin, pale, and its endocardium opaque. The mitral orifice barely adm,its one finger. The left 
 ventricle is large and contains several post-mortem clots, and measures 2.5 cm. at its thickest point, 
 its muscle being firm and pale. The mitral leaflets are thickened, shortened, and adherent, 
 especially at the inner angle. On the posterior surface are numerous small, pendulous, pinkish 
 vegetations, about 4 mm. in length, which are adherent to the leaflets. The aortic leaflets are 
 slightly thickened, especially at their bases. 
 
Fig. 26. 
 
90 STUDIES IN CARDIAC PATHOLOGY 
 
 with somewhat astonishing frequency. In so far as the valves 
 are concerned the structural changes which have been noted 
 are practically those which are met with in other varieties of 
 endocarditis — vegetations, sclerosis, changes in the chordse 
 tendinese, papillary muscles, etc. (See Figs. 23, 24, 28.) In two 
 instances pedunculated tumors have been reported. Perhaps the 
 most frequent finding has been a fusion of the valvular curtains, 
 producing a funnel-shaped stenosis. The degree of the latter, 
 of course, varies with the case. In the older writings several 
 references are made to the case of General Wipple, reported by 
 Corvisart, in which the valves were so extensively calcified that 
 only a small slit-like opening remained. 
 
 Recent vegetations, even when of considerable size, are more 
 apt to produce an insufficiency than a stenosis. Such high degrees 
 of contraction as are met with in mitral disease are very rarely 
 found, and nearly always the aperture will admit two fingers. 
 The crescentic slit so common in mitral stenosis is rarely found 
 on the right side of the heart, whereas calcification seems to be 
 much more common (Crawford).^ 
 
 Inasmuch as the congenital variety of tricuspid stenosis is, so 
 far as we can judge, generally the result of a fetal endocarditis, 
 it is not surprising that the pathologic appearance presents no 
 especial features distinguishing it from the post-natal form. It 
 may, however, be due to true malformation and be associated 
 with other anomalies, such as a persistent ductus arteriosus, im- 
 perforate ventricular septum, patulous foramen ovale, etc. 
 
 Before closing this section, attention should be called to the 
 fact that, owing to the almost constant association of tricuspid 
 and mitral stenosis, it is often very difficult to determine how 
 much or how little effect the latter has had in bringing about 
 the secondary changes in the heart. 
 
 (Figs. 15, 20b, 23, and 24 were from cases of combined lesions; 
 in the first, at least, there was a definite history of rheumatic fever 
 
 ' R. Crawford: Practitioner, 1907, Ixxviii, 191. 
 
Fk;. 27. — Chronic Mitral Endocarditis. 
 
 Female, white, aged forty-three years. (Pennsylvania Hospital. Autopsy No. 309. 
 Pathologist: Dr. Longcope.) 
 
 Clinical Notes: Past history negative. For the last six weeks has had abdominal 
 swelling, post-prandial discomfort, slight loss of weight, and some edema of the feet. 
 
 A systolic murmur is heard at the aortic area which is transmitted down the sternum. 
 There is also a systolic thrill. Ascites is present. Paracentesis abdominalis was twice per- 
 formed. Death occurred gradually, with the symptoms of peritonitis. 
 
 Pathologic Diagnosis: Carcinomatosis of the peritoneum, etc. Chronic mitral endo- 
 carditis. Fatty degeneration of the heart, etc. 
 
 Pericardiu.m: Contains 100 c.c. of clear fluid. It shows no abnormalities. 
 
 Heart; Is not increased in size; it weighs 240 gra., and contains fluid blood and a few 
 postmortem clots. The epicardium contains much fat; it is smooth and glistening and its 
 ve.s.sels are not especially prominent. The heart muscle is of a pale yellowish-brown color, 
 and shows yoUowi.sh flecking beneath the endocardium of the left ventricle, which is 12 to 15 
 ram. in thickness. Tricuspid and pulmonary valves are normal. The mitral valve is thickened 
 along its free edqes, the leaflets are slightly retracted, and the chordm tendine(E are distinctly short- 
 ened. The aortic valves are thickened, not retracted; the corpora? Arantii are knobbed. The 
 aorta show.s moderate sclerosis, in irregular plaques, and one or more calcified plates. The 
 coronary arteries are patent and smooth. The auricular appendages are free from thrombi. 
 
92 STUDIES IN CAKDIAC PATHOLOGY 
 
 four years before death.) The diagnosis is, therefore, obviously 
 often overshadowed bj^ the associated mitral lesion. In the few 
 cases of isolated tricuspid stenosis which have been reported, 
 the diagnosis of mitral stenosis was generally made, although 
 there have been several cases in which the condition has been 
 correctly recognized intra vitam, beginning with Gairdner's case 
 in 1862.' 
 
 Pathologic Physiology. — In case of obstruction of the tricuspid 
 orifice the right ventricle is filled more slowly than normal, and 
 the right auricle hypertrophies. When the stenosis increases 
 or the nutrient blood-supply fails to meet the unusual demands, 
 dilatation follows. Clinically this is well illustrated in the char- 
 acter of the venous pulse. During the first stage the auricular 
 (presystolic) wave is large and well marked; during the second 
 stage, when the auricle becomes overdistended and paralyzed, 
 the veins remain permanentlj^ full and cease to pulsate. At 
 first the venous regurgitation into the cavse is prevented by a 
 hypertrophy of the tenia terminalis and the other fibers which 
 tend to close the caval orifice of the auricle during its systole. 
 Later, stasis and congestion of the portal sj^stem, etc., follows. 
 (See Fig. 46.) 
 
 TRICUSPID INSUFFICIENCY 
 
 Pathologic Anatomy. — The leaflets are generally elongated and 
 thinned, while the free margins are thickened and (contrary to 
 mitral insufficiency) everted. The thickened portion may be 
 soft or indurated, and not rarely on its auricular surface shows 
 localized loss of tissue, resembling ulceration. (This occurred 
 in 17 of Sierro's - 38 cases.) These changes occur oftenest on 
 the free margin of the middle leaflet, with the anterior leaflet 
 next in frequenc3^ The chordae tendinese are often attenuated 
 and elongated, and the tip of the papillary muscle not infrequently 
 is indurated. The tricuspid opening is enlarged. There is also 
 
 1 Gairdner: Clinical Medicine, 1862, p. 602. 
 
 2 Sierro : Contribution a lY'tude des ulcer, chron. dc la valvule tricuspide, These de Geneve, 
 1886. 
 
Fio. 
 
 •Ar't-fE AND Chronic Endocarditis of the Aortic, Mitral, 
 Valves. 
 
 AND Tricuspid 
 
 The uppfT portion of the auricles has been cut away. The three valvular orifices thus 
 e.'cpo.sed show induration and contraction of their component tissues. The mitral valve in 
 nrldition shows a Larue dark mass of vegetations of recent origin which almost completely 
 occlude its orifice. The endocardium and myocardium of 1)(]( h auricles are t hickened. (Photo- 
 graph by Dr. Alfred II. Allen.) 
 
94 STUDIES IN CARDIAC PATHOLOGY 
 
 a diffuse thickening of the endocardium of the right auricle. The 
 right auricular appendix is dilated and the fossa ovalis depressed. 
 In cases in which the foramen ovale is patent, the surrounding 
 endocardium is additionally thickened. The auricular muscle 
 is at times hypertrophied, again seemingly attenuated (Zahn). 
 
 Pathologic Physiology. — Stadler ^ has produced tricuspid in- 
 sufficiency experi'mentalhj in rabbits. The animals lived several 
 weeks (nine to one hundred and seventy-six days), and developed 
 ascites, edema, and hepatic enlargement. The hearts were 
 examined by Miiller's method and showed distinct hypertrophy 
 of the right auricle and ventricle, but in some marked cases 
 atrophy of the left ventricle occurred, due apparently to the 
 smaller amount of blood handled. In the less severe lesions this 
 did not occur, from which it appears that even tricuspid insuffi- 
 ciency may be compensated by increased vascular tone and hyper- 
 trophy of the right auricle, which not only contracts more forcibly 
 but aspirates blood from the veins more powerfully. 
 
 Both the heart and the vense cavte play an important role in 
 maintaining compensation in tricuspid insufficiency. By virtue 
 of the increased venous pressure the right ventricle may be said 
 to contract against a wall of blood which helps to prevent re- 
 gurgitation. Again, this increased venous pressure causes a 
 rapid filling of the chamber during diastole. 
 
 Franke has called especial attention to the role of the liver. 
 Inasmuch as all cases of tricuspid insufficiency are not accompanied 
 by ascites, and since neither suction of the right heart nor elasticity 
 of the venaj cavse are sufficient to explain its non-occurrence, we 
 must assume that the liver plays an important role. During 
 systole venous blood is actually forced out of the hepatic cells 
 into the portal system, by the higher pressure which exists in 
 the arterial system.- (See Fig. 46.) 
 
 Of course, this really means that the left ventricle is doing 
 
 ' Deut. Arch. f. klin. Med., Ixxxiii, 1 and 2. 
 = Franke: Wien. klin. Woch., 1906, No. 31. 
 
DISEASES OF THE TRICUSPID ORIFICE 95 
 
 the work of keeping up excess pressure in tricuspid insufficiency, 
 just as the right ventricle does in mitral insufficiency. ^ When large 
 quantities of blood are penned up in the veins however, the left 
 ventricle has less to handle and maj^ decrease in size.- 
 
 In children the tendency to tricuspid insufficiency is minimized 
 by the more horizontal position of the heart. Gravity has thus 
 little effect. The negative pressure created by ventricular diastole, 
 plus the auricular systole, are the chief factors in filling the ven- 
 tricle (Fetterolf and Gittings). 
 
 Relative tricuspid insufficiency is a common lesion. Structurally 
 this valve is inferior to the mitral, and with dilatation of the 
 right heart incompetency^ is readily induced. This is due not 
 onh' to relaxation of the tricuspid sphincter, but more especially 
 to the fact that in dilated hearts the origins of the chordse tendinese 
 and the papillary muscles are too far from the center of the ven- 
 tricular cavity to permit perfect valvular closure.^ Tricuspid 
 insufficiency may occur during parturition, and in various forms 
 of prolonged and arduous labor which necessitate great muscular 
 and intrathoracic straining. 
 
 Clinical Considerations. — Gibson has stated that tricuspid 
 insuflficiency, far from being a rare lesion, is the commonest of 
 all valvular insufficiencies. This is probably correct if we include 
 the functional regurgitation which occurs after the manner of a 
 safety-valve under great muscular strain, and under other condi- 
 tions of increased right ventricular pressure. The sweeping state- 
 ment of Romberg, that "isolated tricuspid insufficiency has not 
 j^et been described," evidently does not refer to the relative 
 insufficiency above referred to. The safety-valve effect alluded 
 to, which was first emphasized by T. W. King, of "moderator 
 band fame," although it had been described b.y earlier writers, is 
 by no means universally accepted as a fact. 
 
 ' Calvert: Arch. Int. Med., April, 1908. 
 
 ^Stadler: Arch. f. klin. Med., 190.5, Ixxxiii, Heft 1 und 2. 
 
 ' Krehl: Arch, f, Anat. u. Physiol., 1889, p. 289. 
 
VI. DISEASES OF THE PULMONARY ORIFICE 
 
 " Steucturally the pulmonary valve and its surroundings 
 differ from those of the aortic valve in their more delicate texture, 
 and in the fact that in the adult the segments do not, as a rule, 
 show the medial thickening about the corpora Arantii. The wall 
 of the pulmonary artery is thinner than that of the aorta and has 
 not the same tendency to preserve its ring structure in the absence 
 of an internal pressure. The conus arteriosus which leads into 
 the pulmonary arterj^ is more thin-walled than the corresponding 
 part of the left ventricle, and under increased internal pressure is 
 probably capable of considerable dilatation. The structures in 
 relation to the pulmonary valve are obviously directed as a whole 
 to withstanding much less pressure than the corresponding parts 
 of the aorta, and this is borne out by what is known regarding 
 the relative pressures in the two sides of the heart. "^ Among 
 4,547 autopsies and 238 cases of valvular disease Willigk found 
 9 cases of pulmonar}^ endocarditis. 
 
 PULMONARY OBSTRUCTION 
 
 Pathogenesis. — Obstruction of the pulmonary orifice is one of 
 the most rarely acquired, and the commonest of congenital, val- 
 vular lesions of the heart. It maj' be produced by infectious dis- 
 eases, yet often no such history is obtainable. Some of the cases 
 have been due to sclerotic or gummatous syphilitic lesions. Again, 
 pulmonarj^ stenosis may result from pressure from an aortic 
 aneurism or tumor. Some cases have been ascribed to a fetal 
 endocarditis; against this hypothesis is the fact that the inflam- 
 matory condition should remain so localized. In one case re- 
 ported by Dittrich the etiologic factor appeared to be the kick of 
 a horse on the precordium.- From both an anatomic and an 
 
 ' Osier and Gibson: Osier's "Modern Medicine," vol. iv, p. 251. 
 ^ Dittrich: Vierteljahrsch. f. prakt. Heilkunde, 1849, p. 1.57. 
 96 
 
DISEASES OF THE PULMONARY ORIFICE 97 
 
 etiologic standpoint obstruction of the pulmonary orifices is 
 divided into two classes: (a) stenosis the result of acquired patho- 
 logic alterations; (fe) atresia, the result of congenital malformation. 
 Narrowing may occur either at the orifice proper, in the first 
 part of the artery, or in the conus arteriosus. Not infrequently 
 insufficiency of the valve also exists. 
 
 Morbid Anatomy. — In the majority of cases pulmonary stenosis 
 is due to an abnormalitj^ or hypoplasia of some part of the pul- 
 monary tract, such as the conus, in which the leaflets themselves 
 may or may not be involved. "In these cases a defect of the 
 interventricular septum is usually associated and a deviation to 
 the right of the aorta, so that this arises from both ventricles 
 above the defect. Such forms, which seem to suggest a develop- 
 mental origin, make up the great majority of cases of pulmonary 
 stenosis, and the combination of these three conditions, pulmonary 
 stenosis, defect of the septum at the base, and rechtslage of the 
 aorta, is probably the commonest of all cardiac anomalies" 
 (Abbott). Some cases result from induration, thickening, fusion, 
 or calcification of the valve leaflets without other structural defects, 
 and are manifestly the result of an inflammatory process. Ac- 
 cording to Keith, the conus of the right ventricle is involved in 
 90 per cent, of the cases. In most of the cases the right auricle 
 and ventricle are hypertrophied and dilated. With increasing 
 stasis tricuspid insufficiency is often superadded. 
 
 Pulmonarj' stenosis seems distinctly to predispose to tubercu- 
 lous disease of the lungs. Among 449 cases of the former there 
 were 160 of the latter.^ 
 
 Pathologic Physiology. — "In congenital cases the effect on 
 the lioart depends largely on the state of cardiac development 
 at which the pulmonary narrowing is produced. If it appears 
 before the end of the third month, the interventricular septum 
 does not close; if after this date, the foramen ovale and ductus 
 arteriosus may remain patent. The condition of the right ven- 
 
 ' (!. W. .Norris: "Tiiljt-rculo.si.s ami iJcurt Disoasc," Airi. Jour. Med. Sci., Oct., li)0-l. 
 
98 STUDIES IN CARDIAC PATHOLOGY 
 
 tricle varies with the degree of occlusion of the pulmonic orifice. 
 If the opening is completely blocked, the ventricle may remain 
 small and undeveloped, but with less degrees of narrowing the 
 chamber is commonly greatly hypertrophied " (Colbeck). 
 
 PULMONARY INSUFFICIENCY 
 
 Pulmonary insufficiency is a rare lesion. Only one case was 
 found among 8,640 autopsies at the Philadelphia Hospital, and 
 24,000 medical cases admitted to the Johns Hopkins Hospital 
 revealed only 3 cases. 
 
 Pathogenesis. — Pulmonary insufficiency may result from in- 
 fective endocarditis, or from the long-continued pulmonary hyper- 
 tension which occurs in mitral disease, emphysema, and other 
 forms of chronic lung disease. Pitt has called attention to its 
 relative frequency as a result of gonorrheal endocarditis. It occurs 
 in both sexes, is a disease of early life, and is usually associated 
 with obstruction. Sometimes pulmonary sclerosis may be simply 
 a part of a general systemic process. Pulmonary incompetence 
 may result from congenital malformation, although as a rule such 
 abnormalities, which are relatively frequent and generally consist 
 either of an increase or a diminution of the number of leaflets, 
 are unproductive of leakage. Among the Philadelphia Hospital 
 autopsies (8,640) there were 5 cases of supernumerary leaflets, 
 other anomalies 4, fenestration 17. (See Fig. 81.) At times 
 pulmonary incompetence results from aneurism or rupture of a 
 valve. 
 
 From a study of 172 reported cases of sclerosis of the pulmonary artery 
 Posselt found the following conditions associated: mitral stenosis, 47; myo- 
 carditis, 25; arteriosclerosis, 21; polyarthritis, 20; aneurism of the pulmonary 
 artery, 18; other cardiac lesions, 17; patulous ductus Botalli, 15; adhesive 
 pericarditis, 15; syphihs, 12; emphysema, 12, etc' 
 
 It is probable that a relative insufficiency due to dilatation 
 also occurs when pressure in the pulmonary circuit is much in- 
 creased. Gibson has shown that in a normal human heart post 
 
 ' Lubarsch and Ostertag's Ergebnisse d. allg. Path., 1909, i, 444. 
 
DISEASES OF THE PULMONARY ORIFICE 99 
 
 mortem the pulmonary valve begins to leak when pressure is 
 raised to from 16 to 26 c.c. of mercury. 
 
 Pathologic Anatomy. — Well-marked changes in the endocardium 
 of the right heart in cases of pulmonary insufficiency are not 
 often found. The pathologic alterations which are frequently 
 encountered in the left heart when the valves are incompetent 
 are generally absent or but slightly marked. The pulmonary 
 leaflets are less thickened and atrophy or sclerosis of the endo- 
 cardium is less markedly evident. There is, however, generally 
 a dilatation of the right ventricle and of the conus arteriosus.^ 
 
 An unusual case of pulmonary endocarditis causing perforation of the ven- 
 tricular septum followed by embolic gangrene of the nose and ears, and multiple 
 infarcts in the kidneys, has been reported by Fisher and Longcope.- Reitmann ' 
 has reported symptomless pea-sized hyalo-fibromas in the nodules of Arantius 
 of the anterior pulmonary leaflet in a patient of seventy-four years. 
 
 Isolated atheroma and dilatation of the pulmonary artery has been generally 
 regarded as of considerable variety. Romberg's case has been extensively 
 quoted in the literature, and a few other cases are on record. L. Rogers has 
 recently reported 10 cases, and states that the condition is not infrequent in 
 Bengal, where his material was collected. 
 
 Marked hypertrophy of the right ventricle was observed, the patients dying 
 with symptoms of right heart failure, and frequently showing hydropericardium, 
 resulting from dilatation of the coronary veins. The valve leaflets nearly always 
 escaped. Contrary to other forms of arteriosclerosis, it occurred most frequently 
 in women. The explanation seems to lie in the fact that these cases are syphilitic 
 in origin. Disease of the pulmonary artery has also been attributed to the arti- 
 ficial plethora of prolonged and excessive beer-drinking.'* While doubtless most 
 cases of sclerosis of the pulmonary artery are secondary to such cardiac lesions 
 as lead to tricuspid insufficiency, yet some cases have been reported in which the 
 pulmonary sclerosis seemed to be the primary lesion.^ The most important 
 factors are mechanical — increased or variable blood-pressure, in which intoxica- 
 tion and infection perhaps also play a role." 
 
 ' Zahn: Vcrhandl. d. Konsr. f. inn. Med., 190.5, p. 359. 
 
 ^ Fi.sher and Longcope: Proc. Path. Soc. Phila., 1903, p. 98. 
 
 ' Reitmann: Zeit. f. Heilk., xxvi, Abth. f. path. Anat., Heft. I. 
 
 * Kitamura: Zeit. f. khn. Med., Ixv, Heft. I and II. 
 
 •'■ Sanders: Arch. Internal Medicine, April, 1909. 
 
 ' Laubry and Parvu: Tribune Med., 1909, p. 485. 
 
VII. ACUTE PERICARDITIS 
 
 Occurrence.^ — Pericarditis may occur in any form of general 
 infection. Brooks and Lippincott^ found that 46 out of 67 cases 
 were due to general bacterial infections. Some of these diseases, 
 such as rheumatic fever and pneumonia, however, are much more 
 prone than others to be thus complicated. It is apparently more 
 common in children than in adults, especially in the rheumatic 
 fever of the second decade, and, as might be expected, in chorea 
 (19 out of 73 autopsies — Osier). Andrew among 1,474 cases of 
 heart disease found 25 cases of pericarditis. 
 
 Pathologic Anatomy. — The earliest manifestation of pericarditis 
 consists in a vascular engorgement, which spreads from the course 
 of the larger vessels as the process advances. Small localized 
 granulomas occur chiefly at the base of the heart. Associated 
 with this vascular injection the normally transparent and glistening 
 membrane becomes cloud}' and roughened as the result of fibrous 
 exudation and of tumefaction of the endothelium. If the deposi- 
 tion of fibrin increases, it is formed into ridges by the friction of 
 cardiac contraction, producing a reticulated appearance which 
 has been compared to honeycomb, the rippled sea, the rugse of 
 the second stomach of the calf (Corvisart), buttered bread, two 
 slices of which have been separated (Laennec). 
 
 Following the inflammatory engorgement there may be more 
 
 'Brooks and Lippincott: Am. Jour. Med. Sci., Dec, 1909. 
 
 Fig. 29. — Fibhinopurulent Pericarditis. 
 
 D. AI., male, aged thirty-six years. (Philadelphia Hospital, vol. xvii, p. 141. Physician: 
 Dr. Hawke. Pathologist: Dr. A. J. Smith.) 
 
 P.\THOLOGic Diagnosis: Croupous pneumonia of right upper lobe, plastic pleuritis, 
 fibrinopurulent pericarditis, etc. 
 
 Autopsy Notes: The pericardium contains 300 c.c. of slightly brownish, thin, turbid 
 fluid. Both the visceral and parietal layers are covered with a layer of yellowish plastic exudate, 
 mth the characteristic villosities and lines. The heart with its contained blood and with the peri- 
 cardium weighs 880 gm. Circumference at the base 78 cm. External length of ventricle, 1 1 cm. 
 
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102 STUDIES IN CARDIAC PATHOLOGY 
 
 or less liquid exudation, which may be simply serous or a mixture 
 of serum with fibrin, blood, or pus. In rheumatic fever the exudate 
 is generally serofibrinous. Purulent cases are particularly frequent 
 in childhood, and when the pneumococcus is the offending organism. 
 Blood-stained exudates are met with in tuberculous, cancerous, 
 purpuric, scorbutic cases, and in the terminal stages of Bright's 
 disease. At times considerable blood may be found without 
 evident cause; such cases probably result from microscopic vas- 
 cular lesions. 
 
 A simple serous effusion may be absorbed without permanent 
 damage. If fibrin is present, adhesions are apt to form when the 
 parietal and visceral layers again come in contact. Sometimes 
 such adhesions may be broken up, or. again, permanent synechiae 
 may remain. The distinction between fibrinous and serofibrinous 
 pericarditis is one of degree only; the essential process is the same. 
 According to Ziegler, vascularization of the exudate from the 
 vessels on the pericardial surface begins by the third or fourth 
 day. Under favorable circumstances more or less complete 
 resorption of even a fibrinous exudate may occur, only a small 
 circumscribed macula or adhesion remaining. As a rule, the 
 visceral layer shows the most marked changes on account of its 
 
 Fig. 30. — Subacute Fibrinous Pericarditis. 
 
 ,J. M., male, aged thirty years. (Pennsylvania Hospital. Autopsy 1.57. Phj-sician: 
 Dr. Stengel. Pathologist: Dr. Longcope.) 
 
 Clinical Notes: Never ill until two months ago, when he developed pain in the left side 
 of the thorax. This eventually proved to be an empyema, which was opened and drained at 
 the hospital (Dr. Spellissy). Heart dullness was increased laterally. The apex-beat was 
 neither palpable nor visible. Death occurred gradually. 
 
 Pathologic Diagnosis: Subacute fibrinous pericarditis. Fibroid tuberculosis; bronchi- 
 ectasis, etc. 
 
 The left lung is densely adherent to the pericardium along its entire length, both lungs 
 being adherent to the parietal pleura, just below the opening of a small sinus which leads from 
 the abscess cavity. 
 
 The pericardium is adherent to epicardium, and its sac contains a small amount of purulent 
 fluid. Between the pericardium and epicardium there is a thick fibrinous network of adhesions, 
 giving it a "bread and butter" appearance. The heart muscle is soft and moderately pale. 
 The epieardial fat is abundant, and strands of connective tissue can be seen running into 
 the heart muscle. The left ventricle measures 2 cm. in thickness. The valves are normal; 
 pulmonic orifice S..5 cm., aortic 8 cm., in circumference. 
 
104 STUDIES IN CARDIAC PATHOLOGY 
 
 greater vascularity and activity. When pyogenic organisms are 
 present, a great outpouring of leukocytes occurs; the liemorrhagic 
 form is merely the result of the addition of erythrocj^es. Trauma 
 may play both a direct and an indirect role in the production of 
 pericarditis. Puncture, the injection of turpentine, blows upon 
 the precordium, mediastinal irritation due to prolonged passage 
 of a stomach-tube, may produce pericarditis. The scant blood- 
 supply of the sac doubtless favors infection, and the toxin developed 
 in its neighborhood seems to have a predisposing effect (Charrin). 
 The experimental work of Kuelbs showed that when pericardial 
 lesions resulted from precordial blows, they were generalh' slight 
 and consisted of small hemorrhages. 
 
 The serofibrinous form occurs very frequently in pneumonia, 
 infection seeming to take place through the pleura or mediastinum. 
 The auricles are first and chiefly involved, the visceral layer show- 
 ing changes later. As the disease advances small inflammatory 
 areas coalesce until the whole heart may be enveloped in a thick, 
 yellowish, fibrinous mold. 
 
 The chemical constituents of an inflammatory pericardial exudate 
 are practically those of the normal secretion. In some cases, 
 especially the nephritic ones, both alcohol- and water-soluble 
 extractives are somewhat increased (Erben).^ 
 
 A normal pericardium has a capacity of from 180 to 200 c.c. 
 As large an amount as 800 c.c. can be forced into the sac, but 
 anything beyond this is due to stretching — actual enlargement 
 of the membrane (Schaposchikoff and Damsch). The effusion of 
 disease is often much larger than could be forced into a normal 
 pericardium. As was pointed out by Smith and Lusk, this is 
 accounted for by a softening and stretching of the sac which 
 results from the inflammatory processes. The fact that exudates 
 are not absorbed from an inflamed pericardium as they are if 
 drained into a healthy serous cavity, as, for example, the pleura, 
 
 ' Erbcn : Klin. u. Cheni. Beitrage z. Lehre der exud. Pericarditis, Vienna, 1905. 
 
ACUTE PERICARDITIS 105 
 
 is perhaps due to pressure of the exudate upon the stomas, and 
 upon the fact that these are plugged with fibrin.^ 
 
 Purulent pericarditis arises if pj^ogenic organisms are introduced 
 either by way of the blood-stream or the lymphatics, or by direct 
 rupture of an abscess into the sac. Two instances of the latter 
 cases occurred among my 8,640 autopsies. When a serofibrinous 
 exudate undergoes transition into a purulent one, the fibrin becomes 
 more or less liquefied. As a rule, suppurative exudates are smaller 
 than serofibrinous ones. Gas is sometimes found in the sac, 
 produced by the bacillus aerogenes capsulatus. Some j^ears ago 
 James- collected 38 cases of pneumopericardium. Twenty-six 
 were fatal. Among those which recovered, 4 were due to stab 
 wounds and 4 to other forms of trauma. 
 
 Penetrating wounds generally produce the purulent form of 
 the disease. Rareh' such perforation may occur from some object 
 lodged in the esophagus. Flint reported such a case in which 
 the offending object was a set of false teeth. Some very large 
 liquid exudates have from time to time been reported: Sir A. 
 Clark, 4 liters of seropurulent effusion; Osier, 2 to 3 liters; Hirtz, 
 2,790 c.c; Thayer, 4,000 c.c. 
 
 The different varieties of pericarditis have been reported with 
 the following freciuency: 
 
 BreITUNG. NORRIS. NORRIS. 
 
 (Charite, (Philadelphia (Pennsylvania 
 
 Berlin.) Hospital.) Hospital.) 
 
 Sero-fibrinous 108 132 44 
 
 Purulent 24 23 39 
 
 Hemorrhagic 30 18 3 
 
 Tuberculou.s 2(5 (2 primary?) 22 9 
 
 Chronic fibrous Ill .304 24 
 
 Obliterative 23 16 6 
 
 Calcification 2 7 1 
 
 Total number of cases .324 .529 126 
 
 Among 120 cases of ])ericarditis at th(! Pennsylvania Hos})ital 
 
 ' JJerginann (Charitd Annalen, 1909, p. 92) ; A case of large pericardial effusion was tapped 
 .so that it emptied itself into the healthy pleura, whence it was rapitlly and spontaneously 
 absorbed within throe days. 
 
 ^.James: American Medicine, .July 2, 1904. 
 
106 STUDIES IN CARDIAC PATHOLOGY 
 
 cultures were made from the exudate in 54 cases, with the following 
 bacteriologic findings: 
 
 Micrococcus lanceolatus 14 
 
 Pneumococous 10 
 
 Sterile 10 
 
 Unidentified species 6 
 
 Streptococcus pyogenes 5 
 
 Bacillus coli communis 3 
 
 Bacillus lactis aerogenes , 2 
 
 Bacillus proteus vulgaris 1 
 
 Micrococcus zymogenes 1 
 
 Mixed infections (included above) 4 
 
 Tubercle bacillus 1 
 
 Streptococcus mucosus 1 
 
 Contaminated cultures 2 
 
 The following pathologic conditions were associated with 
 pericarditis: Lobar pneumonia, 43; bronchopneumonia, 9; acute 
 endocarditis, 20; chronic endocarditis, 28; tuberculosis, 18; 
 empj^ema, 11; mediastinitis, 3; typhoid fever, 4. 
 
 Previous disease or trauma may prepare the soil for subsequent 
 pericardial infection. Such infection may occur by way of the 
 blood-stream, the lymphatics, hj direct extension, or by perfora- 
 tion. 
 
 The parietal layer of the pericardium, according to Bizzozero and Salvioli,^ 
 contains a single network of lymphatics, which lie deeply embedded in the con- 
 nective-tissue stroma, and consist of interlacing vessels. Schwartzoff - has shown 
 
 ' Bizzozero and Salvioli: Arch, delle Scienze Mediche, vol. ii. 
 
 ^ Schwartzoff: Materialen z. Anat. u. Histol. d. Herzens u. s. Huellen, 1874 
 
 Fig. 31. — Fibrinous Pericarditis. 
 
 G. B., laborer, negro; aged twenty-six years. (Pennsylvania Hospital, November 16, 
 1909. No. 2763. Autopsy: 9.34. Pathologist: Dr. Crispin ) 
 
 Anatomic Diagnosis: Lobar pneumonia of whole right lung. Fibrinous pericarditis 
 with effusion. Fibrinous pleuritisof right side, etc. Cloudy swelling of heart, liver, kidneys, 
 etc. 
 
 Heart: Is of usual size, weighs 330 gm. It is covered with a thick, boggy, shaggy, yellow, 
 fibrinous exudate. The pericardial cavity contains 600 c.o. of yellow fluid, turbid with fibrin- 
 ous shreds and flecks. The right auricle is of normal size, its tips free from thrombi. Tri- 
 cuspid normal; also the pulmonary. The anterior leaflet of the mitral valve has quite a thick 
 fibrous edge, but the chordos are not much thickened or shortened. Papillary muscles are pale and 
 thickened. Ventricular wall IS to SO mm. and very cloudy. There are a few yellow plaques on 
 the arterial wall about the aortic valves. 
 
 Microscopic Examination: The exudate covering the pericardium contains a moderate 
 number of polynuclear cells. The muscle-cells are much swollen and have a waxy appearance 
 (parenchymatous degeneration). 
 
 Bacteriologic Examination: From both lungs and from the pericardial exudate small 
 cocci were obtained, occurring in pairs, and Gram-positive. 
 
108 STUDIES IN CARDIAC PATHOLOGY 
 
 that these vessels drain into the glands which lie in the areolar tissue between the 
 pleura and pericardium. The lymphatics in the visceral layer are much richer 
 and intercommunicate. Nystrom ' considers the question debatable as to whether 
 the lymphatics of the pericardial cavity communicate with those of the external 
 layer. It would have to be assumed, therefore, that when the pericardium is 
 infected from the bronchial glands the micro-organisms travel in a direction 
 opposite to the lymphatic current, as may occur in carcinoma metastases. 
 
 Pathogenesis. — Pericarditis occurs chietij" in infectious dis- 
 eases — rheumatic fever, pneumococcic, gonococcic, streptococcic 
 septicemias, also in tuberculosis, syphilis, and scarlatina. It 
 occurs as a terminal infection in dyscrasic states, such as chronic 
 nephritis, diabetes, leukemia, etc. More rarely it follows from 
 the direct extension of an empyema, a subdiaphragmatic, medias- 
 tinal abscess, or from penetrating wounds or the infiltration of 
 neoplasms. Frequently pericarditis and endocarditis are asso- 
 ciated. In rheumatic fever, for instance, this is common. In the 
 suppurative pericarditis of childhood, however, which is nearly 
 always secondary to pulmonar}^ disease, the endocardium gen- 
 erall}^ escapes. Sixty per cent, of the pericarditis of childhood 
 results from empyema, the rest being made up by abscesses, 
 osteom3'elitis, pyemia, etc- 
 
 At the Philadelphia Hospital among 75 cases of acute aortic 
 endocarditis there were 20 cases of pericarditis; among 75 cases 
 
 ' Nystrom: Arch. f. anat. u. Physiol. Anat., Abth.. 1S97, p. 361. 
 - Poynton: Heart Disease and Thoracic Aneurism, 1907, p. 168. 
 
 Fig. 32. — Adhesive Pericarditis — Cor Villosum. 
 
 Wm. M., male, aged fifty-six years. (Philadelphia Hospital, vol. xvii, p. 217. Physician: 
 Dr. Musser. Pathologist: Dr. Coca.) 
 
 Pathologic Diagnosis: Chronic parenchymatous and interstitial nephritis, with renal 
 infarction. Adhesive pericardilis — cor villosum — acute valvulitis, etc. 
 
 Clinical History: The patient, a moderate consumer of alcohol, was admitted complain- 
 ing of dyspnea, cough, and asthenia, the first-named having been present for a number of 
 years. Temperature 101°, pulse SO, respiration 30, on admission. 
 
 Physical Examination: The apex-beat was not palpable. The heart -sounds were al- 
 most entirely obscured by rales. The pulse was weak and irregular. The heart-sounds at the 
 base were inaudible and this organ was enlarged to percussion. A sudden convulsion was 
 followed by unconsciousness, ending in death from edema of the lungs. Exploratory puncture 
 of the pericardium had given negative results. 
 
110 STUDIES IN CARDIAC PATHOLOGY 
 
 of acute mitral endocarditis there were 18 cases of pericarditis; 
 among 10 cases of acute tricuspid endocarditis there were 5 cases 
 of pericarditis. 
 
 Among the other lesions found there were fatty infiltration 
 of the pericardium 99, hydropericardium 199, pigmentation 1, 
 maculae albidse (exclusive of chronic pericarditis), 84. Brooks 
 and Lippincott found pleural lesions in 136 of 150 cases, acute 
 endocarditis in 10 out of 46, chronic endocarditis in 28 out of 67, 
 acute mj^ocarditis in 2 out of 67. 
 
 Hemopericardium results from rupture of a blood-vessel into 
 the sac. Such vessels ma}' be the aorta, the coronary arteries 
 or veins, superficial vessels injured during aspiration, or new 
 vessels formed in the course of inflammatory changes. In the 
 latter case the blood is generall}^ mixed with the exudate. At the 
 Philadelphia Hospital there were 16 cases of hemopericardium 
 in 8,640 autopsies. In cases in which death has resulted from 
 asphj^xia, small subpericardial ecchymoses are sometimes found, 
 especially at the base in the neighborhood of the epicardial vessels 
 — "spots of Tardieu." (See Figs. 40 and 41.) 
 
 Anthracosis of the pericardium has been reported by Askanazy.^ 
 
 From a clinical standpoint rheumatic fever is generallj^ stated 
 to be the most common cause of pericarditis. Among 1,000 
 cases of this disease at the Bethanien Hospital in Berlin, peri- 
 carditis occurred in 100, and endocarditis in 250 of the cases. 
 Well-marked effusion was present in 35 per cent, and slight effusion 
 in 14 per cent, of these; aspiration was necessarj' in 16 cases. - 
 
 Rheumatic fever has been credited as the causative factor of pericarditis, as 
 follows: Von Schroetter, 30 per cent.; Harras, 7 per cent.; McCrae, 5.9 per 
 cent.; Williams, 75 per cent.; Leudet, 22 per cent.; Bamberger, 30 per cent.; 
 Bauer, 16 to 20 per cent. ; Chambers and Thompson, 20 to 30 per cent. ; Phillipps, 
 4.7 per cent.; Ball and Sibson, 20 per cent.; WunderHch, 19 per cent.; Duchek, 
 16 per cent.; Latham, 5 per cent. ; Telter, 4.7 per cent.; Eichhorst, 3 per cent. ; 
 Taylor, 50 per cent. ; Poynton, 75 per cent, (fatal cases) ; Dunn, 19 per cent. 
 
 ' Askanazy: Zcntralb. f. path. Anat., 1906, No. 16, 17. 
 - Zinn: Therap. d. Gegenwart, September, 1909. 
 
I'lc. '4'-j. — Chronic Adhesive Pericarditis. 
 
 Showing almost complete obliteration of the sac, with marked thickening and extensive 
 extrapericardial adhesions. (Specimen from the German Hospital.) 
 
112 STUDIES IN CARDIAC PATHOLOGY 
 
 (children) ; Flint, 38 per cent. ; Ormerocl, 37 per cent. We must bear in mind, 
 however, that "rheumatism" is, and to an even greater extent was, a much 
 abused disease; many different forms of sepsis being included in the term. In 
 Sears' 100 cases of rheumatism, pericarditis occurred in 51 per cent. The fre- 
 quency of rheumatic infection as an etiologic factor has also been corroborated 
 by the experimental investigations of Wassermann, Poynton and Paine, Cole, 
 Walker and others. Sturges in 100 fatal cases of heart disease, of which 54 were 
 of rheumatic origin, found pericarditis in all but 6. Although there are many 
 exceptions, the pericarchtis of rheumatic fever generally occurs relatively early 
 in the attack — within the first two weeks. Chronic valvular lesions with hyper- 
 trophy, dilatation, and overaction undoubtedly predispose to it. 
 
 As long ago as 1600, Guarinon called attention to the frequency 
 of pneumonia as a causative factor of pericarditis; in fact, this 
 infection was blamed for the majority of cases until Bouillaud 
 emphasized the importance of rheumatic fever. Acute pericarditis, 
 either serous, plastic, or purulent, occurred 289 times among 2,439 
 pneumonia autopsies (11.8 per cent.), and 499 times among 
 40,773 cases of pneum^onia (1.2 per cent.) collected by the author. 
 It is bjf far the commonest cardiac complication, therefore, and 
 stands high up among complications in general. The wide varia- 
 tion in the frequency with which the condition has been reported 
 by different observers shows that, even allowing for errors, the 
 condition is more frequent at certain times. ^ That pericarditis is 
 frequently found unexpectedl.y at autopsy is well known. 
 
 Infection may occur through the blood- or the lymph-streams, but quite 
 often results from direct extension from infected areas of the lungs and pleurae. 
 In a large proportion of Jiirgensen's cases the hngual process of the left upper 
 lobe was cHseased. Sears and Larrabee found the right lung diseased in 10 out of 
 18 cases. Chatard noted the right lung in 13, the left in 5, and both lungs in 13. 
 Kerr found the left lower lobe involved in 12, the right lower in 9, the right middle 
 in 2, and both lower in 3 cases. J. A. Scott, in 76 autopsies on lobar pneumonia 
 at the Pennsylvania Hospital, Philadelphia, found pericarditis in 38 (50 per cent.). 
 In 20 (52.56 per cent.) the exudate was serofibrinous, in 17 (44.7 per cent.) puru- 
 lent, and in one case the pericardium was obliterated by chronic inflammation. 
 Among 40 cases of pericarditis 22 occurred in pneumonia ; in all of these pleuritis 
 coexisted, and in 6 cases both the pericarditis and the pl(?uritis were fibrinopuru- 
 lent. In 170 autopsies in pneumonia. Lance and Kanthack found pericarditis 
 
 1 Netter found pericarditis in pneumonia during the years 1837, 1876, 1882, 1886, and 
 1890 much more frequently than in the intermediate years. 
 
ACUTE PERICARDITIS 113 
 
 37 times. It was associated with the following conditions: acute endocarditis, 
 4; pleuritis or empyema, 8; peritonitis, 1; meningitis, 1; synovitis, 1; pleuritis 
 and peritonitis, 2 ; meningitis and peritonitis, 1 ; pleuritis and endocarditis, 1 . 
 Chatard found the pneumococcus in the pericardium in 19 out of 29 cases, no 
 other important organisms being cultivated. 
 
 Some j^ears ago the writer collected from various hospitals in 
 Philadelphia accurate data regarding 1,780 autopsies performed 
 on the subjects of tuberculous disease, and found 82 cases of 
 tuberculous pericarditis.'^ Among these statistics cases of simple 
 macular albidse were omitted, as were also all cases in which there 
 was a reasonable possibility that the pericarditis may have been 
 due to other causes than tuberculosis. 
 
 Actual tubercles were found in 32, and of the remaining 49, a careful study 
 of the records failed to disclose the evidence of an etiology other than tuberculosis. 
 While there were in the majority of instances no data as to the microscopic ap- 
 pearance of the tissues, it seems reasonable, to credit the existence of these lesions 
 to a tuberculous process; for it is well known that the majority of pleural scars 
 and adhesions, so frequently found at autopsies, arise in this manner, although 
 even the microscope fails to reveal either the tubercle bacillus or its characteristic 
 changes. Jaccoud,^ in 1893, reported a case of complete pericardial symphysis 
 in which all other causes could be positively excluded, and in which tubercle 
 bacilli containing mechastinal glands were the only other pathologic lesions found. 
 In 1885 the same author recorded a case in which the pericardium was macro- 
 scopically normal, but in which tubercle bacilli were microscopically demon- 
 strable. In Wells' ^ 24 cases of obliterative pericarditis the bronchial glands were 
 caseous in 10 instances. 
 
 In tuberculous pericarchtis the heart muscle at times undergoes caseous 
 infiltration and degeneration. This occurred in 5 of my 82 cases; other forms 
 of myocarditis, fatty or fibroid change, are more common. In one of Osier's 
 cases a thin film of auricular appendix alone was found intact ; the remainder of 
 the cardiac muscle in that region having undergone caseous necrosis. In the 
 chronic varieties of this disease the heart is frequently enlarged; at first hyper- 
 trophied by an effort to overcome the abnormal resistance caused by synechise, 
 effusion, or constriction of the large vessels; later, dilated through overwork, 
 malnutrition, and degeneration of its muscle-fibers. The site of the hyper- 
 trophy, of course, dopenrls on the location of the increased resistance. The 
 (|uestion as to whethtT liypcrtropliy will or will not occur depends largely on the 
 
 ' G. W. Norris: Univ. of Pennsylvania Med. Bull., .luly, 1!)()1. 
 ^ .Jacfoucl : Semainc M(jdif;ale, vol. xiii, ISOo, p. '21. 
 •■• \\i-\\<: .(.iiir. Am. .Med. Assoc, May 25, lOOI. 
 
114 STUDIES IN CARDIAC PATHOLOGY 
 
 integrity of the blood-supply and the state of the myocardium at the time when 
 the adhesions form. 
 
 Tuberculous pericarditis may occur as miliary tubercles, as large caseous 
 masses, or as simple fibrous thickening, with or without adhesions, in which 
 microscopically no specific tuberculous changes may be demonstrable. With 
 mixed infections any variety of exudate may be formed. 
 
 The effusion in tuberculous pericarditis may consist: (1) Of clear serum, its 
 nature being only demonstrable through the presence of pericardial tubercles or 
 tubercle bacilli. (2) Turbid or flocculent fluid is sometimes encountered; 
 usually if fibrin is present, it is adherent to the serous membrane. I found this 
 condition 17 times. (3) Hemorrhagic effusion occurred only 4 times, once coin- 
 cidently with uremia. Some authors have stated that the aspiration of sanguin- 
 eous pericarcUal fluid should lead one to suspect a tuberculous origin, a 
 statement which must be accepted with reservation. (4) Fibrinopurulent 
 exudate was encountered 7 times. In none of these cases was the condition 
 caused by the rupture into the pericarchum of a tuberculous lymph-node, as 
 happened in the cases reported by Zenker,' Kast,- Mickle,^ Heineman,'' and Finzi.' 
 The amount of effusion in tuberculous pericarditis is sometimes enormous. 
 The largest recorded in my series was Musser's" well-known case, in which 1,559 
 c.c. of hemorrhagic fluid was removed at autopsy. 
 
 The varieties of pericarditis as occurring in my series of tuberculous peri- 
 carditis may be tabulated as follows : 
 
 1. CHRONIC FIBROPLASTIC. 
 
 (a) Complete obliterative 24 
 
 (b) Partial obliterative 19 
 
 (c) Non-obliterative 3 
 
 2. ACUTE VARIETIES. 
 
 (ti) Serofibrinous 12 
 
 (6) Fibrinopurulent 7 
 
 (c) Fibrinoplastic .' 3 
 
 (d) Hemorrhagic 4 
 
 (e) Miliary 10 
 
 Tuberculous pericarchtis has been found more commonly in men; in the 
 present series it was overwhelmingly so — 86 males, 11 females — the sex of 4 hav- 
 ing been unrecorded. The ages ranged from seven weeks to seventy-seven 
 years, showing that no age is exempt. The former is, I think, the earliest time 
 of life at which a case has been reported; 22 cases occurred in negroes, being 
 probably about the same proportion to the entire series as the percentage of 
 negroes admitted to the hospitals. 
 
 ' Zenker: Quoted by Osier, Am. Jour. Med. Sci., 1S93. 
 
 ^ Kast: Virohow's Archiv., Bd. xcvi. 
 
 ' Mickle: Lancet, 1883. 
 
 ' Heineman: Lancet, Dec. 28, 1901. 
 
 ^ Finzi: La Riforma medica, Sept. 16, 1903. 
 
 " Musser: University Medical Magazine, Oct., 1888, p. 32. 
 
Fig. oi. — Chronic Adhesive Pericarditis. 
 
 The visceral layer shows marked thickening and opacities in places. Near the apex there 
 is a large, thick, firm arlhesion between the visceral and parietal layers, which presents the 
 evidences of prolonged traction, and doubtless played a considerable part in prodviction of 
 cardiac hypertrophy. 
 
116 STUDIES IN CARDIAC PATHOLOGY 
 
 Bamberger was one of the first to point out the frequency of 
 tuberculous pericarditis, he having stated that tuberculosis was 
 second only to rheumatic fever as an etiologic factor, a view 
 which has been reiterated by Osier. 
 
 The occurrence of pericarditis in nephritis was noted by Bright 
 himself in 8 per cent, of the acute and 6 per cent, of the chronic 
 cases. This was further emphasized by Thomas Taylor, who 
 among 50 autopsies found 5 acute and 7 chronic cases. Sibson 
 among 285 cases of nephritis at St. Mary's Hospital found it in 
 8.8 per cent., and in 8.17 per cent, of his 1,691 collected cases. 
 Lately it has been found in about 10 per cent, of the cases of in- 
 terstitial nephritis. 
 
 The pericarditis which complicates nephritis is generally a 
 terminal injection. Among 255 patients Avho died from cardiac 
 or renal lesions, Flexner found distinct evidences of terminal 
 infection in 213. The bacteriologic findings in the pericarditis 
 cases were as follows : Micrococcus lanceolatus, 11; streptococcus, 
 4; staphylococcus aureus, 1; bacillus pyocyaneus, 1; bacillus 
 influenzae, 1; mixed infections, 2; unidentified species, 1.^ In 
 8 of the cases the infection apparently followed pneumonia. 
 
 Some observers still believe that purely toxic cases may occur. - 
 Thus, Chattin found the exudate sterile in 3 out of 4 cases 
 of pericarditis occurring in nephritis: "The existence of asep- 
 tic amicrobic pericarditis in certain cases of Bright's disease 
 is well established." Furthermore, pericarditis did not occur in 
 32 of Flexner's cases of general infection in nephritis, whereas it 
 did occur in 23 in which there was a local infection.-* 
 
 The pericarditis which occurs in nephritis may assume any 
 of the acute or chronic types. A sanguineous exudate seems to 
 be more common than in the rheumatic varietv. Both onset 
 
 ' Flexner; Journal Experimental Medicine, 1S96, p. 1559. 
 
 = Banti: Zentralbl. f. path. Anat,, 1894, p. 461. 
 
 ' Babcock: Diseases of the Heart and Arterial System, 1903, p. 45. 
 
ACUTE PERICARDITIS 117 
 
 and course are often insidious, and the termination is usually 
 rapidly fatal. ^ 
 
 Gonococcus pericarditis, which is sometimes also associated with 
 endocarditis, generally occurs only in the severe and fatal cases 
 of gonococcus septicemia. In a study of the autopsy records 
 from such cases Tyree found pericardial involvement in 40 per 
 cent.; all forms of exudate were encountered.'^ 
 
 Syphilitic disease of the pericardium is probably less rare than 
 has generally been supposed. It is generally a tertiary manifes- 
 tation which occurs secondaril}^ to myocardial disease, as in the 
 cases reported by Ricord, Mragek, Herxheimer, and Virchow. 
 Well-marked gummatous lesions have been reported only three 
 times (McPhedran). Often the lesions appear as ordinary fibrous 
 changes. An especial variety has been described by Baker,' 
 consisting of numerous minute aneurismal dilatations of the peri- 
 cardial vessels, together with thickening or obliteration of the sac. 
 It is not unlikely that future studies based on the finding of the 
 spirocheta pallida will throw much light on the subject. Wacher 
 has recently reported a case occurring as an acute secondary 
 manifestation with recovery under specific treatment.* 
 
 Laennec himself excluded "milk spots'' as not being the results 
 of pericarditis. Recent corroboration of this view is forthcoming 
 as the result of the investigations of Herxheimer,-^ who has de- 
 scribed the microscopic appearances as found in a number of 
 specially studied cases. He invariably found the endothelial 
 layer of the pericardium destroyed, and replaced by fibrin, but 
 noted no round-cell infiltration in the underlying or surrounding 
 tissue. He believes, therefore, that milk patches have a mechanical 
 
 ' H. B, Mlyn: Pennsylvania Medical Journal, 1902, p. 120. 
 
 ^Tyrec: International Clinics, Scries 18, vol. ii. (A considerable number of cases of 
 Konococcus pericarditis are now on record, reference to which may be found in v. Hoffmann's 
 article, Centralb. f. d. (Irenzengeb. der Med. u. Chir., 1903, p. 312.) 
 
 ^ IJalzer: Archiv. d. .Med., 18S3, vi, 93. 
 
 ' Wachor: Wien. klin. Woch., 1909, xxii, p. 96. 
 
 '■' Hcr.vheimer: Centralblatt f. .all. Path, u. path. Anal., 1903, .\iv, 737. 
 
118 STUDIES IN CARDIAC PATHOLOGY 
 
 origin, being produced by pressure or friction, and not by inflam- 
 mation. 
 
 These conclusions have been corroborated from both an 
 anatomic and an experimental standpoint of Tsunoda,^ who likens 
 the mechanism of milk spots to the development thickening of 
 the epidermis on the palms and soles as the result of long-continued 
 friction. He also found that milk spots occurred with increasing 
 frequency as age advanced. 
 
 Up to 10 years 8.5 per cent. 
 
 10 to 20 years 10.0 " 
 
 20 to 30 years 23.0 " 
 
 30 to 40 years 28.0 
 
 40 to 50 years 47.0 
 
 50 to 60 years 54.0 " 
 
 Beyond 60 years 65.0 " 
 
 Primary endothelial atrophy is followed bj^ proliferation of 
 the subendothelial connective tissue. Many modern text-books, 
 disregarding these researches, still class milk spots as the result 
 of an antecedent pericarditis. 
 
 Calcification of the pericardium sometimes occurs. There 
 were two such cases at the Philadelphia Hospital. The condition 
 seems to be most commonly a sequel of a suppurative pericarditis. - 
 
 Oberndorfer has reported a case of board-like pericardial 
 thickening somewhat in the shape of a horseshoe, measuring 11x4 
 cm., occurring in a woman of seventy years and unassociated with 
 symptoms. 
 
 At the Philadelphia Hospital an extreme case of myocardial 
 calcification occurred in a man of sixty-five years, in which the 
 process spread from the anterior flap of the mitral valve, involved 
 the whole auriculo-ventricular orifice, the wall of the left ventricle 
 just beneath the endocardium, and the interventricular septum, 
 the heart weighing 550 gm. (Phila. Hospital Autops}^ Records, 
 vol. xi, p. 19). 
 
 Actinomj'-cosis may produce plastic or suppurative pericarditis. 
 
 ' Tsunoda: Frankfurter Zeit. f. Path., 1909, iii, 220. 
 2 Oberndorfer: Miinch. med. Woch., 1906, p. 2081. 
 
Fiu. 35. — Chronic Adhesive Pericarditis. 
 
 J. T., male. (Pennsylvania Hospital. Specimen 46. Physician: Dr. .J. M. DaCosta.) 
 
 Clinical Notes: Was admitted unconscious and delirious. A diagnosis of meningitis 
 was made. 
 
 The pericardium, which was adherent to both the epicardium and the surrounding struc- 
 tures, has been partially dissected back, and shows very marked thickening, and adhesion. 
 
 The heart weighed 1,0.57 gm. 
 
120 STUDIES IN CARDIAC PATHOLOGY 
 
 Primary neoplasms of the pericardium are rare. Disease due to 
 the cysticercus, the echinococcus, and trichina has been reported. 
 Pathologic Physiology. — "The increase of pressure in the peri- 
 cardial sac is an obstacle to the inflow of blood into the heart, 
 for normally the inflow of blood into the right auricle is greatly 
 favored by the difference in pressure inside and outside the thorax, 
 or, more strictly speaking, outside the thorax and inside the great 
 veins at their entrance into the heart. Since the right auricle 
 receives less blood than normal, it can pass on less blood to the 
 right ventricle, the right ventricle in its turn ejecting less blood 
 into the pulmonary artery; the pulmonary blood-pressure falls, 
 therefore. For the same reason — i. e., because the pulmonary 
 artery receives less blood than normal — less blood reaches the 
 left auricle, and through it the left ventricle, by way of the pul- 
 monary veins. Since the left ventricle receives less blood, its 
 output into the aorta is diminished, and diminution of output of 
 the left ventricle, unaccompanied as in this case by a corresponding 
 increase in the peripheral resistance, is of necessity associated 
 with fall of the aortic blood-pressure. "The venous blood- 
 pressure, on the other hand, rises .... because a new 
 condition has been introduced into the circulation which disturbs 
 the hitherto existing equilibrium between the inflow into and out- 
 flow from the heart. It is evident, since the aortic blood-pressure 
 is dependent upon the two factors, (a) output of the heart, and 
 (b) peripheral resistance in the arteries, and since the output of 
 the heart, cceteris -paribus, depends entirely upon the inflow into 
 the heart, that, for the maintenance of a constant mean level of 
 aortic blood-pressure, the inflow into the heart and the output 
 must be exactly equal. But the blood which constitutes the 
 'inflow' is nothing more than that amount of blood which, as the 
 result of hyperdistention, passes from the arteries into the veins 
 during cardiac diastole. In other words, for the maintenance of a 
 constant aortic blood-pressure the amount of blood which passes 
 from arteries to veins during a given cardiac diastole must be 
 
Fig. 36. — Chronic Adhesive Pericarditis. 
 
 iiil)laiiec of 
 w i 1 1 1 " ] leri- 
 
 This specimen illustrates the "Zuckergusshertz," so called owing to the 
 the exudate to the sugar icing on a cake. It is generally met with in associa 
 cardial pseudocirrho.sis of the liver." (Specimen from the German Hospital, I'liilaildphia.) 
 See page 124. 
 
122 STUDIES IN CARDIAC PATHOLOGY 
 
 exactly equal to the amount of blood which has been thrown into 
 the arteries during the previous cardiac systole, and vice versa. 
 
 "In the case of a dog into whose pericardial sac oil is injected, 
 the output of the heart is diminished, but since, at the moment 
 before this occurred, the hyperdistention of the arteries corre- 
 sponded to a greater output, the amount of blood which passed 
 from arteries to veins also corresponded to that greater output. 
 More blood, therefore, leaves the arterial system during any given 
 diastole than enters it during the succeeding systole; an additional 
 amount of blood, therefore, becomes stored up in the veins with 
 each heart's diastole until equilibrium is once more established, 
 gradually leading to the rise in venous pressure which we have 
 
 noted It is this rise of venous pressure which renders 
 
 maintenance of the circulation possible under the altered conditions, 
 for it is obvious that if the pericardial pressure were raised to, 
 say, 25 mm. of oil, while the pressure in the external jugular and 
 other veins outside the thorax remained at their normal point, 
 no blood would flow into the right auricle at all and the circula- 
 tion would immediatel}' cease As it is, however, the 
 
 venous pressure rises with the intrapericardial pressiire, and always 
 maintains a slight superiorit j^ ; blood, therefore, flows into the 
 right auricle, and though the pressures in arteries and veins are 
 
 altered, the circulation goes on But the pressure 
 
 which can be attained in the venous system has a limit which 
 varies with many factors So long as the intraperi- 
 cardial pressure is below (the extreme limit), the circulation 
 continues, however poorly; but once the intrapericardial pressure 
 reaches this point, all possibility of inflow from veins to auricles 
 ceases and circulation comes to a standstill — the whole of the blood 
 of the body collected in the veins The heart, how- 
 ever, in experimental cases, for a minute or thereabouts continues 
 to contract, and if, during this time, the intrapericardial pressure 
 be reduced, circulation re-establishes itself." (Lazarus Barlow.^) 
 
 ' Quoted, McFarland, Textbook of Pathology, 1904, p. 39S. 
 
ACUTE PERICARDITIS 123 
 
 Pericarditis, although a serious condition, is per se rarely the direct cause of 
 death. Brooks and Lippincott only found 6 such cases among 150. In 86 death 
 was due to septic processes; 17 were terminal infections. In the serofibrinous 
 cases death was due to inflammatory processes outside the pericardium as 
 follows: lobar pneumonia, 30; bronchopneumonia, 4; empyema, 1; acute en- 
 docarditis, 9. Not included in the above there were 4 cases of myocarditis and 
 4 cases of acute tuberculosis. Pericarditis greatly increases danger of endocar- 
 ditis during both the acute and the chronic stages. 
 
 According to Theodore Fisher, pneumococcus and septic pericarditis does 
 not produce cardiac dilatation in the way that the rheumatic variety does, a fact 
 which he explains as due to the deleterious effect of the toxin of the latter disease 
 upon the myocardium. 
 
 There is some ground for supposing that under normal conditions the peri- 
 cardium acts as a support which prevents undue sudden cardiac dilatation, as 
 suggested by Hill and Barnard, and that an inflamed and softened and relaxed 
 sac may be a factor in the production of dilatation. 
 
 In chronic pericarditis death is seldom dependent directly upon the peri- 
 cardial lesion. Of the last-named author's cases, 5 died of cardiac dilatation, 
 1 of acute endocarditis, 8 of lobar pneumonia, 9 of sepsis, 1 of empyema, 9 of 
 tuberculosis, 6 of alcoholism, 4 of syphilis, 2 of traumatism, 4 of non-specific 
 myocarditis. 
 
 Until recently there has been much discussion regarding the. 
 position of the heart in cases of pericardial effusion. A good deal 
 of light has been thrown upon the problem by Damsch, Schap- 
 oschnikoff^ and Calvert.- The position of the heart seems to 
 depend entirely upon its specific gravity; in other words, upon its 
 size and upon the amount of blood it contains, and these factors, 
 in turn, depend upon the amount of intrapericardial pressure and 
 the efficiency of compensation. With advancing severity of the 
 disease the heart contains less blood and the pericardial pressure 
 increases. While the heart is normal in size it remains in a normal 
 position; when it becomes smaller, it is pushed upward and back- 
 ward, the apex being pushed slightly to the right. 
 
 ' Schapcschnikoff: Revue de Medecine, 1905, p. 789. 
 ^ Calvert: Bull. Johns Hopkins Hosp., Oct., 1907. 
 
VIII. CHRONIC PERICARDITIS 
 
 Pathogenesis. — If the exudate of an acute pericarditis is 
 absorbed slowly, or if it is mainly fibrinous in character, adhesions 
 are apt to form as the result of gradual organization of the exudate. 
 These adhesions may remain as localized circumscribed white 
 areas, or they may, in the form of bands or threads, unite the 
 visceral to the parietal layers, or bind the external surface of the 
 pericardium to the surrounding mediastinal tissues. The most 
 frequent site for such adhesions is on the surface of the right 
 ventricle; next upon the auricles; and lastly, upon the left 
 ventricle.^ (See Fig. 34.) Mediastinitis may precede or follow 
 pericarditis. In the former case the infection generally spreads from 
 the bronchial or mediastinal lymph-nodes or from the lungs them- 
 selves. 
 
 Mediastinitis has been divided into three classes: (a) Obhteration of the 
 pericardial cavity with marked increase of mediastinal connective tissue, with 
 or without caseation, (b) Obliteration of the pericardium with extensive ad- 
 hesions to the surrounding structures, without much increase of mediastinal 
 tissue, (c) Mediastinitis without pericardial involvement.''' 
 
 The most important adhesions are those which occur between 
 the external surface of the sac and the surrounding structures, 
 since it is in these cases that the heart is to the greatest extent 
 hampered and restricted in its action. 
 
 When in addition to the pericardium, the mediastinum, pleurae, 
 liver, and omentum are also involved, we have what has been de- 
 scribed as pericardial pseudo-cirrhosis of the liver (Pick's disease). 
 Both the heart and the liver are covered with a thick white laj^er of 
 inflammatory product, so that they have the appearance of being 
 coated with "icing," hence the German name "Zuckerguss Leber 
 
 ' Sicard: New York Med. Jour., 1907, p. 488. 
 - Harris: Medical Chronicle, 189.5. 
 124 
 
I'K 
 
 -AcTTE Fibrinous Pericarditis. 
 
 A specimen from the University of Pennsylvania Museum showing the typical "cor 
 villosum," or "shaggy heart." (The entire heart could not be better reproduced owing to the 
 difficulty of photographing through the convex surface of the hermetically sealed jar in which 
 the specimen was preserved.) 
 
126 STUDIES IN CARDIAC PATHOLOGY 
 
 und Herz."^ This condition is generally a part of an extensive 
 multiple serositis, often tuberculous in origin, and is associated 
 with ascites and signs of portal stasis. Head collected 55 cases of 
 this kind, and added 4. He found that one-third of the cases 
 occurred in persons under twenty years of age. The commonest 
 causal factor was rheumatic fever, although tuberculosis, pneu- 
 monia, nephritis, and chorea were also accountable. Pericardial 
 pseudo-cirrhosis has been approximately reproduced experimentally, 
 by the injection of iodin into the pericardium. The inflammatory 
 reaction which followed, by constricting the vena cava, produced 
 congestion and ultimately cirrhosis of the liver.- (See Fig. 36.) 
 
 Clinically, two varieties of chronic adhesive pericarditis may 
 be distinguished: (a) adhesions followed by marked hypertrophy; 
 (6) complete obliteration without or with only vague s.ymptoms 
 and with few or no adhesions between the pericardium and the 
 
 ' Study of 39 cases, A. O. J. Kelly: Am. Jour. Med. Sci., Jan., 1903. 
 - Hess: "Ueber Stauung u. chron. Entzundung. i. d. Leber u. d. seroesen Hoelen," Mar- 
 burg, 1902. Fletch and Schlossberger: Zeit. f. klin. Med., 1906, lix, 1. 
 
 Fig. 38. — Tuberculous Pericarditis. 
 
 J. L., male, negro. (Pennsylvania Hospital. Autopsy No. 277. Pathologist: Dr. 
 Longcope.) 
 
 Clinical Notes: Patient was admitted to the surgical wards with a history and physical 
 signs of appendicitis. Death occurred from purulent peritonitis. 
 
 Pathologic Diagnosis: Tuberculous pericarditis, etc. 
 
 Pericardium: Both layers are firmly adherent, and have to be dissected apart. On 
 separation, they are found to be covered with small, more or less discrete, opaque, while eleva- 
 tions. Occasionally these coalesce aiid form a lobulated mass about 1 cm. in rlinmclrr. the smaller 
 ones being of a millet-seed size. Both parietal and visceral pericantliini (in murli Ihn-l.-ciied, the 
 former in many places measuring 5 mm. On section the entire pcricunliiim scctii.^ to be com- 
 posed ofnodides, all of which are very firm and never umbilicated. They do not invade the myocar- 
 dium, which is firm and dark reddish-brown in color. The tissue between the nodules is dark 
 purplish-red in color and appears to contain hemorrhages. There are no nodules on the 
 external portion of the visceral pericardium. The left ventricle measures 1.5 cm. in thickness. 
 The heart is somewhat enlarged; the cavities are of fair size, and all the valves are thin and 
 delicate. 
 
 Microscopic Examination: No especial changes are noted in the myocardium. The 
 pericardium is the seat of extensive tuberculosis. Covering the heart muscle there is a thick 
 layer of granular tissue, composed chiefly of epithelioid cells and small round-cells. Every- 
 where throughout this tissue one sees enormous giant-cells and typical tubercles. In the 
 granulation tissue surrounding the tubercles blood-vessels are fairly numerous. There are 
 no areas of caseation. 
 
 (Case reported by the author, Univ. of Pennsylvania Med. Bull., July, 1904.) 
 
Fig. 38. 
 
128 STUDIES IN CARDIAC PATHOLOGY 
 
 surrounding structures. The latter is met with chiefly in males, is 
 independent of valvular lesions, and often occurs in individuals 
 who give no history of antecedent infections. The former variety, 
 which is often seen in valvular disease, is associated with marked 
 hypertrophy and dilatation, and with extensive extrapericardial 
 adhesions. Calcification of the pericardium sometimes follows, 
 and myocardial atrophy resulting from constriction has been 
 described. 
 
 Fenton ' found that "out of 150 cases of adherent pericarditis, in which the 
 cause of death was specifically stated in the postmortem records to have been 
 the direct result of the heart lesions, 65 were found during the first three dec- 
 ades, and 17 during the last four; while where death followed upon causes 
 unconnected with the heart, 13 only were found during the last three decades, 
 and 55 in the last four." He also found a history of rheumatic fever in most of 
 the cases under thirty years, and in relatively few beyond this age; and, further, 
 that the rheumatic cases were generally the serious ones. 
 
 Valvular disease was present in 91 cases, absent in 76; total, 167. General 
 adhesions were found in 153 cases, partial adhesions in 17; total, 170. 
 
 The extent of the adhesion is certainly no index of the severity 
 of the lesion, but extrapericardial adhesions doubtless play a part 
 in the production of hypertrophy and dilatation, as does also 
 valvular disease when present. Probably the most important 
 etiologic factor in the production of hypertrophj^ and dilatation is 
 the myocardial damage which so commonly begins just beneath 
 the pericardial lesions, and tends to progress. 
 
 "Valvular incompetence will exaggerate the tendency to heart 
 failure by an additional demand ujDon cardiac reserve; at the same 
 time everything depends on the extent of original damage sustained 
 by the muscle." "Dilatation takes place during the acute and 
 subacute periods of the phase which precedes the chronic adhesion. 
 In a few mild cases it may pass off, but in the great majority it 
 does not, and hj^Dcrtrophy and external adhesion follow; resulting 
 in a condition of unstable equilibrium in which the constant ten- 
 denc3' is to increase dilatation and failure, owing partly to a 
 
 'Fenton: Practitioner, 190S, Ixxxi, 637. 
 
i'lG. 39. — Tuberculous Pericaeditis. 
 Section of the heart and pericardium from a case of tuberculous pericarditis, sliowing 
 complete obliteration of the sac, with thickening and caseation. (Photograph by Dr. Alfred 
 Fv. Allen.) 
 
130 STUDIES IN CARDIAC PATHOLOGY 
 
 certain amount of embarrassment to systole caused by external 
 adhesions, but mainly to permanent damage to the heart muscle, 
 in a manner resembling those cases of chronic cardiac failure in 
 more advanced life" (Fenton). 
 
 Pathologic Physiology. — "The mechanical effects upon the 
 circulation due to pericardial adhesions may be threefold: (1) 
 The work of the ventricle is increased by the tug upon the adhe- 
 sions. (2) The filling of the heart may be hindered bj^ strangula- 
 tion of the vena cava. At each contraction the heart must not 
 only drive out the blood, but must pull on its harness of adhesions. 
 The additional work which it thus has to perform depends both 
 upon the tightness of the adhesions and upon the weight or rigidity 
 of the structures pulled. The latter factor depends upon the posi- 
 tion of the adhesions, whether it is the ribs, pleura, mediastinum, 
 or the diaphragm and liver that are tugged upon, being greatest 
 for adhesions to the ribs and diaphragm. (3) The emptying of 
 the heart and the flow through the aorta may, as claimed bj' 
 Kussmaul, be hindered by the tugging of the adhesions upon the 
 arch of the aorta. This can readily be shown experimentally if 
 such traction be made in a dog whose chest has been opened. 
 The pulse may be made to disappear absolutely in spite of the fact 
 that the heart-rate remains unchanged and the heart dilates from 
 overfilling; enough blood flows in from the venae cavse to dilate 
 the heart. 
 
 "When this additional work is imposed upon a heart already 
 weak, it may succumb to the strain, and death may occur with 
 all the manifestations of broken compensation. The importance 
 of adherent pericardium in causing death from heart disease is 
 shown by the fact that it was present in almost all the cases of 
 Sturges' series. 
 
 "Usually, however, the ventricles gradually recover from the 
 strain and simply undergo a gradual work hj^pertrophy j^ropor- 
 tional to the additional strain, and an additional amount of work 
 may be done at each systole sufficient to balance the amount 
 
Fk;. 40. — Hemopericardidm. 
 
 The pericardium has been reflected to the left and shows the heart covered with a thick, 
 dark, massive blood-dot which has resulted from the rupture of an aortic aneurism into the 
 pericardium. The aorta is greatly dilated and its endocardium is roughened by extensive 
 calcareous depo.sits. (Specimen from the Philadcliiliia Hospital.) 
 
■132 STUDIES IN CARDIAC PATHOLOGY 
 
 required. During exercise, emotion, disease, or other strains, 
 however, not only the work of the heart in the circulation is in- 
 creased, but with the increased systolic output and systolic excur- 
 sion of the walls the tug upon the adhesions is increased enor- 
 mously, and the heart is thus readily overstrained. The heavy 
 beating of the heart under emotional excitement is especially 
 likely to bring this about. 
 
 "Moreover, the process of hypertrophy is not a pure one. 
 With the fibrosis of the pericardial adhesions outward, the process 
 of fibrosis also extends inward into the somewhat injured myo- 
 cardium, and this process goes on progressively with each moment 
 of overstrain until the mj^ofibrosis cordis is advanced and the heart 
 failure complete. 
 
 "The site of the adhesions determines not only the degree but 
 the character of the heart failure. If the densest adhesions are 
 over the left ventricle, the effect is to inhibit the action of the latter 
 alone. Nature performs the experiment of Welch, and gives rise 
 to the clinical picture of broken pulmonary compensation with 
 dyspnea, cardiac asthma, or pulmonary edema. 
 
 "If the chief adhesions are over the right ventricle, broken 
 systemic compensation sets in, with venous stasis, tricuspid insuf- 
 ficienc}'^, enlargement of the liver, and collection of fluid at 
 various sites, but particularly in the peritoneal cavity. 
 
 "On the other hand, the tugs of the adhesions on auricles and 
 ventricles may act as mechanical extra stimuli and produce an 
 extrasystolic arrhythmia, which in itself hinders the circulation." 
 (Hirschfelder.) 
 
 Frequency. — Among 2,000 autopsies at the Presbyterian 
 Hospital in New York, Sicard found 77 cases of fibrous pericarditis 
 {314, per cent, of all autopsies). It was extensive in 45, and sUght 
 in 32 cases. Mediastinopericarditis occurred only once, endo- 
 carditis was associated in 33, severe aortic sclerosis in 4, marked 
 coronary sclerosis in 15, aneurism in 4, chronic nephritis in 33, 
 
I'll;. 41.— K 
 
 Jl' THIC .\(litT.' 
 
 Clinical Notes: Sudden death without premonitory symptoms durinfi convalescence, 
 six days after an operation for hemorrhoids. 
 
 Patholo(;ic Notes: Two and one-half centimeters above the attachment of the aortic 
 valve.s there is a rough, uliijhlly nhaggy looking tear running direcUy across the aorta. It is 2 cm. 
 in length and leads directly from a small aneurismal pouch into the pericardial cavity. The 
 .surface of the aorta along the ascending arch shows small, scattered, yellowish nodules. (Spec- 
 imen from the Pennsylvania Hospital. Pathologist: Dr. G. C. Robinson.) 
 
134 STUDIES IN CARDIAC PATHOLOGY 
 
 tuberculosis in 9. Leudet in 1,002 autopsies found partial adhesion 
 in 5 per cent., total adhesion in 2.5 per cent. 
 
 Congenital defects of the pericardium are very rare. The sac 
 may be wanting in acardiac monsters, and sometimes even when 
 the heart is present, or it may only partially cover the heart. 
 Ebstein collected 32 cases of congenital absence, and found that 
 the clinical picture in many respects resembled the "movable 
 heart."' 
 
 The following pericardial lesions were encountered among 9,940 autopsies: 
 
 Philadelphia Hospital Pennsylvania Hospital 
 
 Carcinoma (metastatic) 3 
 
 Sarcoma (metastatic) 5 1 
 
 Calcificition 7 1 
 
 Rupture of abscess into 2 
 
 Ctumma 1 
 
 Rupture of aneurism into 2 
 
 Neither the sarcomas nor the carcinomas enumerated in the 
 foregoing statistics were primary. In the case of tumors origi- 
 nating in the heart, pericardial involvement is very rare. Among 
 61 cases of cardiac neoplasms Schoepplcr'- found the pericardium 
 involved only once. 
 
 Clinical Considerations. — The existence of primary pericarditis 
 is no longer admitted. Whenever a true inflammation of this sac 
 occurs, it is due to an antecedent infection of the blood-stream, 
 lymphatics, or contiguous structures. The cases which were at 
 one time believed to have a toxic origin are now known to be 
 infections. "Milk spots" have a mechanical origin which is of 
 a non-inflammatory nature. 
 
 No serious cardiac lesion is so frequently overlooked. Cabot ^ 
 found that of 54 cases of acute pericarditis at the Massachu- 
 setts General Hospital, 70 per cent, were not recognized ante 
 mortem. Any one who is familiar with autopsy records will 
 realize that a similar state of affairs is the general rule elsewhere, 
 
 ' Ebstein: Mtinch. med. Woch., March 8, 1910. 
 
 - Schoeppler: Miinch. med. Woch., 1906, hii, No. 45. 
 
 = Cabot: Jour. Am. Med. Assoc, 1910, p. 134:3. 
 
CHRONIC PERICARDITIS 135 
 
 owing to the fact that the onset of a pericarditis is general!}' 
 insidious, and that such symptoms and physical signs as it does 
 present are usually completely overshadowed by the conditions 
 which it complicates. The obvious lesson to be learned, there- 
 fore, is to look actively for signs of pericardial involvement in 
 conditions such as pneumonia, rheumatic fever, nephritis, tuber- 
 culosis, emp3'ema, etc., in which it so often occurs. 
 
IX. CARDIAC HYPERTROPHY 
 
 DIMENSIONS OF THE NORMAL HEART.— (Bizol.) 
 
 Males Females 
 
 (Meters) (Meters) 
 
 Length of the heart 0.097 0.092 
 
 Breadth of the heart 0.107 0.099 
 
 Thickness of the heart 0.038 0.031 
 
 Length of the left ventricle 0.066 0.072 
 
 Breadth of the left ventricle 0.119 0.104 
 
 Length of the right ventricle •. . . 0.084 0.075 
 
 Breadth of the right ventricle 0.188 0.172 
 
 Thickness of the Walls of the Left Ventricle: 
 
 At the base 0.010 0.009 
 
 At the middle 0.011 0.010 
 
 Near the apex 0.008 0.007 
 
 Thickness of the Septum Ventriculorum: 
 
 At the middle 0.011 0.009 
 
 Thickness of the Walls of the Right Ventricle: 
 
 Base 0.004 0.003 
 
 At the middle 0.003 0.002 
 
 Near the apex 0.002 0.002 
 
 Breadth of the Auriculo-Ventricular Orifices: 
 
 Left ventricle 0.100 0.091 
 
 Right ventricle 0.122 0.106 
 
 Breadth of the origin of the aorta (above the 
 
 valves) 0.069 0.063 
 
 Breadth of the origin of the pulmonary artery 0.071 0.066 
 
 The heart of an adult man averages 300 gm. ; of a woman, 250 gm. 
 The size of the cardiac orifices is given by Perls as follows : 
 
 Under Between Forty .\nd Over 
 
 Forty Ye.vrs. Fifty Ye.\rs. Fifty Years. 
 
 Aortic orifice, cardiac 70.9 mm. 74.6 mm. 74.3 mm. 
 
 Aortic orifice, arterial 63.5 " 72.2 " 80.1 " 
 
 Pulmonary orifice, cardiac 81.5 " 84.9 " 85.7 " 
 
 Pulmonary orifice, arterial 71.9 " 74.6 " 81.3 " 
 
 Mitral orifice, periphery 102.5 " 105.1 " 102.0 " 
 
 Tricuspid orifioe, periphery 121.0 " 122.0 " 122.8 " 
 
 It appears, therefore, that there is a difference not only in the size of the 
 aortic and pulmonary orifices, depending upon whether they are measured at 
 the opening of the heart proper or at the attachment of the semilunar valves, 
 but also that the proportion of these two dimensions to each other is directly 
 reversed before and after forty years of age. "In middle Hfe the unfolded valves 
 take up a greater space than that which they must actually cover, while in old 
 
 136 
 
CHRONIC PERICARDITIS 137 
 
 age they generally take up a smaller space." These facts help to explain the 
 greater frequency of insufficient valves in old age.'- This increase in the size 
 of the vessels is due to diminished elasticity of arteriosclerotic vascular walls. 
 Arteriosclerotic aortae are often overlooked because they simply show dilatation, 
 without sclerotic patches.'' 
 
 The size of the heart is proportionate to bodily weight,^ and 
 to a lesser extent to stature. In adolescents, in corpulent subjects, 
 and in women the size of the heart is relatively smaller than in 
 adult men of the same proportions, especially those with good 
 muscular development. It also increases with age, but enlarge- 
 ment to the left, as shown by percussion or b.y the orthodiagram, 
 is not solely due to hypertrophy, but also to the fact that in ad- 
 vanced years the organ lies more to the left. The dome of the 
 diaphragm sinks, and with this descent the heart moves downward 
 and to the left. 
 
 In early life the upper cardiac border reaches the second, and 
 in adult life the third, costal interspace. The diaphragm being 
 more highly placed in women, the heart is correspondingly higher 
 in position. The lower cardiac border is found in 52 per cent, of 
 male adults at the angle of the costosternal junction, in women 
 in 70 per cent. (Muller, Hirsch, Dietlen).^ In men the weight 
 of the heart to the whole body is about 1 to 170; in women it is 
 1 to 183. 
 
 Occurrence. — Hypertrophy of the heart consists of an increase 
 in either the number or the size of the muscle-cells, or both. 
 Practically, however, hypertrophy of the heart as generally seen 
 is in part also due to an increased amount of connective tissue, fat, 
 and blood-vessels. It is directly due to an increased demand for 
 work, arising either within or without the heart — valvular lesions, 
 
 ' Quoted, Ro.senstein: Ziemssen's Cylcop. of Med., vi, p. 13. 
 
 ^ Scheel: "Study of .500 Autopsies," Norsk Mag. f. Laegevidenskaben, June, 1907. 
 
 ' In animals which have been starved the heart diminishes in proportion to the loss of 
 bodily weight, and regains its original size (as shown by the orthodiagram) when feeding is 
 resumed. This decrease in size seems to be due partly to actual loss of substance, and partly 
 to a decreased volume of blood. One animal in the course of nine days lost .'31 per cent, of its 
 total blood. (SchielTcr: Dcut. Arch. f. kHn. Med., 1907, xcii, Dec. 28.) 
 
 * Muller: Die MassHnverhaeltnisse des monschlichen Ilerzens, Berlin, 1S7S;. Ilirsch: 
 Deut. .Xrch. f. klin. Med., 1899, p. .597. Dictlen: Dcut. Arcli. f. l<Hii. Med., Orl. 24, 1906. 
 
138 STUDIES IN CARDIAC PATHOLOGY 
 
 congenital defects, pericarditis, scoliosis, cardiac thrombosis, 
 aneurisms, neoplasms of the mediastinum, arteriosclerosis, gout, 
 lead-poisoning, etc. Although hypertrophy may affect only 
 one chamber, this is unusual. Hypertrophy has also been as- 
 cribed to defective innervation. Although a common cause of 
 hypertrophy is arterial hypertension, yet the continued rapidity 
 of action which occurs over years of time in hypotension may 
 produce a similar result. Thus we see hypertrophy associated 
 with hyperthyroidism. 
 
 Systematic writers have been wont to recognize three types of 
 cardiac hypertrophy: (1) Simple enlargement, without change 
 in the size of the cavities; (2) concentric enlargement, with dimi- 
 
 FiG. 42. — Concentric Cardiac Hypertrophy. 
 
 W. B., negro, laborer, aged forty-five years. (Pennsylvania Hospital. No. 1442 (1908). 
 Physician: Dr. A. Newlin. Pathologist; Dr. Krumbhaar.) 
 
 Clinical Notes: Delicate as a child. Healthy at eighteen years. Hard worker. 
 Alcohol and tobacco to excess. Syphilis probably. Six months ago nausea and vomiting, 
 with increasing headaches. Brought to hospital unconscious and soon died. 
 
 Pathologic Diagnosis: Tumor of the pituitary body, etc. Acute mitral endocarditis. 
 Chronic mitral and aortic endocarditis — concentric cardiac hypertrophy. Arteriosclerosis of the 
 aorta, etc. 
 
 Pericardium contains 10 c.c. of clear fluid; no adhesions. 
 
 Heart: Weighs 530 gm., enlarged and firm. Normal color. Epicardium grayish, and 
 diffusely thickened. In spots, dense white, opaque areas, which cut with resistance. Epi- 
 cardial fat increased. Epicardium over right auricle tessellated with slight raised, grayish, 
 pin-point nodules. Right ventricle 6 to 10 mm. Auricular and pulmonary valves normal. 
 Left heart empty, its musculature enormously increased; measures IS to SB mm. Its cavity 
 smaller than would he expected. Endocardium smooth and glistening, though on the septal wall 
 some of the vessels seem dilated. Mitral orifice 10.5 cm. and shows, especially on the anterior 
 leaflet, diffuse fibrous plaques. Along the whole line of closure are minute grayish vegetations of 
 pin-point size. Aortic orifice 7 cm.; shows some fibrous thickening along the base of the leaflets, 
 the line of closure being normal. Aorta: nodular yellowish thickenings, and a certain amount of 
 branching contractions like the willow-tree type of sclerosis. Coronary arteries: except at the 
 origin are normal. 
 
 Microscopic Diagnosis: Chronic interstitial myocarditis. The muscle shows well- 
 marked stria;, and not much pigment about the nuclei. The fibers, especially on cross-section, 
 are much shrunken from the sarcolemma, and occasionally extensive areas with large rectangular 
 nuclei are found. Interstitial tissue is diffusely thickened, especially about the blood-vessels, 
 whose walls are also thickened. At the edges of the fibrosed areas the muscle-fibers are often 
 vacuolated, while others are small and shrunken, having lost their striae. The process is more 
 advanced and extensive in the papillary muscles than in the ventricular wall. Sections of the 
 mitral valve show that both the ventricular and the auricular endocardium are thickened, espe- 
 cially the former. In some areas the endothelial layer is broken, and fibrous tissue directly 
 continuous with the adherent masses of fibrin is seen, which occasionally includes red and 
 white blood-cells. There is considerable coarse fibrous tissue between the two endocardial 
 layers. 
 
Fig. 42. 
 
140 STUDIES IN CARDIAC PATHOLOGY 
 
 nution in the size of the cavities; (3) eccentric enlargement, with 
 enlargement in the size of the cavities (also spoken of as hj^per- 
 trophic dilatation). The second type, regarding the existence 
 of which there is some difference of opinion, may be simulated if 
 death occurs during sj^stole. (See Figs. 43, 44, 45.) In such a 
 case prolonged immersion in water will bring about a relaxation 
 of the heart muscle. 
 
 Pathogenesis. — Excessive demand for work on the part of 
 the heart calls forth the latent reserve force which every normal 
 heart possesses, and which represents the surplus energy which 
 has been stored up under periods of rest. When the demand for 
 increased work becomes constant, hypertrophic changes are brought 
 about. If the demands exceed the limit of the field of response, 
 or the nutritional possibilities, dilatation occurs. 
 
 As has been intimated above, the term "concentric hyper- 
 trophy" is justly falling into disuse because there is no actual 
 diminution in the size of the chambers in such cases. When 
 hypertrophy is due to an obstruction to the outflow of blood, 
 simple hypertrophy^ is induced; when it arises from diastolic 
 overfilling, hypertrophy and dilatation occur. This does not 
 result from mere stretching of the muscle-fibers (because even 
 with increased diastolic filling there is no increase in muscular 
 tension), but owing to the fundamental attribute of the heart 
 muscle, by virtue of which every contraction is maximal. Although 
 the contraction time is prolonged when obstruction to outflow or 
 increased diastolic filling occur, this increase is not in proportion 
 to the amount of the hindrance or of the overfilling imposed 
 (Romberg). 
 
 Hypertrophy affects only such parts of the heart muscle as 
 are actually called upon to do extra work. An associated or 
 sympathetic hypertrophy, or one due merely to increased nutri- 
 tional advantages, is never found (Romberg). Atrophy and hy- 
 pertrophy of different chambers of the same heart are often 
 encountered, as has been shown by Hirsch. Hypertrophy of the 
 
1 ii.. 4o. — Vi^KTK'AL Section of the Thorax. (See also Fig. 44. J 
 
 Figs. 43 and 44 show what appears to be a most extraordinary concentric hypertrophy of 
 Ike left ventricle. The walls of this chamber are enormously thickened and the chamber itself 
 almo.st obliterated as the result of it. This specimen was found among the anatomic material 
 at the University of Pennsylvania. Nothing is known regarding the history of the individual, 
 but it is inconceivable that such an extreme concentric hypertrophy should have developed 
 without more adequate cause than is demonstrable. The aorta above the valves shows the 
 results of a syphilitic aortitis, but the valve.s themselves are only moderately thickened. We 
 have a.s.sumftd, therefore, that an explanation must be sought in the fact that the heart ceased 
 HCtiriK ill .systole. ('Sfctions prepared by Dr. flcorgc I'V'lterolf.) 
 
142 STUDIES IN CARDIAC PATHOLOGY 
 
 conducting fibers — auriculo-ventricular bundle, etc. — does not 
 occur (Aschoff and Tawara).' 
 
 The mechanism by which hypertrophy is produced probably 
 varies; the most important being that due to increased intra- 
 cardiac pressure. This factor normallj^ acts as a stimulus to 
 contraction, as has been shown by v. Frey." Before birth the 
 walls of the two ventricles are of equal thickness, but afterward, 
 when much greater work is demanded of the left ventricle, its 
 walls become much thicker than those of the right. That this 
 pressure or stretching hypertrophy is independent of nervous 
 influences seems likely from the investigations of Rieder.-* 
 
 A considerable number of cases of hypertrophy are due to 
 chemical factors. In this group are included adrenalin, and 
 metabolic products of more or less undetermined composition, 
 such as occur in renal disease and intestinal autointoxication. 
 
 As opposed to a mechanical origin of cardiac hypertrophy 
 we have the "irritation" hypothesis of v. Dusch, it being assumed 
 that increase of intracardiac pressure by stimulation of the cardiac 
 nerves and ganglia produces an increased force of contraction, 
 and this in turn hypertrophy.* 
 
 Still another non-chemical explanation has been offered by 
 Albrecht,^ who discards the internal pressure or nervous hjq^othesis 
 as untenable, and regards hypertrophy as the result of a chronic 
 proliferative myocarditis — an inflammatory hyperplasia — which 
 exists not as an isolated manifestation, but as an attribute of a 
 chronic process which is often associated with, it may be, nephritis, 
 valvular disease, etc. Other varieties of hypertrophy not ex- 
 plainable on this basis are assumed to result from chemical and 
 bacterial and metabolic toxins. 
 
 1 This statement is also corroborated by Moenkeberg, " Untersuchungen li. d. Atrio-ven- 
 trikular Biindel im menschliclien Herzen," 1909. 
 
 2 Frey: Deut. Arch. f. Idin. Med., 1889, xlvi, p. .398. 
 
 3 Rieder: Arch. f. Win. Med., 1895. 
 
 ■"Asch; Zur Hypertrophie d. Quergestreiften Muskeln, speziel des Herzmuskels', Berlin, 
 1906. 
 
 ^Albrecht: Der Herzmuskel u. s. Bcdeutung f. Physiol., Pathol, u. Klinik d. Herzens, 
 Berlin, 1903. 
 
Fifi, 44. — Vertical Section of the Thouax. (Sep doscriptivc legend for rig. 4'A.) 
 
144 STUDIES IN CARDIAC PATHOLOGY 
 
 It has been found that chronic nephritis with hypertension is very fre- 
 quently associated with enlargement of the suprarenal gland,' and, further, that 
 in some cases an abnormally large amount of the secretion of this gland can be 
 demonstrated in the circulating blood. Again, it appears that removal of the 
 suprarenals produces a fall of blood-pressure, and that the serum of clogs thus 
 treated has a hypotensive action. - 
 
 Finallj^, nervous factors are probably responsible for hyper- 
 trophy in a certain number of cases. Thus, for instance, neurotic 
 individuals with a permanently rapid pulse-rate often develop 
 minor grades of hypertrophy. 
 
 While cardiac hypertrophy is most common in the sulDJects of aortic disease, 
 of interstitial nephritis, and in the sons of heavy toil, it is by no means a negligible 
 factor exclusive of the just mentioned conditions. Lubenau^ in the sanatorium 
 for heart diseases at Beehtz, from which valvular diseases are excluded, found 
 that 40 per cent, of the admissions were on account of "idiopathic hypertrophy," 
 35 per cent, were carchac neuroses, and 10 per cent, primary cardiac weak- 
 ness. 
 
 When the left ventricle is hypertrophied, the arterial system is subjected to 
 violent alterations in pressure, which produce minute ruptures in the vascular 
 coats ; this leads to fibrosis, and ultimately to an arteriosclerosis, which in turn 
 demands a greater hypertrophy, and thus a vicious circle is established. 
 
 Since increased work on the part of the heart produces hypertrophy, animals 
 which are fleet of foot — deers, hares — have larger hearts than less active animals 
 of an equal size. The wild rabbit has a larger heart than his tame cousin. The 
 same law holds good for birds of long flight." Animals of the same size and 
 breed which are forced to exercise, develop larger hearts than the controls which 
 are prevented from exercising." We also know that not only the left, but also 
 the right ventricle hypertrophies in these cases, due apparently to increased 
 pressure in the pulmonary circulation during exercise, since it has been shown 
 that activity produces a physiologic emphysema, and this in turn increases 
 tension in the pulmonary capillaries. Athletes, especially those accustomed to 
 prolonged contests, such as rowing, bicycling,'^ and long-distance running, gen- 
 erally develop more or less hypertrophy. They are said to be two and one-half 
 times as subject to carchac chseases as other people.' Participation in record- 
 breaking feats has been shown to be especially harmful.^ 
 
 1 Philpot: Quart. Jour. Med., Oct., 1909. 
 
 ^ Reneau: Thftse de Lyon, 1909. 
 
 ■' Lubenau: Zeit. f. klin. Med., 1906, Ix, p. 134. 
 
 •' Grober: Deut. Arch. f. klin. Med., 1907, xoi, p. .502. 
 
 ^ Kulbs: Munch. Kongr. f. inn. Med., April, 1906. 
 
 '• Sliieffer: Deut. Arch. f. klin. Med., Ixxxix, 604. 
 
 ' Hutchinson, quoted Davy: Lancet, Feb. 16, 1907. 
 
 SSeUg: Mediz. Klinik, March 29, 1908. 
 
Fig. 45. — Cardiac Hypertrophy. 
 
 A specimen from the Museum of the University of Pennsylvania, illustrating the type 
 known as "concentric hypertrophy." The wall of the left ventricle shows an enormous degree 
 of thickening; the cavity has apparently not enlarged in proportion. The aorta shows well- 
 marked atheroma ami calcification .-ibout the sinus of Valsalva. 
 
146 STUDIES IN CARDIAC PATHOLOGY 
 
 A hypertrophied heart is never as efficient as a ndrmal organ, 
 because associated with its increase in size there has been no 
 corresponding increase in the size or number of its ganglion-cells, 
 nerve-cells, or nutritional possibilities. Although the existence of 
 a pure "work hypertrophy" may be accepted as proved, despite 
 the denial of its existence by some well-known clinicians, neverthe- 
 less hypertrophies of this sort never attain the enormous dimen- 
 sions which are met with in the hypertrophy of disease. An 
 increase of 50 odd per cent, may be produced by the former, and 
 an increase of 200 or 300 per cent, may occur in the latter. Thus, 
 some enormous hypertrophies have been recorded — 1300 gm. 
 (Jackson^), 1700 gm. (Osier), 2500 gm. (Norristown Hospital). 
 Among 32 arteriosclerotic hearts studied by Jackson, only 4 
 weighed less than 400 gm. 
 
 Great cardiac enlargement naturally takes up considerable 
 intrathoracic space. When there is insufficient room, we see 
 bulging of the precordial ribs and compression of the lungs. How 
 great this compression may be, is shown in a case at the Philadelphia 
 Hospital in the service of Dr. Lloyd, in which actual erosion of 
 the thoracic vertebrae was thus produced.^ Lack of space, if 
 of sufficient degree, may mechanically interfere with heart action 
 and be the direct cause of cardiac symptoms. This fact has been 
 especially dwelt upon by Herz.-' 
 
 ' Jackson: Boston Med. and Surg. Jour., 1896. 
 
 2 Philadelphia Hospital Autopsy Records, vol. x, p. 17. (April 4, 1897.) 
 
 ' Herz: Wien. med. Woch., 1908, xxxiii, 397. 
 
 Fig. 46. — Sagittal Section op the Thorax. (See also Figs. 47 and 48.) 
 Figs. 46, 47, and 48 demonstrate how little room for expansion there is for the heart 
 between the vertebral column, and the anterior thoracic wall. Displacement to the right is 
 impracticable, since the antero-posterior thoracic dimensions are smallest in the median hne. 
 Movement to the left is hindered by the increasing convexity of the ribs. If any displacement 
 takes place, therefore, it must be backward and downward. When the possibility of motion 
 in these directions is exhausted, a squeezing of the heart must occur. It is plainly evident that 
 such a state of crowding, whether it results from enlargement of the heart or of the lungs 
 (pericardial effusion) or from deformity of the chest — empyema, etc. — must have a deleterious 
 effect not only on the functionation but also upon the nutrition of the heart. The most 
 striking effects which result from diminished intrathoracic space are noted in cases of valvu- 
 lar insufficiency, especially when associated with dilatation and myocarditis (Herz) . (Sections 
 from the Laboratory of Anatomy of the University of Pennsylvania, Dr. George Fetterolf.) 
 
Bight pulmonarj'^ arterj- 
 
 Left superior pulmon- 
 ary vein 
 I>eft auricular appendix 
 Left inf. pulm. vein 
 
 Left auricle 
 
 Mitral valve (anterio 
 
 ■ Aortic'Ieaflets 
 
 , Left ventricle 
 . Kight \'-entricIe 
 
 Via. 40. 
 
148 STUDIES IN CARDIAC PATHOLOGY 
 
 Probably a part of the dyspnea seen in high grades of pulmonary emphysema 
 is due to this crowding of the heart. The great lessening of dyspnea in cardiac 
 patients by the simple procedure of propping them up in bed, so that with lower- 
 ing of the diaphragm the heart is afforded more room, is another example of the 
 importance of external pressure. 
 
 This is well illustrated in Figs. 43 and 44, a glance at which 
 will show how snugly the heart is fitted in between the lungs and 
 diaphragm. 1 
 
 Exclusive of valvular lesions, chronic nephritis is perhaps the 
 most frequent cause of cardiac hypertrophy. The exact modus 
 operandi by virtue of which it occurs is still unsettled. In many 
 cases arterial hypertension seems to be accountable for the con- 
 dition, but this factor, while usually, is not invariably, present. 
 Then, again, we have still to learn the cause of such hypertension, 
 whether it is reflex or toxic, whether it is due to arteriosclerosis, 
 especially of the splanchnics or the renal arteries; whether it is 
 due to overactivity of the adrenals, and if so, why such an over- 
 secretion occurs. The hypertrophic changes are apparently closely 
 associated with contraction of the smaller arteries, which, in 
 turn, seems to be due to a toxic factor. 
 
 The importance of arteriosclerosis or constriction of the splanch- 
 nic area as a cause of hypertension and cardiac hypertrophy, 
 which was prominently brought to the fore through the investi- 
 gations of Hasenfeld- and Hirsch,^ and widely accepted, has 
 apparently been overestimated. Marchand," as well as Longcope 
 and McClintock,= were unable to corroborate the above-mentioned 
 observations. Neither experimentally or at autopsy could the 
 last-mentioned investigators find any definite association between 
 cardiac hypertrophy and sclerosis of the abdominal aorta or the 
 splanchnic vascular domain. 
 
 Cystic kidneys and hydronephrosis are often associated with 
 
 ' These sections were prepared by Dr. George Fetterolf . 
 = Hasenfeld: Deut. Arch. f. klin. Med., 1897, p. 193. 
 'Hirsch: Ibid., 1899, p. 579. 
 
 ' Marchand: Verhandl. d. Kong. f. inn. Med., 1904, p. 60. 
 ' Longcope and McClintock: Arch. Int. Med., 1910, p. 439. 
 
Superior vena cava 
 
 Right auricle 
 Coronary sinus 
 
 Tricuspid valve 
 
 Via. 47.— SAr;irrAr> Skction of thk 'J'hohax. fSco (Icsrriplivf legend under Kifr. 46.) 
 
150 STUDIES IN CARDIAC PATHOLOGY 
 
 cardiac hypertrophy. Myocardial changes and disease of the 
 coronary arteries are often relatively slight in nephritis, and death 
 from heart failure is more frequent in secondary than in primary 
 nephritis.^ 
 
 It was formerly taught that the hypertrophy which occurs 
 in chronic nephritis, and even in acute nephritis if its duration 
 exceeds four weeks,- affected chiefly, if not entirely, the left 
 ventricle. Careful examinations by MuUer's method have shown 
 that all the cardiac chambers are affected'' in 82 per cent, of the 
 cases. It is true, however, that the left ventricle shows the most 
 pronounced changes, and that right-sided enlargement appears 
 to be definitely a sequel (Paessler) . The hypertrophy is generally 
 regarded as due to increased work of the left ventricle in over- 
 coming abnormal resistance. With a normal blood-pressure the 
 heart handles about 10 pounds of blood per minute, and with 
 hypertension this work may readily be doubled. The nephritis 
 in which interstitial changes preponderate is the type in which 
 cardiac hypertrophy most frequently occurs, although cases of 
 this type are sometimes seen without either hypertension or 
 cardiac hypertrophy. Some cases of diffuse nephritis are ac- 
 companied by hypertrophy, although this is unusual. Hyper- 
 trophy is said never to occur in amyloid renal disease. It may, 
 according to Cohnheim, follow obstruction of the ureter. 
 
 The interrelationship between disease of the heart, the arteries, 
 and the kidneys has been a fertile topic of discussion. It has been 
 explained: (a) as part of a general process; (6) by the fact that 
 disease of the kidneys produced an increased blood-pressure 
 reflexly, this being nature's compensatory method of maintaining 
 an adequate urinary output; (c) by assuming that the heart 
 lesion produces the renal lesion by means of hypostatic congestion. 
 The occurrence of combined disease is very common. 
 
 1 Friedl.ander: Arch. f. Physiol., 1881, p. 168. 
 
 2 Hasenfeld: Arch. f. klin. Med., hx, 210. 
 
 'Scheel: Ugeskrift f. Laegevidenskaben, Aug., 1909, Ixxi. 
 
Papillary muscle 
 
 Right pulmonary 
 
 artery 
 Descending aorta 
 Left bronchus 
 
 Fig. 48. — Sagittal Section of the Tiiohax. (See descriptive legend under Fig, 46.) 
 
 This figure illustrate.s: (1) the too often insufficiently appreciated posterior position of 
 the left auricle, (2) the comparatively fixed and unyielding structures by which it is surrounded: 
 the descending aorta, esophagus, and spinal column behind; the left ventricle and diaphragm 
 below; the left ventricle and right auricle in front. When dilatation of the left auricle occurs 
 it mu.st be upward mainly. (.3) It is also evident that direct pressure from the auricle upon the 
 aortic arch i.s, on account of the intervening structures — the pulmonary arteries, veins and the 
 left bronchus — impossible. (Sec also the Figs. 46 and 47, and compare text, page 70.) 
 
152 STUDIES IN CARDIAC PATHOLOGY 
 
 Among 165 autopsies on cases of cardiac and aortic disease at Warsaw, the 
 kidneys were normal in only 6. Fifty-four were cases of mitral, and 50 of aortic 
 disease.^ In 66 cases of chronic interstitial nephritis the left ventricle was hyper- 
 trophied in 30.5 per cent.; normal or atrophied in 58 per cent.; both ventricles 
 hypertrophied in 11.5 per cent. In 22 cases of arteriosclerosis the left ventricle 
 was hypertrophied in 27 per cent.; right and left ventricles hypertrophied in 
 9 per cent.; normal in 64 per cent. In 25 cases of parenchymatous nephritis 
 the left ventricle was hypertrophied in 12 per cent.; right and left ventricles 
 hypertrophied in 4 per cent.; normal in 84 per cent. 
 
 Cohnheim's explanation of the cardiac hypertrophy in nephritis was based 
 on mechanical grounds. He attributed the rise of blood-pressure to diminution 
 in the size of the renal capillaries resulting from interstitial nephritis. But 
 Alwen- was unable to produce any considerable degree of hypertension by renal 
 compression. Furthermore, Heinike and Paessler's' progressive resection of the 
 kidneys did not prove that the increased arterial pressure was not toxic, rather 
 than mechanical. Finally, Jores* found less actual destruction of capillaries 
 in the red granular kidney than in the atrophic kidneys of late parenchymatous 
 nephritis, and in amyloid disease, in both of which conditions arterial hyper- 
 tension is infrequent. Schur and Wiesel,* on the other hand, found a constantly 
 increased amount of adrenalin in the blood of nephritics, and believe that the 
 high blood-pressure results from stimulation of the medullary portion of the 
 adrenal glands. These experiments have, however, not been corroborated by 
 others.^ Pearce ' has described a nephrotoxic substance in the blood of dogs in 
 which nephritis had been produced, which when injected into normal dogs pro- 
 duces the urinary evidence of nephritis. The evidence thus far, then, indicates 
 a chemical rather than a mechanical origin of the arterial hypertension of 
 nephritis. 
 
 Reicher ^ has shown that in experimental nephritis produced by cold, adren- 
 alin is found in increased amounts in the blood immediately succeeding the cold 
 bath, indicating that perhaps this substance is the cause of the hypertension in 
 the early stages of the natural disease. 
 
 Hypertrophy in Valvular Disease. — The myocardial changes 
 which follow experimental section of the aortic and tricuspid 
 valves indicate a mechanical and not an inflammatory origin. 
 The primary dilatation which follows the operation produces first 
 
 'Bronowski: Presse M6dicale, 1904, No. 99. 
 2 Alwen: Deut. Arch. f. klin. Med., xcviii, 137. 
 
 ^ Heinike and Paessler: Verhandl. d. deutsch. path. Gesellsch., 1905, p. 99. 
 ^ Jores: Verhandl. d. deutsch. path. Gesellsch., 1908, p. 187. 
 ■^ Schur and Wiesel: Verhandl. d. deutsch. path. Gesellsch., 1907, p. 17.5. 
 '5 Asohoff and Cohn: Verhandl. d. deutsch. path. Gesellsch., 1908, p. 31. Goldschmidt : 
 Deut. Arch. f. klin. Med., xcix, 186. 
 
 ' Pearce: Jour. Med. Research, 1908, 2. 
 
 " Reicher: Berlin, klin. Woch., 1908, No. 31. 
 
Fig. 49. — Left Ventricular Hypertrohpy. 
 
 A ca.se of aortic and mitral stenosis. The aortic valves have unfortunately been destroyed 
 through handling. The mitral valve shows marked induration oj the leaflets and chordw tendinem, 
 together with a Jew old fibrous vegetations. The papillary muscles are hyperlrophied. (Specimen 
 from the German Hospital, Philadelphia.) 
 
154 STUDIES IN CARDIAC PATHOLOGY 
 
 an increase of connective tissue, later a muscular hypertrophy. 
 These changes may occur independently of each other. ^ This is 
 opposed to the older teaching of Albrecht, whose views were 
 based upon a study of human hearts, mostly in cases of nephritis, 
 in which condition serositis and other inflammatory^ changes are 
 common. TangP has shown that even in the most emaciated 
 animals hypertrophy of the left ventricle will develop after arti- 
 ficially produced valvular lesions. 
 
 Hypertrophy is a result of the prolonged overexertion of the 
 heart muscle which is required to supply the demands of some 
 abnormal condition of the circulation. It is the result of cardiac 
 compensation under these conditions, not the cause of it. The 
 experimental section of an aortic valve is followed by dilatation 
 of the ventricle, and almost equall}^ soon a dilatation of the auricle, 
 together with a mitral sj^stolic murmur. There is no faltering 
 of the circulation; the animals are active and playful and ap- 
 parentlj^ never suffer from edema or dyspnea; all of which facts 
 show that a normal myocardium is instantly able to do an 
 enormously increased amount of work without being prepared 
 for it by any process of hypertrophy. Even in long-standing- 
 experimental lesions there do not seem to be produced any 
 of those chronic myocardial changes which we find in human 
 hearts. 
 
 Schnackers^ found that even when domestic animals develop 
 endocarditis by natural channels of infection, these lesions are 
 not followed by myocardial changes at all comparable to those 
 which occur in human beings. The Purkinje fibers, on the other 
 hand, seem to be seriously damaged. 
 
 Hypertrophied hearts of large dimensions are also met with 
 as a result of excessive beer-drinking over prolonged periods — 
 "beer heart," "Munich heart." This lesion results not so much 
 from any poisonous effect of the beer, but from an increased 
 
 ' Stadler: Deut. Arch. f. klin. Med., Aug., 1907, xci. 
 
 ^ Virchow's Archiv, cxvi, 432. 
 
 » Schnackers: Frankfurter Zeit. f. Path., 1909, p. 658. 
 
Fig. 50. — HypisnTROPHY and Dilatation of the Left Ventricle. 
 
 The miirnl valve .-ihrni-s inniirroiis olil injlammalnry vegelaliotts, wilh more or less deslrucliort 
 of lisHue. The left aunri/lnr u-nll in itUcniKiliil iiml its cavity enlarged. (Specimen from the 
 Episcopal Hospital, Pliihi'lilphin.! 
 
156 STUDIES IN CARDIAC PATHOLOGY 
 
 artificial plethora caused by the ingestion of excessive quantities 
 of fluid, which in turn necessitates an increased systolic output. 
 
 The left ventricle is hypertrophied in cases of aortic aneurism 
 only if there is an insufficiency of the aortic valves. 
 
 "Idiopathic hypertrophy" has been reported as occurring even 
 in infancy. Some of these cases occurred in nurslings. All sorts 
 of explanations have been offered, from Virchow's suggestion that 
 we were dealing with a diffuse form of rhabdomyoma, to Michaud's 
 belief that the chromaffin system is at fault. ^ The majority of 
 the cases, however, occur in the fourth or fifth decade of life. 
 More or less constant arterial hypertension is generally present, 
 which cannot be satisfactorily explained by the urinary examina- 
 tion. Not infrequently such cases terminate after the manner of 
 nephritics. The hypertension seems to be in part the result of 
 metabolic toxemia, and in part the result of adrenal overactivity, 
 and until the relationship between these conditions and chronic 
 interstitial nephritis is better understood we can hardly expect 
 definite knowledge concerning this so-called "idiopathic hyper- 
 trophy." 
 
 Many of the discordant reports which have from time to time 
 appeared in medical literature regarding the presence or absence 
 of hypertrophy of certain heart chambers have been due to inexact 
 methods. The most satisfactory, although a time-consuming, 
 method of determining this question is known as "Mailer's 
 method," which consists of careful weighing of the separated 
 heart chambers after the blood-clots, excess fat, etc., have 
 been removed. This is much more satisfactory than measurement, 
 since with the latter procedure marked variations occur which 
 depend on whether the heart has ceased to contract in systole or 
 in diastole. 
 
 The question as to why a hypertrophied heart fails in compensation has not 
 been definitely settled. Krehl regards it as due to a progressive myocarditis. 
 
 ' References to this subject together with a criticism of the cases reported in the litera- 
 ture will be found in Hedinger's article, Virchow's Archiv, vol. cxxviii, 1904, and in that 
 of Michaud, Correspondenzbl. f. Schweitz. Aerzte, 1906, p. 779. 
 
VUi. 51. Hvi'KRTItOl'HY AND DILATATION OF THE LeFT VeNTRICLE. 
 
 Chronic miiral and aortic endocardilis. The left ventricular wall is enormously thickened 
 and the cavity enlarged. The mitral valve shows extensive sclerosis. Many of the chordce ten- 
 dinete have ruptured; the rest are thickened and contracted. Numerous old sclerotic elev- 
 ated patches are seen on the auricular .surface of the mitral leaflets — the remnants of a former 
 endocarditis. The pupillary 7nuscles are hypcrlrophicd anil the left iiuricte is diluted. (R])('ci- 
 mnn from tho Philadolphia Hospital.) 
 
158 STUDIES IN CARDIAC PATHOLOGY 
 
 On the other hand, the careful researches of Aschoff and Tawara failed to find 
 such changes sufficiently constant to account for the condition. So, too, the 
 studies of Lissauer^ fail to decide the question as to whether the cardiac paralysis 
 results from a progressively increasing demand upon the heart muscle, or from 
 lesions in the nervous mechanism. 
 
 A chemical explanation of the cause of myocardial weakness has been offered 
 by Rzentkowski, who found that the myocardium of the left ventricle from cases 
 dying of prolonged illness, but without actual cardiac disease, contained more 
 proteid, fat, glycogen, etc., and much less sodium chlorid than the right ventricle. 
 He has endeavored to explain heart failure by an insufficiency of these substances, 
 or by disturbances in their distribution or in their utilizability.- 
 
 Bence, on the other hand, found that neither hypertrophy nor exhaustion of 
 a heart chamber was associated with any abnormality in the distribution of 
 nitrogen in the heart muscle, and, further, that in normal and simple hj^per- 
 trophied hearts the proportion of nitrogen bore a constant relation to weight. 
 During exhaustion the relation between muscular weight and nitrogen content 
 departs from the normal, inasmuch as the fixed nitrogen becomes proportion- 
 ately less.' 
 
 Merkel * suggests that stasis in the coronary veins plays a role in preventing 
 a removal of waste products, especially since this blood is not carried off by 
 collateral circulations. Pratt' failed to find sufficient fatty change to account 
 for it, and Faverges'" investigations indicated that the austere prognosis in 
 fatty degeneration was very much overrated. Aschoff was unable to find the 
 interstitial changes in either muscle-, nerve-, or ganglion-cell which Daddi ^ had 
 described. Merkel and Jannin* have demonstrated by means of injection of 
 the coronary arteries the fact that in cases of left ventricular hypertrophy there 
 is an enormous increase in the vascular supply which is given off from the left 
 artery, and, further, the fact that the right and left coronary arteries anastomose 
 both as arterioles and as capillaries, and that anastomotic branches from the 
 pericardium to the heart exist. In some cases, of course, the hypertrophy fails 
 as the result of those changes which are associated with advancing years. It 
 also fails in many cases because the pathologic changes in other organs \vith 
 which it is associated are progressive and have a direct physiologic as well as 
 anatomic relation to it. For the present we must conclude that the insufficiency 
 of hypertrophy rests upon a variable basis, and that although some cases can be 
 explained upon anatomic grounds, in others we have to assume a physico- 
 chemical or functional basis. The role of the vasomotor system is, as it is in 
 infectious diseases, more important than is generallj' recognized. 
 
 ' Lissauer; Mtinch. med. Woch., 1909, No. 36. 
 
 - Zent. f. klin. Med., 1910, Ixx, 337. 
 
 ' Zeit. f. klin. Med., Ixvi, Nos. .5 and 6. 
 
 ' Merkel: Mtinch. med. Woeh., 1907, p. 753. 
 
 * Pratt: Quoted Zentralb. f. path. Anat., 190.5, p. 531. 
 
 " Faverges: Wien. klin. Woch.. 1905, No. 19. 
 
 ' Daddi: Zentralb. f. inn. Med., 1904, p. 119. 
 
 ' Merkel and Jannin: Centralb. f. allg. Path. u. path. Anat., 1907, xvii, 876. 
 
I''iG. 52. — Cardiac Dilatation. 
 
 The heart is lar^c ainl fl:il)by, its walls thinned. Its form k .somcwlint (inadrannulur. 
 'Photograph by Dr. Alfred R. Allen.) 
 
160 STUDIES IN CARDIAC PATHOLOGY 
 
 In a study of the cause of compensatory failure in 34 cases of hj'pertrophy, 
 Schltiter' found fatty degeneration of the muscle-fibers relatively frequently, 
 together with enlargement and chstortion of the nuclei. Connective-tissue or 
 round-cell infiltration was less common and more localized. He behaves that 
 these manifestations are not the anatomic expression of heart weakness, but the 
 results of insufficient cardiac activity — slowed circulation and lymphatic stasis. 
 Insufficiency of the hypertrophied ventricle is the result of inadequate reserve 
 power, which he attributes rather to chminished excitabihty than to actual 
 muscular disease. 
 
 ' R. Schliiter: Die Erlahmung des hypertrophieten Herzmuskels, Vienna, 1906. 
 
 Fig. 53. — Hypertrophy and Dilatation of the Heart. 
 
 W. B. (Philadelphia Hcspital. November 28, 1901. xiii: 103. Patliologist: Dr. 
 Prince.) 
 
 Pathologic Diagnosis: Myocarditis; bilateral pleural effusion; hypertrophy and dila- 
 tation of the heart; mitral insufficiency; aortic stenosis; advanced arteriosclerosis; edema of 
 the lungs; acute nephritis. 
 
 Pericardium: Contains 100 c.c. of fluid. 
 
 Heart: Weighs 760 gm. The muscle is pale, the mills fn'uhlr. Tlir hf I rentricle averages 
 1.5 cm. in thickness. The aortic valves are incompetent. I In n-chiixi/urLi ikiI a ml Indurated. The 
 mitral ring admits five fingers; its valve leaflets are sliyhllij llilcl.-i ncil. The mnia is practically 
 one mass of atheromatous plates, with excavations. The left ventricular cavity shows many cal- 
 careous plates, and is about twice the normal size. 
 
X. CARDIAC DILATATION 
 
 Pathogenesis. — By dilatation of the heart we mean an increase 
 in the size of its chambers, which results from stretching of its 
 muscular walls. Such a condition may occur acutely under sud- 
 den, prolonged, or excessive strain, especially in subjects out of 
 training, or as the result of toxic processes, such as diphtheria, 
 typhoid fever, pneumonia, also as the result of prolonged nervous 
 strain and sudden mental or moral shock. The emotional stress 
 acts on the vasomotor nerves, the arterial spasm inducing a hyper- 
 tension which reacts on the myocardium. It has also been sug- 
 gested that the moral shock has further a direct action on the 
 centers regulating the innervation of the heart. Such cases were 
 observed among the Jews during the massacres in Odessa. ^ Chronic 
 dilatation of the heart is generally associated with or a sequel 
 of hypertrophy. It is usually due to two factors: inadequate 
 nutrition and. increased endocardial pressure, such as occurs in 
 the gradual occlusion of sclerotic coronary arteries, together with 
 valvular disease and an increased demand for hypertrophy. 
 Increased endocardial pressure may result not only from dim- 
 inished outflow, but also from increased inflow — from a rise of 
 venous pressure. 
 
 When extra work is suddenlj' required of tlie ventricle, as, for instance, if 
 the aorta is clamped, there first results a dilatation of the chamber associated 
 with a diminution of the systolic output; following this in healthy hearts there 
 occurs as the result of increased tonicity an increase of the systohc output, so 
 that the ventricle again empties itself properly. But if the heart is unable to 
 meet the emergency, or the obstructive force is too great, dilatation ensues 
 (0. Frank, Hirschf elder). 
 
 From what has been said it will be readily understood that, as 
 seen at autopsy, dilatation of the heart is generally associated 
 
 ' Cheinisse: Semaine Medic, 1907, xxvii, No. 9. 
 162 
 
I'u;. .54. — Ax ExTKK.MK Grade of .Sclerosis and Calcification of the Aortic Valves 
 
 AND OF THE AoRTA ItSELF. 
 
 The valves are shrunken, thickened, stiffened, and show calcareous change; the aorta is 
 dilated and consists of great masses of calcareous infiltration, for the purpose of showing 
 which the vessel has been everted. The mitral valve is sclerotic. The aortic valves are cal- 
 cified, the ventricular endocardium is thickened, and the left ventricle is hypertrophied and 
 dilated. The aorta .shows as saccular aneurismal dilatation. (Specimen from the Philadel- 
 phia HoHpital.) 
 
164 STUDIES IN CARDIAC PATHOLOGY 
 
 with more or less hypertrophy, in those cases in which the causa- 
 tive factors have been of prolonged duration. 
 
 Simple dilatation without a preceding hypertrophy may result 
 from the toxemia of infectious disease, especially diphtheria, from 
 metabohc poison, as in uremia, from lack of nutrition or the 
 ingestion of poison, or from sudden exertion, and apparently at 
 times from psychic shock. ^ 
 
 There can hardly be a doubt that toxins play an extrem^ely 
 important role in the production of dilatation. The microscopic 
 examinations by Tawara on the hearts of patients dead of cardiac 
 failure in a large number of cases showed no changes which could 
 account for death. The sudden death in infections such as 
 diphtheria is an example. In diphtheria this sudden death is 
 usually attributed to toxic action on the vagus, inasmuch as it is 
 often associated with unexplained and sudden vomiting, and since 
 post-diphtheritic paralyses are well known. So, too, the question 
 has been brought up whether diphtheria does not more or less 
 often irreparably damage the heart so that sudden death may 
 occur months, or even years, after the original infection. 
 
 Morbid Anatomy. — The heart, in addition to being enlarged, 
 is relaxed, flabby, and distended with blood. Dilatation generally 
 affects chiefly the right side. The auriculo-ventricular orifices 
 are enlarged, the septa may bulge toward the less affected side, 
 while chronic mj^ocardial changes of a fatty or fibroid nature are 
 more or less evident. (See Fig. 52.) 
 
 It is doubtful if all cases of cardiac dilatation could be ex- 
 plained on an anatomic basis, even if our methods of examination 
 
 ' Two cases reported by Marmorstein, Wien. med. Woch., Aug. 4, 1906. Starck: Mlinch. 
 med. Woch., 1905, lii, No. 7. 
 
 Fig. .5.5. — Calcification of the Aorta. 
 
 Specimen showing the left ventricular cavity. The .aortic valves are thickened, slightly 
 retracted, and contain calcareous deposits. The aorta is greatly thickened and its entire sur- 
 face is covered with white and dark yellow, roughened and projecting calcareous plates. 
 (Yellow being a relatively non-actinic color, these plates appear as black and brown in the 
 reproduction.) The mitral valve is moderately thickened. (vSpecimen from the Philadelphia 
 Hospital.) 
 
166 STUDIES IN CARDIAC PATHOLOGY 
 
 were more searching and exact. Dilatation is essentially the result 
 of diminished muscular tone, and while doubtless many cases 
 can be explained by structural microscopic changes in the muscle- 
 fibers or nerves, yet we know that muscular tone varies greatly 
 within functional limits. 
 
 Clinical Considerations. — There has been much discussion and 
 investigation regarding the existence of a functional cardiac 
 dilatation. It was at one time taught that the so-called "second 
 wind" of the well-trained athlete depended upon the appearance 
 of a physiologic dilatation by virtue of which the heart was enabled 
 to handle more blood. The investigations of Dietlen, Moritz, 
 De la Camp,^ Raab,'' and others indicate that such is not the case. 
 On the contrary, the normal heart becomes smaller during severe 
 exertion, and when dilatation occurs, we are in all probability 
 dealing with an organ whose reserve power is not up to par. 
 
 We must also bear in mind that the normal heart is smaller in the erect 
 than in the recumbent postures, due to the fact that in the former a larger amount 
 of blood is pent up in the vessels below the heart by the action of gravity.^ 
 It is also possible that, pressure-tension of the pericardium being greater in the 
 standing position, a greater pressure is exerted not only on the heart itself, but 
 also upon the venae cavae, both of which would tend to lessen the blood-content 
 of the heart, as would also lowering of blood-pressure and increase of pulse-rate. 
 
 Dilatation sometimes results from pure fatigue of the muscle, 
 no structural changes being demonstrable. Dilatation by bulging 
 of the ventricle drags on the papillary muscles and makes it more 
 difficult for the auriculo-ventricular valves to close, thus producing 
 valvular incompetency^ 
 
 Although the consideration of myocarditis properly belongs to 
 a work which concerns itself with microscopic pathology, yet the 
 subject is so intimately associated with the conditions which we 
 have discussed that a brief allusion to certain phases seems war- 
 ranted. 
 
 Acute myocarditis may occur as a result of infectious processes 
 
 ' De la Camp: Zeit. f. klin. Med., vol. li. 
 " Raab: Milnch. med. Woch., 1909, No. 11. 
 ^Dietlen: Habilitationsschrifft, 1909. 
 
Fk;. 56. — CALCiFirATioN of the Aorta. 
 
 The entire aorta is one hard, brittle, rough, thickened, calcareous mass, which fractures 
 with an audible snap when the vessel is flexed. The aortic valves share in this process of 
 calcification. The wall of the left ventricle is greatly thickened. The pericardium is thick- 
 ened and the subpericardial fat increased in amount. (Specimen from the German Hospital, 
 Philadelphia.) 
 
168 STUDIES IN CARDIAC PATHOLOGY 
 
 either as the result of micro-organismal or toxic action. It is 
 met with more especially in diphtheria, typhoid and typhus 
 fevers, rheumatic fever, scarlatina, and influenza. Embolic and 
 thrombotic affections of the coronary vessels, and septic processes, 
 may also be causative factors. The toxemia of pregnancy, 
 especially when eclampsia has occurred, often causes myocardial 
 degeneration. 
 
 Chronic myocarditis is often the result of poor cardiac nutrition, 
 which, in turn, means that the coronary circulation has in some 
 way been rendered inadequate. Thus, sclerosis of these vessels 
 leads to fibroid or fatty changes according to the amount of vas- 
 cular damage. Again, valvular lesions, especially aortic obstruc- 
 tion, lead to myocarditis, because with an increased demand for 
 cardiac work there is a relative diminution of blood-supply. 
 Coronary sclerosis may arise from conditions similar to those 
 which cause arteriosclerosis elsewhere. We must bear in mind, 
 however, that the mouths of these vessels, arising as they do from 
 the aorta in close proximity to the heart, are often seriously con- 
 stricted at their point of origin as the result of disease of the aorta, 
 without there being anj^ marked pathologic changes in their later 
 course. It is in this respect especiallj;' that syphilitic aortitis 
 plaj^s so important a role, producing, as it does with great fre- 
 quency, aortic aneurism, aortic insufficiency, and myocarditis. 
 That this statement does not invariably apply, however, is indi- 
 cated by the experimental work of Fleisher and Loeb, who found 
 that adrenalin injections, when combined with certain other 
 substances, such as spartein sulfate and caffein sodium benzoate, 
 produce both macroscopic and microscopic myocardial changes.^ 
 
 The direct cause of these lesions seems to be a mechanical one. "The 
 typical seat of the lesion at the base of the left ventricle, where the greatest 
 strain is exerted, favors this theory. Furthermore, analogous conditions have 
 been shown to occur in striated muscle in conditions of overexertion. The fact 
 
 1 Fleisher and Loeb's article, Arch. Int. Med., Feb., 1909, contains also a resumd of the 
 literature concerning experimental myocarditis. See also a second article by the same authors, 
 Arch. Int. Med., Oct. 15, 1910. 
 
Fig. 57. — Sclerotic .\nd Calcified Coronary Arteries. 
 
 Specimen from the Museum of the University of Pennsylvania, showing the root of the 
 aorta and the coronary arteries, the myocardium being removed by dissection. The vessels 
 are greatly thickened, and consi.st of masses of calcareous nodules and plates. 
 
170 STUDIES IN CARDIAC PATHOLOGY 
 
 that the injection of spartein and aclrenahn into dogs, whose hearts are relatively 
 stronger than those of rabbits, does not cause the appearance of myocardial 
 lesions, adds further support to this theory. These lesions are in all probability 
 not clue to lack of nutrition of the muscle-fibers as a result of contraction of the 
 coronary vessels, inasmuch as it has been shown that adrenalin does not cause a 
 contraction of these vessels." 
 
 Even small doses of adrenalin in the rabbit produce well-marked myocardial 
 changes, although these lesions show a tendency to heal. Pearce' has shown 
 that large quantities of this substance injected into animals may produce sudden 
 death from acute dilatation or from insidious myocardial changes which occur 
 independently of coronary sclerosis. 
 
 Bjorksten succeeded in producing myocardial changes in animals by the 
 injection of micro-organisms (bacillus coli, pneumococcus, typhoid bacillus, 
 staphylococcus), and also of their toxins.- Similar results were obtained by 
 Arloing and De Lagoanere with streptococci and staphylococci.'' 
 
 Rheumatic myocarditis is etiologically one of the most im- 
 portant varieties. It accompanies most cases of rheumatic endo- 
 carditis, and it is to this pathologic process that many cases of 
 cardiac hypertrophy and chronic myocarditis owe their origin. 
 Macroscopically rheumatic myocarditis shows httle that is char- 
 acteristic. Microscopically an inflammatory tissue proliferation 
 which manifests itself as small interstitial nodules is noted. This 
 process spreads to the neighboring muscle-fibers and produces 
 degeneration in them.* The hypertrophy and dilatation affects 
 both ventricles, and is often considerable, more so than the 
 microscopic changes seem to account for. Ventricular hyper- 
 trophy and dilatation are evidently the result of toxic action. 
 Death in the rheumatic carditis of childhood is generally directly 
 due to the myocardial lesions.'^ The nodules above referred to 
 are by some considered characteristic of rheumatic infection, but 
 they have also been described as occurring in chronic nephritis 
 and in non-rheumatic infections. Rheumatic myocarditis tends 
 to be progressive, a progression which is often considerably en- 
 hanced by subsequent reinfections. 
 
 ' Pearce: Albany Med. Annals, Jan., 1907, p. 42. 
 
 - Bjorksten: Arbeit, path.-anat. Institut Helsingfori?, 1908. 
 
 ■' Arloing and De Lagoanere: These de Lyon, 190S. 
 
 ' Geipel: Deut. Arch. f. khn. Med., Ixxxv, p. 75. 
 
 = Coombs: Quart. Jour. Med., Oct., 1908, p. 26. 
 
Fia. 58. — Cardiac Aneurism. 
 
 'rhc lower part of the loft ventricle shows a marked protuberance both to the right and to 
 the left of the incision. On the external surface of this bulging area the pericardium is densely 
 adherent. The ventricular wall at this point is thinned and the muscle appears dark and softer 
 than elsewhere. The interior of the sac communicates directly with the left ventricular cavity. 
 At the lowermost end of the incision, part of a dark blood-clot is seen which extends into, and 
 to a certain extent fills, the sac. The left ventricle is hypcrtrophicd and dilated. The aorta 
 shows .slight arteriosclerotic change, fSpecimen from the Philadelphia Hospital.) 
 
172 STUDIES IN CARDIAC PATHOLOGY 
 
 Fig. 59. — Aneurism of the He.\rt. 
 
 J. N., white, male, aged seventy-seven years. (Pennsylvania Hospital. Autopsy No. 
 -125. Pathologist: Dr. Longcope.) 
 
 Clinical Notes: Admitted nine days ago, having been ill for two or three weeks, with 
 cough and chilliness. In delirium he had wandered from his bed, to which he was returned 
 only after a tussle. He died suddenly two hours later. 
 
 Physical Examination: No heart murmurs. First sound faint. Action of heart 
 irregular. 
 
 Pathologic Diagnosis: Aneurism of the he%rl, with rupture ifito the -pericardium. 
 Occlusion of the descending branch of the left coronary artery. General arteriosclerosis. Chronic 
 diffuse nephritis. 
 
 Pericardium: Is filled with blood. 
 
 Heart: Is much enlarged. The epicardium is filled with fat, which measures 0.5 cm. in 
 some places. The organ has a peculiar shape, due to buljing of the left ventricle, so that the heart 
 from apex to base is elongated. In the bulging tip of the left ventricle there is a rupture 4 cm. 
 in length and 2 cm. in width. The surface of the heart about the tear is mottled deep red and 
 brownish-gray in color. On opening the heart the right ventricle is normal, as are also the 
 tricuspid and pulmonary valves. The left auricle is thickened but not dilated. The mitral 
 leaflets are moderately thin and delicate. The tip of the left ventricle shows a tear corresponding 
 in position to that described externally. It is 6 cm. in diameter. The heart muscle, which is 
 fairly firm and yellowish-brown in color (near the base of the left ventricle measuring 2 cm.), 
 gradually thins out until the deepest portion of the aneurismal sac is reached, where scarcely 
 any muscle-fibers can be found. At the beginning of the sac the heart muscle is pale brown 
 and soft. The sac is almost entirely filled with soft blood-clot, which shows very beautifully "the 
 lines of Zahn." The clot is attached to the wall of the heart, and measures 11 cm. in thickness; it 
 Jills the sac except in the lower portion, in which the tear occurred. The aortic valves are somewhat 
 retracted, thickened, and calcified, about the sinus of Valsalva. The descending branch of the 
 left coronary artery becomes very much narrowed about 3 cm. from its origin, and as it reaches 
 the region of the dilatation, is completely calcified and practically occluded. The circumflex 
 branch and the right coronary artery are patent, but their walls are absolutely stiff and cal- 
 careous. The aorta shows moderate arteriosclerosis associated with large areas of ulceration 
 and atheromatous ulcers. 
 
 Microscopic Examination: The pericardium contains a good deal of fat, but is normal. 
 The heart muscle is to a large extent degenerated. Certain areas are composed of pinkish 
 granular material, mixed with the remains of muscle-fibers, and some young connective -tissue 
 cells. About the margin of these areas the muscle-fibers are swollen or atrophied, filled with small 
 granules, and destitute of cross-strije. The nuclei often do not stain. Between the muscle- 
 fibers there is either connective tissue or fat. In some places isolated masses of muscle-fibers 
 are seen, which still retain their structure, but are entirely necrotic. The cells are filled with a 
 golden-brown pigment in the degenerated areas. A few polynuclear leukocytes are found. 
 The thickness of the muscular wall of the heart measures in some sections only 1 mm. Thrombi 
 composed of erythrocytes, leukocytes, and fibrin, all of which take a rather definits eosin 
 stain, are attached to the endocardial surface in some sections. There is no definite organiza- 
 tion, but the clot is so clearly welded into the muscular wall that it is impossible to determine 
 where the one ends and the other begins. The intima of some of the small arteries is so much 
 thickened that the lumen in some places is almost occluded. 
 
 Diagnosis: Myomalacia; chronic interstitial myositis; thrombosis. 
 
Fk; 59. 
 
174 STUDIES IN CARDIAC PATHOLOGY 
 
 The whole subject of chronic myocarditis is still far from 
 satisfactorily understood. There have been great discrepancies 
 of results among different observers, and hence diversities of 
 opinion. 
 
 Mj^ocarditis has been attributed to a great number of other 
 factors, such as a strenuous life, physical toil and hardship, chronic 
 infections, and intoxications — metabolic, alcoholic, nicotinic, etc.; 
 but it is very evident that the majority of these factors are of 
 etiologic importance in exact proportion to their tendency to 
 produce vascular damage. 
 
 Myocardial changes have also been produced bj^ high temperatures, by the 
 injection of staphylococcus pyogenes aureus, diphtheria bacillus and toxin, strep- 
 tococcus, adrenalin, and ligation of the branches of the coronary arteries. 
 
 Of all infectious diseases, diphtheria is most commonly accompanied by 
 cardiac dilatation, scarlatina being next in frequency. In the majority there 
 is a gradual return to the normal. In rheumatic fever 8 out of 18 showed dilata- 
 tion; 7 of these patients also had endocarditis. Three with endocarditis showed 
 no dilatation. None of these cases returned to a normal size (for bochly weight). 
 In typhoid fever the return to normal was variable. Five cases of pneumonia 
 out of 11 had dilatation which appeared chiefly at the time of the crisis.' 
 
 The depressing effect of the diphtheria toxin upon the heart has long been 
 recognized, and has been experimentally demonstrated.- According to Gossage,''' 
 the diphtheria toxin depresses contractility, the rheumatic toxin tonicity, hence 
 the greater frequency of death as a result of the former, and dilatation as that 
 of the latter. 
 
 In diphtheria the myocardial complications increase with age: 14.3 per 
 cent, in children under two years; 88.5 per cent, between eleven and fifteen 
 years. Cardiac dilatation occurred in 29 out of 40 cases.'' 
 
 Influenza, although occasionally causing endocarditis or myocarditis, gen- 
 erally manifests its cardiac effect by making some already existing lesion worse. ^ 
 
 Acute syphilitic myocarditis as a secondary manifestation has been described 
 by Jesionek. 
 
 Suppurative myocarditis includes two distinct types: (1) Puru- 
 lent infiltration of the heart muscle, generally secondary to such con- 
 ditions as infectious endocarditis, pericarditis, cardiac thrombosis, 
 
 ' Dietlen (orthodiagraphic studies): Munch, med. Woch., 1908, p. 2077. 
 
 2 Chevalier and Clerc: Soc. Biolog., June 26, 1909. 
 
 ' Gossage: Lancet, Aug. 21, 1909. 
 
 ' Foerster: Deut. Arch. f. klin. Med., 1905, No. 13. 
 
 '^ Ruheman: Beriin. klin. Woch., 1910, p. 201. 
 
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 Fiii. GO. — CAHDiAf Thiiombosis. 
 
 A large rounded thrombus about the size of a large walnut is attached to the auricular 
 surface of the mitral valve. The valvular leaflets themselves are sclerosed and indurated. 
 Another and much larger thrombus is seen occupying the lower and anterior surface of the left 
 ventricle. This has undergone partial organization and is firmly attached to columna; carneie 
 and the ventricular r^ndocardium, and very materially reduces the size of the cavity. 
 
176 STUDIES IN CARDIAC PATHOLOGY 
 
 septic myocardial infarction, as in pyemia; (2) acute interstitial 
 myocarditis, such as may occur in scarlatina, diphtheria, etc. 
 Beck and Stokes ^ were able to find only one true case of the 
 last-named type recorded, although thej^ collected a number of 
 cases of circumscribed abscess formation. Suppurative myo- 
 carditis generally results from septic thrombosis, and the abscesses 
 resulting may vary in size from a pinhead to several centimeters 
 in diameter. Among the 9,940 autopsies studied by the author 
 there were 6 cases of acute suppurative myocarditis. 
 
 Clinical Considerations. — While it is doubtless true that the 
 myocardium plays a role in all forms of heart disease the im- 
 portance of which it is difficult to overestimate, yet the term 
 "myocarditis" is often vaguely applied, and such a diagnosis 
 made without ample justification. Thus, in acute diseases death 
 is often attributed to myocarditis when it is really the result of 
 toxic vasomotor paralysis. In these cases blood-pressure, both 
 systolic and diastolic, will be found unduly low, and careful 
 microscopic examination of the heart may show no structural 
 alterations meriting the appellation of myocarditis. Surgical 
 shock, too, is now known to be a vasomotor paralysis, and not 
 to be a result of heart weakness. Sweet has suggested that it 
 may be the result of an acute adrenal insufficiency. A clinical 
 diagnosis of myocarditis is generally based upon evidences of 
 cardiac insufficiency^ the symptoms of which may be produced 
 by a host of extracardiac and intracardiac causes, associated with 
 which ver}^ little myocardial degeneration may be demonstrable 
 at autopsy. On the other hand, cases with well-marked lesions 
 often exhibit disproportionately few symptoms. Cabot found a 
 myocarditis correctly recognized in 22 per cent., overlooked , in 
 26 per cent., and diagnosticated when not present in 52 per cent, 
 of the cases studied by him. We must bear in mind, however, 
 that very small lesions localized to important areas, such as the 
 sinus node, the auriculo-ventricular node or bundle, etc., may 
 
 ' Beck and Stokes: Jour. Am. i\Ied. Assoc., 1910, p. 1065. 
 
In;. 01. — CAiii)[.\r A.\i;i;ris,m a.vd Tiuiombosis. 
 A larce o'/ati; llirombus i.s .s.ion in tho lower part, of the left ventricle, the walls of which are 
 visibly thinncfl and stretchetl below and behind the thrombus. The endocardium of the 
 vonlriclo in thickened anrl riparnic, the aorta xhow.s slifrhl artcrio.sclorotic chango, in part in- 
 volving the mouth of thf cdronary artery. 
 
178 STUDIES IN CARDIAC PATHOLOGY 
 
 Fig. 62. — Mural Thrombosis. 
 
 Pathologic Diagnosis: Mural cardiac thrombosis. Dilatation of the heart, chronic 
 myocarditis, bronchopneumonia. 
 
 Pathologic Notes: Pericardium: The pericardium contains approximately 20 c.c. of 
 clear yellow straw-colored fluid. The visceral surface is smooth and glistening, with injected 
 vessels. Its visceral surface contains a large, smooth, opaque, white patch measuring 3x2 cm. 
 This patch is apparently on the external surface of the middle portion of the right ventricle. 
 There are a few scattered areas similar to the above on the external surface of the right heart. 
 The superior portion of the exterior surface of the right auricle contains a few yellowish-white 
 ■ spots, pinhead size. There is a larger yellowish-white patch, 5 mm. in diameter. 
 
 Heart: The heart weighs 530 grams. The heart's flesh is quite firm in consistency and is 
 of a dark red color streaked, in areas, with spots of a lighter red. Both the right and left heart 
 are markedly dilated. The right ventricular walls measures 5 mm. in thickness. The papil- 
 lary muscles are of a pale reddish-gray color. Clinging to portions of the right ventricular 
 wall, especially toward its tricuspid portion, are masses of a quite firm reddish material spotted 
 with areas of yellow. These masses are quite well attached to the muscular wall, and for the 
 most part lie between the papillary muscles. The right auricle is completely thrombosed 
 by the masses of what appear to be organized blood-clots. The muscle of the right ven- 
 tricular wall, especially, shows on its under surface very many reddish-yellow patches with 
 small strands of reddish tissue coursing between them, which gives to the surface a mottled 
 appearance. At the base of many of the papillary muscles small whitish patches are seen. 
 The tricuspid valve is well formed and normal in all respects. The pulmonary valve shows no 
 apparent pathologic change, nor do the pulmonary vessels. The endocardium of the right 
 side seems to be intact. The lefl rntiriciilar cavity is dilated, measuring at its middle transverse 
 portion 10.5 cm. The muscuhir imll i-nrirf; in thickness; thus, at the apex it is but 1 cm. in thick- 
 ness, while toward the valvular end it measures 1.7 cm. in thickness. Attached to its walls are 
 masses oj an organized tissue of a reddish-gray appearance, streaked with coarse strands of a 
 definite yellow-while. These masses cling to nearly all portions of the left ventricular wall, measur- 
 ing from 0.5 to 2.5 cm. in diameter, and do not appear to cling to the endocardium at 
 any point. The condition of the heart muscle, at its .junction with these clots, has a most 
 peculiar appearance. Where the clots nice! the true muscular wall there appears to be a 
 dcHiiitc yellow line, in many portions shouinii ilisiiiici (Iciiiarkation. These clots interweave 
 among the papillary muscles, are quiti' finu in coiisislcncy, and show definite evidences of well 
 organized tissue. The mitral valve is normal. The left auricle contains the same kind of 
 thrombi as does the ventricle. The aortic ring measures 6 cm. The aortic valves are well 
 formed and are normal in all respects. There is no evidence of any sclerosis of the larger 
 vessels. The coronary arteries are patent; their walls are smooth and no sclerosis can be 
 found. (Pennsylvania Hospital, No. 1060.) 
 
Fig. 62^ 
 
180 STUDIES IN CARDIAC PATHOLOGY 
 
 apparently be responsible for serious damage when the rest of the 
 myocardium is comparative!}' healthy; and that disease of these 
 structures is generally undemonstrable during a routine autopsy. 
 It is to be hoped tliat the careful routine examination of these 
 areas in large series of cases will throw much light upon the at 
 present unsatisfactory status of "myocarditis." 
 
 CORONARY ARTERIOSCLEROSIS 
 
 The nutritional suppl}', and hence the functional integrity^, of 
 the whole heart depends very largely upon the condition of the 
 coronary arteries. As long as the blood-supply is adequate the 
 heart can cope with the most surprising mechanical odds. It is 
 not surprising, therefore, that sclerosis of the coronary arteries 
 should be the most serious form of heart disease. 
 
 As a general rule, gradual narrowing of a coronary artery is 
 followed by fibroid or fatt_y change in the mj^ocardium, whereas 
 sudden occlusion, as may occur from embolism or thrombosis, 
 produces an area of softening somewhat smaller than the anatomic 
 area supplied by the vessel. (See Section IX.) 
 
 Although the earlier teaching, that the coronaries are end- 
 arteries which practically do not anastomose, has been in a strict 
 sense disproved by the researches of Hirsch and Spalteholtz, ^ Jannin 
 and Merkel;- and although cases have been reported in which 
 occlusion of large arteries, such as the right coronary, may occur 
 without subsequent myocardial change (Marchiafava,^ Chiari); 
 and although the last-named arterj^ has been ligated in man with- 
 out subsequent muscular degeneration (Pagenstecher^), yet these 
 cases are exceptional, and must be explained as due to anomalous 
 blood-supply or incomplete occlusion. Cases of the opposite 
 sort have also been noted, as, for instance, that of F. T. Stewart, 
 in which a human heart sutured some years before for trauma, 
 
 ' Hirsch and Spalteholtz: Deut. med. Woch., 1907, p. 790. 
 
 - Jannin and Merkel: Die Koronararterien des Mensehliohen Herzen, etc., Jena, 1907. 
 ^ Marchiafava: Revist. critica di olin. med., 1904. 
 ■" Pagenstecher: Deut. med. Woch., 1901, p. .56. 
 
Fid. 03. — C.\RDi.\c Aneurism and Thrombosis. 
 Thf iiiusculatiiro of Iho left vontricle near the apex i.s thinned and stretehed; its chamber 
 is nearly filled with a large, dark, jiilisteninp;, adherent thrombus, which shows the "Unes of 
 Zahn." The mitral valve is moderately .sclerosed. (Photograph by Dr. Alfred R. Allen.) 
 
182 STUDIES IN CARDIAC PATHOLOGY 
 
 disclosed a fibroid myocarditis originating at the site of the original 
 ligature. 
 
 When the coronary arteries are ligated in animals, death may 
 occur suddenly,^ preceded by fibrillation, or it ma}^ occur in the 
 course of minutes,- hours, ■' or weeks.'' 
 
 But we must bear in mind tiiat in animals we are dealing with healtliy liearts 
 wliich we Ivnow are able to sustain a great deal of traumatic insult. Embolic or 
 thrombotic manifestations, on the other hand, rarely occur in conjunction with 
 a previously healthj^ myocardium. 
 
 Based on original investigation and a review of the literature, Amenomiya " 
 draws the following conclusions regarding the coronary arteries and the papillary 
 muscles. The 7^ight coronary artery supplies the greater part of the right heart, 
 the posterior part of the ventricular septum, and part of the posterior part of 
 the left heart. The left coronary artery supplies the most of the left heart, the 
 anterior part of the ventricular septum, and part of the anterior wall of the right 
 heart. In the papillary muscles the terminal bifurcations occur as straight, 
 longitudinal, and radiating branches. The anterior papillary muscle of the left 
 ventricle is supplied solely by the ramus descendens of the left, and the posterior 
 by both branches of both coronary arteries. The large anterior papillary muscle 
 of the right ventricle derives its nourishment from both arteries, the branch from 
 the left artery being given off relatively high up from the ramus descendens. 
 The vessels supplying the papillary muscles double upon themselves upon enter- 
 ing, thus describing a considerable curve. The foregoing anatomic facts, which 
 are unfavorable to perfect circulatory efficiency, explain why the papillary muscles, 
 especially the anterior ones, are so frequently the seat of infarction and fibrosis. 
 It has been shown that during acute infections the coronary arteries show patho- 
 logic alterations before the other vessels of the body, and that the structural 
 damage thus produced maj^ lead to arteriosclerosis." 
 
 Pathogenesis. — The effects of arteriosclerosis of the coronary 
 arteries may be due either to disease of the artery itself through- 
 out its course, or to constriction of its orifice resulting from disease 
 of the aorta. The types of coronary arteriosclerosis are similar 
 to those affecting other arteries — localized or general thickening, 
 
 ' Magrath and Kenned}': Jour. Exper. Med., 1S97, p. 1.3. Porter: .Jour. Physiol., 1893, 
 p. 121. 
 
 - Cohnheim and v. Schulthess Rechberg: Arch. f. path. Anat., 1881, p. 503. 
 
 ' Panum: Ibid., 1863, pp. 308, 433. 
 
 ■• Baumgarten: Am. Jour. Physiol., 1899, p. 243. 
 
 ^Amenomiya: Virchow's Arch., 1910, cic, 187. 
 
 "Wiesel: Wien. kUn. Woch., 1906, No. 26. Wiesner: Centralb. f. med. Wissensch., 
 1907, No. 3. 
 
Fig. 64. — Aneurism op the Left Ventricle. 
 
 The left ventricular wall, which is elsewhere hypertrophied, is markedly attenuated on its 
 left .side at and above the apex. In this region a marked bulging, about the size and shape of a 
 large duck egg, is seen. The endocardium in this region is covered with calcareous plaques. 
 The aortic and mitral valves show moderate sclerosis. (Specimen from the Philadelphia 
 Ho.spital. Vol. XV, p. 39. Phy.sician: Dr. F. P. Henry.) 
 
184 STUDIES IN CARDIAC PATHOLOGY 
 
 roughening, hardening, or actual calcification being met with. 
 On account of the smaller cahber of some of the branches, occlusion 
 may readily occur and thrombosis result, especially if the blood- 
 pressure is lowered or the orifices are constricted. Such constric- 
 tion is of frequent occurrence. Up to thirty years of age the elastic 
 tissue in the aorta increases.^ Both Adami and Aschoff regard 
 this as a work hypertrophy. For the following fifteen years the 
 amount of this connective tissue remains stationary. After 
 fift}^ 3'ears there is a slow, progressive wasting of the elastica, 
 and a stretching and thinning of the media occurs. "The domi- 
 nant primary event in the arteriosclerotic process — syphilitic, 
 senile, functional — is a localized, or it may be diffuse, weakening 
 of the arterial wall, and especially of the media. This induces 
 increased strain upon the remaining coats; and if this be not 
 excessive, that strain leads more especially to connective-tissue 
 overgrowth and the development of the characteristic lesions of 
 arteriosclerosis" (Adami). Syphilitic disease of the aorta is a 
 relatively frequent manifestation of this infection. It is apt to 
 occur early in life, to be of a serious and progressive nature, and, 
 as already pointed out, to affect just that portion of the aorta 
 from which the coronary arteries arise. In addition to lues, 
 certain acute infections, such as typhoid and rheumatic fevers, 
 and certain chronic infections, such as rheumatoid arthritis, often 
 seem to produce arteriosclerosis. 
 
 Three more or less distinct types of arteriosclerosis of the larger vessels 
 occur in man: (1) The ordinary nodular form; (2) dilatation of the vessels with 
 increased tortuosity, the peripheral arteries being of the "pipe-stem" variety, 
 and (3) the syphilitic type, affecting chiefly the ascending aorta, in which the 
 nodules eventuallj^ cause depressions in the intima. This is primarily a mes- 
 aortitis, with wasting of the media, and with thickening of the other coats. 
 
 In 1,000 consecutive autopsies Brooks- found coronary sclerosis of sufficient 
 degree to "seriously affect the nutrition of the heart " in 270 cases. The earliest 
 instance occurred in a boy of fifteen years, the average age being forty-five years. 
 The following associated conditions were found: Chronic alcoholism, 107;. 
 
 ' Foster: Jour. Med. Research, Sept., 1909. 
 - Brooks: New York Med. Jour., 1906, p. 825. 
 
Fig. 6.5. — Ball Thkombus in the Left Auricle. 
 A largo, dark, ball-shaped thrombus lies free in the left auricular cavity. Numerous 
 smaller mural thrombi are seen enmeshed in the columna; cameae and chorda; tendinea;. 
 The left ventricular wall, which is elsewhere hypertrophied, is noticeably thinned near the 
 ape.x. fPhotOKraph by Dr. .Vlfred R. Allen.) 
 
186 STUDIES IN CARDIAC PATHOLOGY 
 
 nephritis, 35; syphilis, 30; tuberculosis, 20; carcinoma, 1; diabetes, 6; plumb- 
 ism, 2. All but 15 showed macroscopic myocardial lesions. In 215 cases these 
 changes were sufficient to be considered as contributory to the cause of death. 
 The following lesions were observed: Brown atrophy, 64; fibrosis, 24; hyper- 
 trophy, 35; acute dilatation, 20; aneurism, 2; cardiac rupture, 2. At the 
 Philadelphia General Hospital, which is very rich in such material, among 8,640 
 autopsies the following myocardial lesions were encountered : Acute suppurative 
 myocarditis, 5; myocardial thrombosis, 28; sarcoma, 4; carcinoma, 4. At the 
 Pennsylvania Hospital among 1,300 autopsies there was 1 case of coronary 
 aneurism and 10 cases of coronary obhteration. (See page 48.) 
 
 Arteriosclerosis of the coronary artery is the commonest pathologic finding 
 in cases of angina pectoris. 
 
 Among 83 cases of angina pectoris Bouchard found only 12 with a history 
 of syphilis. Among 261 syphilitics, 4.5 per cent, suffered from angina pectoris; 
 among 3,739 non-syphilitics, only 2 per cent. did. Of the above mentioned 261, 
 14 per cent, presented aortic lesions.^ 
 
 The left coronary artery generally shows the most marked sclerotic changes. 
 These appear as localized or diffuse thickening, especially at the points of bi- 
 furcation or branching. Partial occlusion generally results in myomalacia cordis, 
 which, if several contiguous areas are involved, results in aneurismal dilatation. 
 
 The localization and extent of arteriosclerosis is to a certain extent depen- 
 dent upon functional activity. Boveri's ^ experiments on animals tend to con- 
 firm the clinical view that hard muscular work leads to arteriosclerosis. In 
 laborers the location of the most pronounced vascular lesions corresponds to the 
 part of the body which performs most of the work — the lower extremities in 
 knife-grinders, the upper extremities in wood- and stone-cutters. It is not im- 
 probable that fatigue toxins have some effect. It has sometimes been possible 
 to determine post mortem by the amount of arteriosclerosis which organ of the 
 body functionated most actively during life.' An inchcation that such arterio- 
 sclerosis may be the result of increased blood-pressure may be found in the fact 
 that rabbits suspended by the hind legs for three minutes daily over a period of 
 one hundred and twenty days showed well-marked arterial lesions in the upper 
 part of the body.^ A normal pressure with weakened media, or an increased 
 pressure with a normal media, may cause a giving way of the arterial coat with 
 secondary intimal changes. To a certain extent the toxins of disease exert a 
 specific selective action. Klotz and Saltykow^ have shown that diphtheria 
 affects the media, while the typhoid fever exerts its noxious influence on the 
 intima. 
 
 That syphilis is one of the commonest, if not the commonest, causes of 
 sclerosis of the aorta cannot be doubted. In a study of 54 cases byBittdorf' 
 
 ' Arch, du Mai du Coeur, 1909, p. 98. 
 
 = Boveri: Riforma Medica, 1909, No. 30, 31. 
 
 ' Askana: Therapeut. Monatshefte, Sept., 1907. 
 
 •• Klotz: Quoted Adami, Am. Jour. Med. Sci., Oct., 1909. 
 
 » Saltykow: Ziegler's Beitriige, 1908, xlii, 187. 
 
 » Bittdorf : Deut. Arch. f. klin. Med., Ixxxi, 1904, No. 122. 
 
CARDIAC DILATATION 187 
 
 the average age at which this lesion occurred was 55.6; in syphihtics the average 
 age was ten years younger. Huchard' in a study of 1,835 cases of arterio- 
 sclerosis seen in private practice found a history of gout in 323, of rheumatism 
 in 332, of syphilis in 209, of the abuse of tobacco in 181, of infectious disease 
 in 67, of alcohol in 27. 
 
 Although the arteriosclerosis produced by means of adrenalin, barium 
 chlorid, nicotin, etc., differs from that which occurs spontaneously in man, 
 inasmuch as in the former the changes are hmited almost entirely to the mecUa, 
 yet both of these types have as a common basis a giving way of the media. 
 Adami suggests that the intimal changes are lacking in the experimental variety 
 on account of their acuteness, and considers that the arterial thinning of the 
 Monkeberg type, and the intimal thickening of senile arteriosclerosis, are diverse 
 manifestations of a common process. 
 
 'Huchard: Bull, de I'acad. d. Med., July 1.5, 190S. 
 
XL CARDIAC ANEURISM 
 
 Aneurism of the myocardium consists of a localized bulging of 
 the heart, and is brought about through stretching of the softened 
 muscle or the fibrous tissue which displaces a diseased myocardium. 
 At times the septum is involved. Rarely the aneurism is an 
 extension of the aneurismal dilatation of one of the valves, e. g., 
 the mitral, with secondary involvement of the wall of the heart. 
 
 The fibroid degeneration which precedes the aneurism may 
 result from coronary sclerosis, either the mouths or the terminal 
 branches of these vessels being diseased. Chronic endocarditis 
 and the traction of pericardial adhesions are also causative factors 
 in some instances. Cardiac aneurism is distinctly rare, and except 
 in those cases where rupture produces hemopericardium and sudden 
 death, it is often discovered unexpectedly at autopsy. (See 
 "Coronary Sclerosis," p. 180.) 
 
 The condition is generally single, although multiple aneurisms 
 have been noted. The myocardium, which may be greatly 
 thinned and stretched, is replaced to a greater or less extent by 
 fibrous tissue. At times the opening into the aneurism is con- 
 stricted and forms a dilated sac beyond, but this is not generally 
 
 Fig. 66. — Rupture of the Aorta. 
 
 M. S., male, white, aged fifty-one years. (Philadelphia Hospital. Autopsy vol. xix, p. 
 281. Physician: Dr. Mills. Pathologist: Dr. J. D. Wilson.) 
 
 Clinical Notes: Arrhythmia; pulse 90. Sudden death, with marked cyanosis and 
 rigidity of the body. 
 
 Pathologic Diagnosis: Rupture of the aorta; chronic interstitial nephritis, with acute 
 exacerbation; nutmeg liver; general arteriosclerosis. 
 
 Pericardium: Extends from the right border of the sternum to the left axillary line. On 
 incision, blood spurts freel}'. The cavity contains 1,000 c.c. of fluid blood, and an equal amount 
 of blood-clot. 
 
 Heart: Weighs 750 gm., has a normal color. Myocardium is thickened and firm. Endo- 
 cardium normal except } or small patch of atheroma on the aortic valve, hi the aorta, 2 c.c. above 
 the valve margin, there are two openings, one a vertical slit 3 cm. long, which forms an opening 
 from the aorta to the pericardial cavity. The other, 6 cm. long, is situated directly opposite, but 
 extends only to the connective tissue surrounding the vessel. This tissue surrounding the lateral 
 slit is markedly reddened and swollen. 
 
 1S8 
 
190 STUDIES IN CARDIAC PATHOLOGY 
 
 the case. Aneurisms are generally found on the anterior surface 
 of the left ventricle above the apex. Such dilatation has clinically 
 simulated a pericardial effusion to such an extent that aspiration 
 was performed and blood withdrawn from the left ventricle.^ 
 Among the 1,300 Pennsylvania Hospital autopsies there were 5 
 cases of cardiac aneurism; at the Philadelphia Hospital, 3 among 
 8,640. Legg found 3 in 1,899 autopsies. 
 
 To parietal endocarditis has also been ascribed an etiologic 
 
 ' W. Pepper: University of Penna. Med. Bull., vol. i. 
 
 Fig. 67. — Gummas op the Myocardium. (Right heart.) (See also Fig. 68.) 
 
 Male, aged thirty-eight years. (Pennsylvania Hospital. Specimen 239. Physician: 
 Dr. A. V. Meigs.) 
 
 Clinical Notes : Patient's health had been poor for the last few years; he had complained 
 of frequent micturition and asthma. He at one time had swelling of the feet. Before the 
 present attack he had no distinct convulsions, but had had frequently what he called "spells." 
 He denied ever having had syphilis. At the time of his admission to the hospital he was in a 
 state of partial collapse, with cyanosis, cold extremities, vomiting, and retching. The heart 
 action was "excessively slow" and irregular, "there being when the patient first came into 
 the ward two or three respirations taken for each beat of the heart." There was a loud blow- 
 ing murmur at the apex. On the day following the patient frequently complained of feeling 
 faint, and during these attacks objects swam before his eyes. Cyanosis and cold extremities 
 were constant. The murmur still persisted, but was heard louder at the base of the heart. 
 Pulse 34, respirations 18, temperature 98° F. Five days later the patient uttered a shriek and 
 died suddenly. 
 
 Pathologic Report: "The specimen shows a heart with a firm, nodular mass situated 
 in the septum and reaching from the tricuspid valve into the right auricle, and also making a pro- 
 jection into the left ventricle just below the aortic orifice; its size is about that of a walnut. In the 
 right auricle it juts forward directly over the tricuspid orifice, and in the left ventricle it in- 
 volves nearly the whole of the ventricular surface of the aortic cusp. Its tissue is firm, some- 
 what elastic, and on section shows a pretty uniform consistence and a gray color. Numerous 
 firm clots are entangled in the columna? carneaj of the right ventricle, which are continuous 
 through the tricuspid orifice and pulmonary artery. The organ weighs 17 J^ ounces. A micro- 
 scopic examination showed the characteristic appearance of a syphilitic gumma." (Meigs.') 
 "Further examituiUmi of llu' preserved specimen shows that this nodular mass obliterates the un- 
 defended space «/ /lie lull rreiilrindur septum, and entirely fills that part of the septum through 
 which the auricalu-eeiUneidar bundle runs. It is the posterior leaflet of the aortic valve into 
 which the gumma has grown. To the right of this leaflet there is a small second nodule 
 10 X 7 mm. The root of the aorta is corrugated and appears to be the seat of a syphilitic 
 aortitis." (Robinson.) 
 
 There is every reason to believe (although this case was first reported long before the 
 existence of the auriculo- ventricular bundle was known, or its function understood) that we 
 had here to deal with a case of auriculo-ventricular heart block due to a gumma of the myocar- 
 dium involving the interventricular septum. 
 
 ' This case was reported by Dr. A. V. Meigs in the Transactions of the College of Physicians 
 of Philadelphia, 1881, third series, vol. v; further studied and reported by Dr. G. C. Robinson 
 in the Bulletin of the Ayer Clinical Laboratory, 1907, No. iv. 
 
192 STUDIES IN CARDIAC PATHOLOGY 
 
 role.^ Such a case has recently been reported by Bret and Rou- 
 bier.- Cardiac aneurism may also result from traumatic scar 
 formation, suppurative foci, or gummatous myocarditis. 
 
 According to M'Elroy,^ there are now on record in medical 
 literature some 300 cases of myocardial aneurism. Warthin 
 states that the condition may be congenital. Among 208 cases 
 collected by Hare, 74 per cent, occurred in men. Only about 
 7 per cent, of the chronic cases terminate in rupture. 
 
 Actual calcification of the myocardium is distinctly rare, 
 and its pathology not thoroughly understood. Apparently the 
 calcification occurs as a sequel to muscular degeneration. Hart,^ 
 who has collected 13 cases, has suggested that hyaline, glycogenic, 
 and amyloid changes may be the real substratum of the condition. 
 Topham has reported actual bone formation in the heart of a 
 man dying at the age of seventy-one.'' 
 
 CARDIAC THROMBOSIS 
 
 "The term cardiac thrombosis must be reserved for a solid or 
 partly solid structure, primarily formed from the blood-elements, 
 which develops in one or more of the heart chambers during life. 
 Such a mass may be attached to the cardiac wall by a more or 
 less altered base, or may exist as a free foreign body within a heart 
 cavity. When cardiac thrombi are measured bj^ this standard 
 they are uncommon post-mortem findings.'"^ For the production 
 of cardiac thrombosis three factors are necessary: first, local 
 endocardial injury — mechanical, bacterial, or toxic; second, 
 an increase of hemagglutinins in the blood; and, third, slowing 
 of the blood-stream. Thrombi are met with in valvular heart 
 disease, in cachectic states, and in blood dyscrasias. In the first- 
 named class they maj^ begin as vegetations. Infectious diseases 
 
 1 Strauch; Zeit. f. klin. Med., 1900, p. 231. 
 
 - Bret and Roubier: Arch. d. Mai. du Cceur., 1910, p. 445. 
 
 ' M'Elroy: Jour. Am. Med. Assoc, Aug. 1, 1908. 
 
 •" Hart: Zeit. f. Patholog., 1909, iii, 706. 
 
 '^Topham: Brit. Med. Jour., Oct. 1.3, 1906. 
 
 "Smithies: Jour. Am. Med. Assoc, 1909, p. 1347. 
 
Fic. OS. — Gummas of the Myocardium. (Left heart.) (See legend under Fig. 67.) 
 
194 STUDIES IN CARDIAC PATHOLOGY 
 
 except influenza and tuberculosis are rarely complicated by throm- 
 bosis. The most common site is in the left auricle, the right auricle 
 and the left ventricle coming next in frequency, while "primary 
 thrombosis of the right ventricle appears to be unknown." 
 
 Thrombosis is probably more common in mitral stenosis than 
 in any one other condition. It is also met with in cardiac dilata- 
 tion, especially when sclerotic endocardial or myocardial changes 
 are present. Hence it is more common in the later years of life, 
 although it has been described in childhood. The shape of the 
 thrombi varies considerably, but generally they can be classified 
 either as pedunculated or of the ball variety, the former being 
 the more common. The effect of cardiac thrombosis upon the 
 circulation is generally marked. Such a condition interferes 
 considerably with cardiac contraction and with the transference 
 of blood from one chamber to another, so that from a diagnostic 
 standpoint the severity of the symptoms is out of all proportion 
 to the apparent degree of the cardiac lesion. At the Pennsylvania 
 Hospital there were 6 cases in 1,300 autopsies; at the Philadelphia 
 Hospital, 28 among 8,640. 
 
 Cardiac rupture may occur as the result of fatty degeneration, 
 aneurismal dilatation, suppurative myocarditis, acute necrosis, 
 gummatous disease, and brown atrophy. This condition was 
 first described by Harvey, and later by Morgagni. Among 
 Quain's 100 collected cases 77 were due to fatty degeneration. 
 Most of the patients were beyond sixt.y years of age, and sudden 
 death occurred in 71 per cent. The site of rupture was as follows: 
 Left ventricle, 55; right ventricle, 7; right auricle, 3; left auricle, 2. 
 Rupture may be complete or incomplete. It is slightly more 
 frequent in males. In 18 of LetuUe's 110 cases, multiple rupture 
 was found. Occasionally rupture occurs in apparently healthy 
 young people as the result of coronary thrombosis.^ Quain's 
 cases included two between the ages of ten and twenty. Rupture 
 
 ■ Klingmann: New York Med. Jour., 190S, p. 199. 
 
Fig. 69. — Gumma of the Myocardium. 
 
 A larfcc, firm, nodular mass is seen in the septum below the aortic valves which bulges 
 forward into the ventricle. Another mass is seen in the wall of the ventricle. These masses 
 were firm, .slightly elastic, grayish in color, and upon microscopic examination showed typical 
 gummatous structure. 
 
 The heart is that of a patient aged thirty-one years, who had contracted syphilis eight 
 years before. Three years previous to admission he had been incapacitated for three days 
 by an "inflammation of the heart." Six weeks before admission he had had fugacious pains 
 and less of power in the right hand. A few days afterward he had a syncopal attack while at 
 work, following which he developed headache, weakness, numbness of the legs, and diplopia. 
 On admi.s.sion to the hospital he was found to have a right-sided hemiplegia. On auscultation 
 a mitral systolic murmur was noted. During his three months' stay in the hospital he had 
 hemoptysis and cardiac pain. (Pennsylvania Ho.spital, No. .301. Dr. J. M. DaCosta.) 
 
196 STUDIES IN CARDIAC PATHOLOGY 
 
 of a 'papillary muscle is extremely rare. Dennig^ has reported a 
 case, and alludes to the scanty literature on the subject. It 
 may follow great increase of blood-pressure, especially with a 
 diseased myocardium, or it may result from crushing trauma 
 of the thorax or from ulcerative processes. Spontaneous car- 
 diac rupture is to be differentiated from the traumatic variety 
 — the question is often of medico-legal importance — as follows: 
 The former occurs chiefly in advanced years; the parietal peri- 
 cardium shows no lesion, the heart muscle near the site of 
 the tear generally does. The tear is usually near the apex in the 
 left ventricle, and assumes a zigzag outline. Although it has been 
 stated that a perfectly normal heart may rupture under great 
 strain, this is very questionable. Such cases probably always have 
 a preceding pathologic basis which predisposed to the rupture 
 (ThoreP). Geill,^ in an analysis of 90 cases of traumatic cardiac 
 rupture produced by blows delivered with dull instruments, etc., 
 found the right ventricle frequently, and the left rarely, injured. 
 There is much discrepancy' of opinion as to whether the tearing, 
 crushing, or bursting element is the most important in the mechan- 
 ism of traumatic rupture. The mode of death in such cases de- 
 pends upon whether the exudation of blood into the pericardial 
 sac is sudden or gradual. In the former we may have an actual 
 mechanical compression — "tamponade"; in the latter a gradual 
 interference with diastole through the secondary effect of the de- 
 pressor nerve on the vasomotor center (Placzek*). In the former 
 the pericardium will be tensely distended and the heart collapsed; 
 in the latter both of these conditions will be less marked. 
 
 The distribution of cardiac rupture among 8,640 autopsies at 
 the Philadelphia Hospital was as follows : One of the left ventricle, 
 two of the left auricle, one of a papillary muscle. 
 
 ■ Dennig: Deut. Arch. f. klin. Med., 1909, p. 163. 
 ^Thorel: Lubarsch and Ostertag's Ergebnisse, 1907, ii, 425. 
 ' Geill: Viertel Jahrschr, f. Gericht. Med., 189.5, xvii. 
 ^Placzek: Ibid., 1902. 
 
Fif;. 70. — fliMMA OF THE T,i;iT \'jc\Tniri.K. (Specimen I'rom the Fonnsylvania Hosiiital.) 
 
198 STUDIES IN CARDIAC PATHOLOGY 
 
 Among 132 cases Odriozola^ found the site of the rupture to be 
 as follows: Left ventricle, 96; right ventricle, 22; left auricle, 
 2; auriculo-ventricular groove, 2. 
 
 The size of the tear in the spontaneous cases varies, but is 
 generally from one-half to one inch in length. Not infrequently 
 the tear is larger on the outside than on the inside. The rupture 
 is often that of an "X" or a "Y." Ruptures generally occur 
 during muscular strain, but may do so during sleep. As a historic 
 example it may be recalled that George the Second died of a 
 ruptured right ventricle. 
 
 Spontaneous rupture of the aorta without preceding aneurismal 
 dilatation is occasionally met with. It generally occurs in the 
 aged, and is associated with atheromatous or sclerotic vascular 
 disease, but at least two cases have been reported in children 
 under fourteen years of age in whom the aorta showed only yery 
 slight evidences of disease, on account of which a congenital weak- 
 ness of this structure was assumed. - 
 
 TUMORS OF THE HEART 
 
 Primary neoplasms of the heart are extremely rare. There 
 were no such cases among the 9,940 autopsies studied by the 
 author, nor among 3,000 reviewed by Thorel.^ Of 110 cases of 
 heart tumors found in the Index Catalogue of the Surgeon-General's 
 Library the majority were secondary. The mesoblastic origin of 
 the heart accounts for preponderance of sarcomata (Hektoen*). 
 A recent compilation of cases by Link" shows the following 
 data: total number of primary heart tumors, 91. Among 61 of 
 these the character of the growths was as follows: Sarcoma, 13; 
 myxoma, 18; carcinoma, 7; lipoma, 8; myoma, 5; rhabdomyoma, 
 1; teratoma, 1; papilloma, 1. The growths were distributed: 
 
 ' Odriozola: Etude sur le cocur senile, Paris, 18S8. 
 
 = The literature on this subject can be found: Berge: Gaz. d. Hopit., 1906, No. 38. Thorel: 
 Lubarsch and Ostertag's Ergebnisse d. allg. Path., 1907, ii, 577. 
 
 ' Thorel: Lubarsch and Ostertag's Ergebnisse d. allg. Path., 1903, pt. 1; 1907, pt. 2. 
 'Hektoen: Med. News, 1893, p. 571. 
 5 Link: Zeit. f. klin. Med., 1909, p. 272. 
 
CARDIAC ANEURISM 199 
 
 Left auricle, 24; valves, 16; right ventricle, 14; right auricle, 10; 
 left ventricle, 8; interauricular septum, 2; both auricles, 3; 
 both ventricles, 2; right auricle and ventricle, 2; left auricle 
 and ventricle, 2; at the junction of the auricular and ventricular 
 septa, 2. In the foregoing study gummas, cysticerci, and secondary 
 tumors were excluded. The age of the patients in Schoeppler's 
 series ranged from three days to eighty-three years. ^ It has quite 
 frequently happened that the heart has manifested very few symp- 
 toms of insufficiency even with extensive mj^ocardial involvement.^ 
 
 ' Schoeppler: Miinch. med. Woch., 1906, liii, No. 45. 
 
 - Another case of sarcoma has recently been reported by Ehrenberg, Upsala, Lakarefoerings 
 ForhandUngar, 1910, xv. 
 
XII. CARDIAC SYPHILIS 
 
 Occurrence. — SjqDhilis of the heart was first described by 
 Ricord in 1845. Virchow distinguished two distinct types: 
 (a) gumma formation; (6) diffuse interstitial change. In 1904 
 Stockman collected 80 cases of the former type. Mracek has 
 published the pathologic findings of 102 cases, he having found 
 4 cases of cardiac syphilis among 150 autopsies. Loomis found 
 4 cases in 1,500 autopsies, and describes amyloid change resulting 
 from this infection. Among 61 of Mracek's cases gummas oc- 
 curred in about 50 per cent. Any part of the myocardium, 
 endocardium, or pericardium may be involved. A considerable 
 number of cases of the Adams-Stokes syndrome showing gumma- 
 tous lesion in the auriculo-ventricular bundle are now on record. 
 The Pennsylvania Hospital statistics showed 2 cases in 1,300 
 autopsies; the Philadelphia Hospital records, 1 in 8,640. 
 
 Pathologic Anatomy. — Gtimmatous cardiac disease consists of 
 circumscribed tumor-like masses which on section appear dry and 
 yellowish or grayish in color. The lesions are chiefly encountered 
 in the ventricles, though the auricles, and especially the inter- 
 ventricular septum, are often diseased. The involvement is 
 generally multiple, the size ranging from 0.5 cm. upward. If 
 breaking down occurs, cardiac sclerosis or aneurism may result. 
 The gummatous cases are usually accompanied by more or less 
 diffuse fibrous change. The gummas show the characteristic 
 histologic structure. They are generally sharply defined and 
 encapsulated. In the fibrous type involvement of the endo- 
 cardium and the pericardium is more frequent than in the gum- 
 matous variety. As might be expected, vascular changes in the 
 coronary vessels are common findings. Syphilitic endocarditis 
 and pericarditis are generally secondary to myocardial disease. 
 The fibrous type of cardiac sj'philis is essentially a microscopic 
 
 200 
 
Fiu. 71. — .Syphilitic Aortitis. 
 
 Syphilitic me.saortitis occurs characteristically about one and one half inches above the 
 aortic valves, often spreading downward and involving the mouths of the coronary arteries 
 and the leaflets secondarily. The surface of the aorta appears depressed — not elevated as in 
 the ordinary arteriosclerotic lesions. It is a prolific source of aortic aneurism, and aortic 
 rupture. (See "Cardiac Syphilis," p. 200, and "Diseases of the Aortic Orifice," p. 50. 
 Compare Figs. 41, 66, 72.; 
 
202 STUDIES IN CARDIAC PATHOLOGY 
 
 lesion. It is of considerable rarity.^ Warthin has described 
 diffuse myocardial fibrosis due to congenital syphilis,- and produc- 
 tive mesaortitis as a hereditary lesion has been reported by Bruhns,^ 
 Wiesner,* and Klotz." 
 
 That mesaortitis is frequently the result of syphilis has been 
 shown by the demonstration of the Spirochoeta pallida in these 
 lesions.'' The lesion is generally confined to the arch of the aorta, 
 or, as in the case depicted in Fig. 71, extends only about 5 cm. 
 above the aortic valves. It is definitely localized and often ab- 
 ruptly circumscribed. Longcope found 21 cases of chronic aortic 
 endocarditis without involvement of the other valves among 930 
 autopsies at the Pennsylvania Hospital. "In the least extensive 
 areas there were patches of thickening 2 or 3 cm. in diameter. 
 The central portion was elevated, gray, and somewhat succulent 
 in appearance, while the margins were yellowish and crinkled. 
 The sclerosis, when more extensive, was characterized by an 
 irregular corrugated or crinkled thickening of the wall, showing 
 small pits and sometimes minute aneurismal sacculations. Often 
 the bases of these small aneurisms were so thin that they trans- 
 mitted light. There was no calcification except in one instance, 
 but rather a rubbery pliable thickening. In 4 cases the arch of 
 the aorta was the seat of large aneurismal formations. The valves 
 showed the same rubbery thickening when extensively involved, 
 and occasionally there were crescentic lines of whitish-yellow 
 thickening on the endocardium of the ventricle beneath the 
 valves." The diagnoses in these cases were corroborated by mi- 
 croscopic examinations, and extension downward into the aortic 
 
 ' For further information see Mracek, Arch. f. Dermat. u. Syphilis, xxv, 1893, Ergan- 
 zungsheft, p. 279; Landois, ibid., 1908, p. 221; and Stockmann, "Ueber Gummiknoten in 
 Herzfleische bei Erwachsenen," Wiesbaden, 1904. 
 
 -Warthin: Trans. Assoc. Am. Phys., 1910. 
 
 ' Bruhns: BerUn. klin. Woch., xUi, No, 8. 
 
 ■I Wiesner: Centralbl. f. Path. u. path. Anat., 1905, p. 822. 
 
 ^ Klotz: Jour. Path, and Bact., 1907, p. 11. 
 
 " Renter; Mijnch. med. Woch., 1906, p. 778; Ztsch. f. Hyg. u. Infektionskh. 1906, p. 49. 
 Benda: BerUn. khn. Woch., 1906, p. 989. Schmorl: Munch, med. Woch., 1907, p. 188. 
 Wright: Boston Med. and Surg. Jour., 1909, p. 539. 
 
Fig. 72. — Syphilitic Aortitis. 
 In thi.s specimen the syphilitic prooes.s has extended downward along the aortic wall and 
 involved the coronary orifices and the aortic leaflets. The smooth, more or less sharply cir- 
 cumscribed rubbery appearance of the lesions is shown. Also the absence of calcification. 
 (Compare with Fiss. 41, 66, and 71. See also under "Cardiac Syphilis," p. 200, and "Dis- 
 easf» of the .Vonif Orififo," p. 50.) 
 
204 STUDIES IN CARDIAC PATHOLOGY 
 
 leaflets suggested that "the agent which produced the chronic 
 inflammatory and proliferative changes in the wall of the aorta 
 had some part in the disease of the aortic valves." 
 
 Of these 21 cases all but 3 had shown the clinical evidences of aortic leakage. 
 There were 55 other cases of aortic endocarditis among the 930 autopsies 
 in which the etiologic factor was an antecedent acute endocarditis (history 
 of infections and involvement of other valves, 21 cases), and others in which the 
 sclerosis was general, involved the whole aorta, and was associated with marked 
 calcification (endarteritis deformans — pure aortic endocarditis, 34 cases).' 
 
 ' Longcope: "The Association of Aortic Insufficiency with Syphihs," .lour. Am. Med. 
 Assoc, .Ian. S, 1910. 
 
Fig. 73. — This Specimen Show.s a Dissection of the Aukiculo-ventricular Bundle 
 (Bundle of His) in the Heart of a Bullock. 
 The bundle is about 5 mm. in diameter and can be seen grayer than the rest of the mus- 
 culature, running directly up the middle of the specimen in the left ventricle until it disappears 
 beneath the heart muscle. In the right ventricle it runs obliquely upward toward the left, 
 disappearing beneath the auriculo-ventricular valve. (Dissection by Dr. Krumbhaar.) The 
 nujierficial ponlion of the bundle and its 'proximity to the aortic and mitral valves indicate how 
 rea/lily this structure might suffer damage in case of an inflammatory or degenerative process in- 
 volving either of these valves or the intervening endocardium. 
 
XIII. CONGENITAL LESIONS 
 
 IMPERFORATE VENTRICULAR SEPTUM 
 
 An imperforate interventricular septum, like other congenital 
 abnormalities, is a condition which may be associated with other 
 developmental malformations — harelip, cleft palate, polydactylism, 
 supernumerary auricles, nipples, etc. It is the commonest of all 
 congenital heart lesions. It is generally associated with other 
 defects, such as obstruction of the pulmonary or tricuspid orifices. 
 The perforation usually occurs in the undefended space, just 
 beneath the aortic valves. As a result of it hypertrophy, and 
 especially dilatation of the right heart, occur if the child lives long 
 enough. Among the Philadelphia Hospital autopsies the following 
 
 Fig. 74. — Patulous Interventricular Septum. 
 
 C. R., male, white. Italian boy. (Pennsylvania Hospital Autopsy 1111. Spec. No. 
 453. Physician: Dr. M. J. Lewis. Pathologist: Dr. Krumbhaar.) 
 
 Clinical Notes: Patient admitted unconscious, with left-sided paralysis. Has never had 
 any acute illness previously. Was a "blue baby," and had always remained cyanotic. He 
 did not play actively. Fingers and toes are clubbed. For three days he had had fever, head- 
 ache, convulsions, abdominal pain. A loud systolic murmur was heard over the heart. 
 
 Pathologic Diagnosis: Congenital malformation of the heart. Stenosis of the conus 
 arteriosus. Hypoplasia of the pulmonary artery. Patulous interventricular septum. Acute 
 endocarditis. Softening of the right cerebral hemisphere. 
 
 Heart: Weighs 250 gm. Pericardium: negative. The heart is enlarged, especially to 
 the right side. The ductus arteriosus is easily found and measures 9 cm. in length, 2 cm. in 
 diameter. It does not admit a probe. On opening the heart : at the junction of the interauricular 
 and interventricular septa there is a large opening between the right and left sides (undefended 
 space); it is about 9 cm. in diameter, easily admitting an ordinary lead-pencil. Its walls are 
 smooth and lined with endocardium. It is evidently congenital. Foramen ovale closed. Right 
 ventricle 8 mm. Pulmonary artery and the conus arteriosus poorly developed and stenotic. 
 A few millimeters below the base of the valve there are some fine granular vegetations. The 
 left ventricle 12 mm. The heart muscle is deep red, normal in color. The tricuspid valve 
 measures 7 cm. in circumference, the mitral 6 cm., the aorta 3.1 cm. The pulmonary and 
 aortic rings were not measured, in order to preserve the specimen. The coronaries are 
 normal. 
 
 Microscopic Examination: The muscle-fibers are swollen and everywhere the striations 
 are poorly marked or absent, the fibers having a homogeneous appearance. The nuclei are for 
 the most part normal, though occasionally very large ones are found. The papillary muscles 
 on cross-section show vacuolization of many fibers. Interstitial tissue is increased in a few 
 places. The endocardium is normal except for a slight thickening on the internal surface of the 
 papillary muscle. 
 
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208 STUDIES IN CARDIAC PATHOLOGY 
 
 lesions of the interventricular septum were found: aneurism, 1; 
 ulceration, 1; rupture, 1; perforation, 2. (See Figs. 74, 76, 77.) 
 The "observations by His and others have not confirmed 
 Rokitansky's view of this extension upward of the interventricular 
 septum to form the aortic wall, but show that the aortic septum 
 is prolonged downward to assist in closing the interventricular 
 septum at the undefended space. Moreover, independent defects 
 of the interventricular septum, sometimes of large size and evi- 
 dently not of inflammatory origin, and unassociated with any 
 deviation to the right of the aorta, ma,y and do occur. Such 
 conditions cannot be explained on Rokitanskj^'s theory as a 
 deviation of the septa, and must be acknowledged to be a primary 
 arrest of growth of unknown origin." (Abbott.) The effect of an 
 imiDcrforate ventricular septum upon the circulation and upon 
 the rest of the heart dej^ends upon whether it occurs as an isolated 
 lesion or not. In 78 per cent, of Abbott's cases it appeared in 
 combination with other defects; most commonly with pulmonary 
 stenosis. When it occurs alone, it produces hypertrophy of both 
 ventricles, the degree of which is dependent upon the size of the 
 perforation. "As the right ventricle hypertrophies and pressure 
 in the right ventricle increases, the leakage diminishes, so that the 
 effect of the lesion tends to correct itself; on the other hand, the 
 pressure in the pulmonary artery increases. But since the ordinary 
 resistance in the pulmonary circulation is much less than in the 
 systemic, when the forces of both ventricles approximate one 
 another the effect on the pulmonarj^ circulation is the same as 
 though the left ventricle became weaker and the right remained 
 unchanged. Pulmonaiy engorgements may, therefore, result, 
 with consequent dyspnea. In most cases, however, the hyper- 
 trophy does not reach this point, and it is only when the heart is 
 stimulated by effort or exercise that pulmonary engorgement sets 
 in." (Hirschfelder.) 
 
Fig. 75. — Patent Ductus Arteriosus. 
 
 Male infant, thirty-four days old. (Physician: Dr. G.M.Boyd. Pathologist: Dr. A. G. 
 Ellis.') 
 
 Clinical Notes: At birth the baby was cyanotic and weighed 7 pounds. Respiratory 
 difficulty was present at all times, and the cyanosis was marked during the first few days. 
 Later the blueness became less prominent, especially during short periods in which it almost 
 disappeared. Death occurred during an attack of dyspnea associated with cyanosis. 
 
 Pathologic Diagnosis: Transposilion of the aorta and the pulmonary artery; patent 
 diictics arteriosus; hypertrophy of the right ventricle. Patent foramen ovale; partial atelectasis 
 of the right lung; general visceral congestion. 
 
 Pathologic Notes: The heart is essentially normal in size. The wall of the right and 
 left ventricles are respectively 5 and 7 mm. in thickness. Neither the pulmonary artery nor 
 the aorta shows any evidence of stenosis. The foramen ovale is patulous in the form of a 
 slit-like opening 0.5 cm. in length, and the ductus arteriosus allows with ease the passage of a 
 probe 2 mm. in diameter. Neither the ventricles nor the auricles are transposed, and the veins 
 of the latter arc normally placed. (Specimen from the Philadelphia Hospital.) 
 
 ' Case reported by Dr. A. O. Ellis: Am. Jour. Obstet., 1905, lii, No. 6. 
 
210 STUDIES IN CARDIAC PATHOLOGY 
 
 Fig. 76. — Patulous Interventricular Septum with Acute Endocarditis. 
 
 (Pennsylvania Hospital. Physician: Dr. H. M. Fisher. Pathologist: Dr. G. C. Robin- 
 son.) 
 
 Clinical Notes: Patient had dyspnea and cough after exertion, but was otherwise fairly 
 healthy. Heart: hypertrophied, loud systolic murmur at the apex, transmitted to the back. 
 Also a diastolic murmur, loudest over the aortic area. Two years later the patient died after 
 ha,ving suffered from gangrene of the nose, the ear, etc., apparently the result of thrombosis. 
 
 Pathologic Notes: Partial autopsy disclosed hydrothorax, parenchymatous nephritis, 
 capillary hemorrhages, etc., and the following cardiac condition: 
 
 Heart : Is somewhat enlarged ; the epicardium is normal, but shows a very small amount 
 of fat. Tricuspid valve (after hardening) measures 10.5 cm. The wall of the right 
 ventricle measures 8 to 10 mm.; its cavity about normal. Tricuspid valve and the chordae 
 tendineae of its posterior leaflet show a few fresh vegetations. In the seplum ventriculorum, 
 just to the left of the begiyming of the conus arteriosus, there is an oval opening, 3.5 x 2.5 cm. 
 in diameter, which appears as a funnel-shaped excavation in the ventricular septum. The open- 
 ing into the left ventricle is nearly closed by large wart-like vegetations. These vegetations extend 
 from the opening upward into the conus arteriosus and are continuous with those on the right an- 
 terior leaflet of the pulmonary valve. The conus arteriosus is quite narrowed. Its origin, which 
 is but 4.5 cm. in circumference, is surrounded by a row of delicate vegetations. The pulmonary 
 artery at the base of the valves measures 7 cm. in circumference. All of its leaflets show a con- 
 siderable thickening and puckering and are the seats of extensive fresh vegetations. The right 
 anterior and posterior leaflets show round knob-like masses measuring 2 to 5 mm. in diameter, 
 hanging to their free margins, while the left anterior pulmonary leaflet is about half covered by 
 large, rather regular vegetations extending all the way across its free margin. There is a small 
 group of warty vegetations extending 1.5 cm. below this leaflet in the conus arteriosus, and 
 within the sinus of Valsalva above it there is a small nodular vegetation, 6 mm. in diameter, 
 attached to the wall of the pulmonary artery. Upon examining the left side of the heart the 
 auricle is found to be normal in proportions. The mitral valve is somewhat thickened toward its 
 base, but is free from vegetations. The wall of the left ventricle is but slightly thickened {14 mm.). 
 Directly beneath the posterior leaflet of the aortic valve there is an opening in the septum ventriculorum 
 continuous with that seen in the right ventricle. On the left side the opening measures 2.5 x 1.5 cm. 
 It is almost closed, however, by the extensive vegetations springing from its margins. The endo- 
 canliimi of the left ventricle extends into the opening and is apparently continuous luith that of the 
 riijlil rriilnrlr. The direction of the passage between the ventricles is downward and backward 
 from the left to the right side. The aortic ring measures 6 cm. in circumference. All of the 
 aortic valves are much thickened and somewhat contracted. On the anterior and right pos- 
 terior leaflets there are small verrucose vegetations; on the left posterior leaflet there is an enor- 
 mous, irregularly round, nodular vegetation measuring 2.5 x 2.3 x l.S cm. in diameter. The 
 vegetation is attached to the entire ventricular aspect of the leaflet, and extends downward into the 
 opening in the septum ventriculorum, nearly closing the same. No bacteriologic examination 
 was made. 
 
Kjc;. 70. 
 
212 STUDIES IN CARDIAC PATHOLOGY 
 
 TRANSPOSITION OF THE GREAT VESSELS 
 
 Transposition of the great vessels is generally associated with 
 a transposition of the other viscera. It is ascribed to non-rotation 
 of the aortic septum from which these vessels are formed, and it 
 is often accompanied b}' patency of the foramen ovale, interven- 
 tricular septum, or ductus arteriosus. 
 
 "In typical cases the aorta is in front and to the right, the pulmonary artery 
 behind and to the left. At one stage in the normal process both vessels are 
 connected with the right ventricle, the change of the aorta to the left being 
 largely accomplished by the completion of the interventricular septum. Irregu- 
 larities in the formation of this septum, especially its deviation to the right or 
 left, may result in both vessels arising from one or other of the ventricles, more 
 often the right, an anomaly not exceedingly rare. Transposition of the vessels 
 may be accompanied by transposition of the auricles and veins, or of the ven- 
 tricles, or both. The transposed vessels may be normal, but usually are not."^ 
 
 As to the frequency of the condition, Theremin found 21 cases among 106 
 cardiac anomahes at the Foundling Hospital in St. Petersburg, and Vierordt, 
 76 among 383. 
 
 PATULOUS DUCTUS ARTERIOSUS 
 
 In an excellent and comprehensive article Goodman- has re- 
 cently summarized what is at present known regarding patency of 
 the ductus arteriosus. Altogether he was able to collect 71 cases, 
 34 of which were autopsied. A great many different explanations 
 have been offered as to the modus operandi by which the ductus 
 Botalli is normally obliterated during the first four weeks of life, 
 and an equal number of hypotheses offered as to the cause of its con- 
 tinued or renewed patency. Among the former the following may 
 be mentioned: Pressure equilibrium between the aorta and pulmon- 
 ary artery, also contraction of the walls of the duct after the first 
 inspiration; changes in the position of the heart after the last-named 
 act; redundant valve-like intimal folds at the aortic orifice, etc. 
 
 Persistent patulosity may occur: 
 
 1. As an isolated lesion. 
 
 2. In association with other cardiac malformations. 
 
 ' Abbott: Osier's Modern Medicine, vol. iv, p. 370. 
 
 = E. H. Goodman: Univ. of Penna. Med. Bull., Dec., 1910, p. .509. (Complete biljliography.) 
 
I-IG. 
 
 -Patulol's Intehventkutlak Settum with Acute Knuocahditis. 
 
 The interventricular septum is patulous, but this opening is almost entirely closed by a 
 large mass of recent veRetations which are attached to its margins. (Photograph by Dr. A. R. 
 Alien.) 
 
214 STUDIES IN CARDIAC PATHOLOGY 
 
 3. In association with other non-cardiac developmental defects. 
 The form of the ductus arteriosus may be as follows (Gerhardt) : 
 
 1. Extreme shortening of the canal, the great vessels being 
 practically united by a simple opening between them. 
 
 2. A funnel-shaped opening, with the larger opening on the 
 aortic end. (Relatively common.) 
 
 3. A cj'Iindrical shape. (Commonest variety.) 
 
 4. Aneurismal dilatation. 
 
 Patency of the ductus Botalli, both as an isolated lesion and in 
 combination with other defects, is one of the commoner congenital 
 abnormalities. (See Figs. 75, 83, 84.) 
 
 PATULOUS FORAMEN OVALE 
 
 Occurrence. — A patulous foramen ovale is a relatively common 
 autopsy finding (Vierordt, 28 per cent.; Zahn, 22.3 per cent.), 
 but mere patency is not necessarily of pathologic importance. 
 The fact that the channel runs obhquely through the auricular 
 septum, and that, therefore, the openings on the two sides are not 
 directh' opposite to each other, favors competency, for as soon as 
 intra-auricular pressure on the two sides of the membranes rises, 
 the lateral walls of the channel are pressed together, and tend to 
 close. Under normal circumstances obliteration of the opening 
 is said to result from mechanical irritation, as the result of which 
 the endothelial covering of the two surfaces becomes abraded 
 and adhesion follows. The above-mentioned figures apparently 
 include all grades of patency. An opening large enough to admit 
 the small finger occurred only 9 times in 462 autopsies (1.9 per 
 cent.).^ At the Philadelphia Hospital there were only recorded 
 86 cases among 8,640 autopsies (0.9 per cent.). 
 
 "The foramen ovale lies in almost a horizontal plane, and not 
 vertically and facing the left." Neither the right- nor the left- 
 sided posture after birth is, therefore, of any consequence in favor- 
 ing its closure in the newly born infant (Fetterolf and Gittings).- 
 
 1 Hintze and Ogle: quoted Hirschfelder, "Diseases of the Heart and Aorta," 1910, p. 466. 
 'Fetterolf and Gittings: Am. Jour. Children's Dis., Jan., 1910, No. 1. 
 
Fig. 78. — Patulous Foramen Ovale. 
 Hfart of a woman aged seventy years, who died of croupous pneumonia, liaving advanced 
 general arteriosclerosis. The illustration shows a chronic, more or less diffuse, mitral thicken- 
 ing, with contraction of the ehorchc tendineie, and marked hypertrophy of the left ventricle. 
 The foramen ovale is quite large and patulous, but owing to its oblique course it was probably 
 functionally competent. 
 
216 STUDIES IN CARDIAC PATHOLOGY 
 
 Pathologic Physiology. — As has already been intimated, mere 
 patulousness of the foramen ovale need be of but little consequence 
 unless the opening be a very large and direct one. (See Figs. 
 78, 79, 80.) With valvular disease of the heart, especially in 
 mitral lesions with failing compensation, the defect maj^ become 
 important. Thus, for instance, when the left auricle is over- 
 burdened and dilated, and its internal pressure increased, consider- 
 able quantities of blood may regurgitate into the right auricle. 
 Up to a certain point such reflux may be conservative, after the 
 manner of the safety-valve. When the failure of the right heart 
 is superadded, however, a patulous foramen ovale becomes doubly 
 disadvantageous by preventing proper aeration of the blood, and 
 by directly mixing the venous with the arterial currents. Griffiths 
 suggests that slight patency of the foramen may be of actual 
 benefit in case of obstruction in the pulmonary circulation, such 
 as emphysema, since it is less harmful to have some venous blood 
 admitted to the arteries, than to have the individual waterlogged 
 from back-pressure in the right heart. Emboli from the right 
 heart may reach the general circulation by passing through a 
 patulous foramen ovale or interventricular septum or ductus 
 arteriosus. 
 
 ABNORMAL FIBROUS BANDS 
 
 The so-called abnormal fibrous bands of the heart are chiefly 
 found in the ventricles. According to Tawara, they represent 
 a congenital anomaly of the auriculo-ventricular bundle; an 
 opinion based solely on their course and distribution. Roessle^ 
 showed that these fibrous bands contained muscular tissue, but 
 regarded their structure as the result of pressure atrophy. Magnus- 
 Alsleben- examined ten cases and found muscle-cells often similar 
 in microscopic appearance to the auriculo-ventricular bundle. He 
 suggests that, inasmuch as these bands are of no such great rarity, 
 both the hitherto employed terms " abnormale " and " sehnenfaden " 
 are inappropriate. (See Fig. 82.) 
 
 ' Roessle: Arch. f. klin. Med., 1902, p. 224. 
 
 2 Magnus-Alsleben: Centralb. f. Path. u. path. Anat., 1906, p. 897. 
 
Fig. 79. — Patulous but Competent Foramen Ovale. (University of Pennsylvania 
 Museum.) 
 
Fig. so. — P.\tulous but Inxompetent For.v.mex 0\ ale. (Pennsylvania Hospital, Xo. 175. 
 
CONGENITAL LESIONS 219 
 
 ANOMALIES OF THE SEMILUNAR VALVES 
 
 These anomalies may occur in otherwise normal hearts and 
 have little clinical significance, or they may be associated with 
 coarction of the aorta. Theremin has reported an instance in 
 which both the aortic and pulmonic valves were bicuspid. There 
 has been considerable discussion as to whether the condition was 
 most frequently the result of faulty development or of antenatal 
 endocarditis. Fusion of the leaflets resulting from post-natal 
 infections "is distinguished by the presence behind the fused 
 cusps of a high raphe formed by their united adjacent portions, 
 by the absence of compensatory changes in this and in the fused 
 cusp, and by marked thickening, calcification, and other evidence 
 of inflammator}'' action" (Abbott). 
 
 This anomaly may be attended by no pathologic results, but 
 not infrequently acute endocarditis, arteriosclerotic change, or 
 functional insufficiency as the result of valvular stretching is a 
 sequel of this condition. ^ (See Figs. 81, 82, 83.) 
 
 DOUBLE MITRAL- OR TRICUSPID' ORIFICES 
 
 Double orifices have been reported. The abnormal orifice 
 may possess its own papillarj^ muscles and chordse tendinese. 
 "Pisenti explained the condition as the result of a congenital 
 fenestration which had transmitted the blood-stream in early 
 embryonic life, and thought that its transformation into a second 
 valvular orifice was an adaptation of growth or compensatory 
 process, the papillary muscles (which develop at the same time as 
 the cusps) growing up with their chordae tendinese to its borders." 
 f Abbott.) This hypothesis is tentatively indorsed by the last- 
 named authoress, although rejected by Cohn on the ground that 
 the anomaly docs not correspond with what we know regarding 
 any stage of the embryologic process. (See Fig. 85.) 
 
 ' For literature .sec: Dilg, Virchow's Archiv., 1883, vol. xci; Lannois and Villaret, Bull, 
 et Mom. Soc. Anat., Pari.s, July, 190.5. 
 
 ^ (jrtMnfuM: Tran.s. Path. Hot;. U)n(lon, 1876, xxvii, p. 128. Colin: Inauuuial Di.s.sei-l. 
 Konig.'ibcrg, 1800. Abbott: 0«ler's ".VIotU'rn .Medicine," vol. iv, p. 393. 
 
 ' PiHenti: " Di una variwHirna .\nonialia della triouspido," Peiinia, 1888. 
 
-Bicuspid Pulmonary Valve. (Specimen from the Mutter Museum of the College 
 of Physicians of Philadelphia.) 
 
Fig. 82. — Four Pulmonary Valves. (Specimen from the Philadelphia Hospital.) 
 
 This anomaly is somewhat more frequent in the pulmonary artery than in the aorta. It 
 usually has no pathologic significance, but congenitally abnormal valves seem to be more 
 frequently subject to subsequent infection. 
 
222 STUDIES IN CARDIAC PATHOLOGY 
 
 Fig. 83. — Congenital Atresia of the Aorta, with Patent Ductus Arteriosus. 
 
 Male, negro, aged twenty-two years. (W. B.) (Pennsylvania Hospital, 1903. No. 
 1711. Autopsy 472.) 
 
 Clinical History: Pneumonia as a boy; and again 1898. Gonorrhea some years ago. 
 
 Symptoms: dyspnea, tachycardia, arrhythmia. 
 
 Apex-beat in fifth interspace, mid-clavicular line, heart enlarged to the right. First 
 sound booming. No murmurs on admission, but later a soft systolic murmur was heard at the 
 apex from time to time, but not constantly. 
 
 Pathologic Diagnosis: Congenital atresia of the aorta, mth patent ductus arteriosus. 
 Bicuspid aortic valve. Chronic mitral endocarditis. Cardiac hypertrophy, especially of the 
 right side. Thrombosis of the right innominate, internal jugular, axillary, and basilic veins; 
 also of the auricular appendage. Congestion of the viscera, with cardiac hepatic cirrhosis, etc. 
 
 Pericardium and Heart, very large, filling the whole anterior mediastinum. Heart 
 extends 8 cm. to right of mid-sternum, at level of fourth costal cartilage. From above down- 
 ward it measures 13 cm.; from the apex diagonally to the base, 20 cm. Pericardium contains 
 400 c.c. shghtly turbid, straw-colored fluid, containing a few flakes of fibrin. The serous sur- 
 faces are smooth and glistening. Heart weighs 780 gm. It is large and has a peculiar square 
 shape, the apex being very blunt. The right heart is especially large. The epicardium in some 
 places appears thickened, and is rather opaque and grayish. Subepicardial fat decreased. 
 The vessels are much injected and small punctate hemorrhages are seen, especially at the base. 
 The cavities are all filled with postmortem clots. Both the right auricle and ventricle are 
 large and their walls excessively thickened. The tricuspid orifice measures 12 cm. in circum- 
 ference; its valves are thin and delicate. Pulmonary orifice 9 cm. in circumference. Papillary 
 muscles and columnee carnese are exceedingly large and firm. The actual wall of the right 
 ventricle measures 10 to IT mm. in thickness, it being as thick as a moderately hypertrophied left 
 ventricle. Wall of the right auricle 3 to 8 mm. The tip of the auricle is completely filled with 
 a soft, gray, smooth thrombus, the center of which contains a thick, gray, pus-like material. 
 Mitral valves thin and delicate. The aortic valve shows only two large cusps, hut they are 
 thin and delicate. The aortic orifice is 5.5 cm. in circumference (half the size of the pulmonary) ; 
 the aorta above it is about the same size. The cavity of the left ventricle is not very large, but the 
 walls are much hypertrophied, averaging 18 to 20 mm,, in thickness. The endocardium is opaque, 
 thick, and white. Muscular bands extend from one side of the wall to the other, forming a coarse 
 network in the cavity. Coronary arteries are large and patent. A few pinhead-sized, raised 
 points are scattered over the aorta. 
 
 Microscopic Diagnosis: Chronic interstitial myocarditis. Pericardium shows no especial 
 change. Heart muscle shows degenerative changes in places, while a fibrillated connective 
 tissue containing very few cells fills the areas of degeneration and extends between the muscle- 
 fibers, the latter being large and granular. Endocardium is thickened; connective tissue ex- 
 tends from it to the muscle. (Aorta shown in Fig. 84.) 
 
l''ifi. S?>. — Hicrsrin Aortic Valve. 
 
 This hpocinioM also .shows marked left ventricular hypertrophy and "abnoniKd fibrous 
 bands" traversing this chamber. (See p. 222.) 
 
Fic. 84. — Congenital Aortic Stenosis with Patency of the Ductus Arteriosus. 
 
 Pathologic Notes: The aorta is very small, measuring at the arch only 4.5 cm. in di- 
 ameter, while the pulmonary artery is twice this size. The innominate, left vertebral, and sub- 
 (•l:i\ian urlcrifs are normal in position and size. Immeiialdy at the junction of the lower edge of 
 Ihi: li-fl .inhrliii'ian artery and the aorta, the latter vessel shows a sudden and marked constriction, 
 ll.e external diameter of which measures 12 mm., while S cm,, above and below the constriction the 
 aorta mcanureH 2 and 2.5 cm. in diameter. On opening the aorta and looking down toward the 
 fonstriction the ves-iel appears to end in a smooth, rounded, blind pouch, but on closer in- 
 spection a fjinhoad-sissed opening can bo seen, through which a small probe can be passed. 
 Connecting the pulmonary artery just where it branches, and the aorta just at the proximal 
 side of the constriction, is a narrow ve.s.sel, about S mm. in length and .5 mm. in diameter, 
 through which a [jrobc can be passer!.. The aorta throughout its length is narrow, but its 
 branches are about normal in size. (■Pennsylvania Hospital, Xo. .S17. Thae are the vessels 
 belonging to the heart nhown in Fi;i. HS.) 
 13 
 
226 STUDIES IN CARDIAC PATHOLOGY 
 
 Fig. 85. — Double Mitral Orifice. 
 
 C. D., male, aged twenty-two years. (Pennsylvania Hospital 23.5. 349.) 
 
 Clinical Notes: Patient died of typhoid fever, complicated by bronchopneumonia and 
 erysipelas. He had had no circulatory symptoms at any time before, nor physical signs in- 
 dicative of cardiac disease. 
 
 Pathologic Notes: Heart weighs 290 gm. The cavities are normal in proportion, 
 except the left auricle, which is dilated. All of the valves are normal except the mitral, which 
 shows thickening. The chorda; tendineoe are thickened, white, and fibrous. The papillary muscles 
 are large and thick; and beneath their posterior segment the three portions are distinct as three 
 separate muscles. The chiinhi IcmlitKiv micli from two of them to the anterior leaflet, which is 
 large, measuring 3 cm. from I In' iiiiinihi.-i liliriKitiK In I he free edge in a straight line. The papillary 
 muscle, which is normally alUivhnl In Ihc rilgr nf lln- vnlve, attaches here almost at the central portion 
 of the leaflet. The valve is perforated by an opening 1 cm. in diameter, the chordce tendineoe at- 
 taching about the margin of this opening. There are thus two auriculo-ventricular openings, sur- 
 rounded by chordae tendineoe, with normal margins. The entire ventriculo-ventricular ring measures 
 9.5 cm. in circumference. The heart muscle is dark reddish-brown and firm. Left ventricle: 
 18 to 20 mm. Coronaries patent. Foramen ovale closed. Auricular appendages free from 
 thrombi. Aorta smooth. 
 
 Microscopically: Slight edema of the heart muscle with pigmentation of the muscle-fibers, 
 but no other changes. 
 
 (The match-stick passes through the accessory auriculo-ventricular orifice.) 
 
INDEX OF ILLUSTRATIONS 
 
 Aneurism of mitral valve, 45 
 of the heart, 171, 173 
 
 of the left ventricle, with calcification, 183 
 Aortic and mitral endocarditis, acute, 19, 
 25, 33, 41 
 chronic, 69 
 endocarditis, acute, 9, 15, 37 
 
 subacute, 11 
 mitral and tricuspid endocarditis, acute 
 and chronic, 93 
 obstruction, 79 
 obstruction, 61, 65 
 Atresia of the aorta, 224 
 Auriculo-ventricular bundle, 205 
 
 Ball thrombus of the left auricle, 185 
 Bicuspid aortic valve, 223 
 pulmonary valve, 220 
 
 Calcification and dilation of the aorta, 163 
 
 of the aorta, 161, 165, 167 
 
 of the coronary arteries, 169 
 Cardiac aneurism and thrombosis, 177, 181 
 
 hypertrophy, 145 
 
 Dilatation of the heart, 159 
 
 Endocarditis, acute and chronic, 35 
 chronic, 57 
 
 Gumma of the heart, 191, 193, 195 
 of the left ventricle, 197 
 
 Hemopericardium, 131 
 
 Hypertrophy and dilatation of the heart, 139 
 of the left ventricle, 153, 155, 157 
 
 Mitral and aortic endocarditis, acute, 5 
 and mural endocarditis, acute, 7 
 
 Mitral endocarditis, acute and chronic, 89 
 ulcerative, 3 
 chronic, 91 
 insufficiency, 83 
 obstruction from the auricular aspect, 73 
 
 from the ventricular aspect, 53 
 orifice, double, 226 
 Mural and aortic endocarditis, chronic, 59 
 endocarditis, acute, 29 
 thrombosis, 179 
 
 Patulous ductus arteriosus, 209 
 
 foramen ovale, 215, 217, 219 
 
 interventricular septum, 207 
 
 with acute endocarditis, 211, 213 
 Pericarditis, acute fibrinopurulent, 101 
 serofibrinous, 109, 125 
 
 chronic adhesive. 111, 115, 119, 121 
 
 fibrinous, 107 
 
 subacute fibrinous, 103 
 
 tuberculous, 127, 129 
 
 QuADRicuspiD pulmonary valve, 221 
 
 Rupture of the aorta, 133, 189 
 
 Syphilitic aortitis, 201, 203 
 
 Thorax, sagittal section (No. 1), 147 
 (No. 2), 149 
 (No. 3), 151 
 transverse section (No. 1), 141 
 (No. 2), 143 
 Thrombosis of the heart, 175 
 Tricuspid and mitral endocarditis, chronic, 47 
 obstruction, 75 
 
 Vertical .section of the thorax, anterior half, 
 141 
 posterior lialf, 143 
 
INDEX OF SUBJECTS 
 
 Actinomycosis of the pericardium, 118 
 Aneurism of the heart, ISS 
 Angina pectoris, 186 
 
 Anomalies of the auriculo-ventricular valves, 
 218 
 of the semilunar valves, 218 
 Aorta, arteriosclerosis of, 186 
 coarction of, 51 
 rupture of, 198 
 syphihs of, 168, 186, 202 
 Aortic disease due to rheumatic fever, 50 
 in locomotor ataxia, 62 
 in syphilis, 62 
 spirocheta paUida in, 62 
 Wassermann reaction in, 62 
 insufficiency, 55 
 
 clinical considerations, 63 
 functional, 62 
 
 occurrence and pathologic anatomy, 55 
 pathologic physiology, 60 
 obstruction, clinical considerations, 54 
 occurrence and pathogenesis, 50 
 pathologic anatomy of, 51 
 physiology, 52 
 orifice, diseases of, 50 
 valve, embryologic formation, 56 
 Aortitis, syphilitic. 168, 186, 202. See also 
 
 Diseases of the A ortic Orifice 
 Auricular thrombosis, 8, 185 
 Auriculo-ventricular bundle, 142 
 
 B.^cTERioLoov of acute endocarditis, 12, 13, 
 26 
 of pericarditis, 106, 116 
 
 Chemical changes of mj'ocardium in cardiac 
 
 hypertrophy, 158 
 Congenital heart Icsion.s, 206 
 Cor bovi.s in aortic disease, 60 
 Coronary arterie.s, 180 
 
 effects of obliteration, 180 
 
 experimental ligation of, 182 
 arteriosclero.si.H, 180 
 
 frequency of, 184 
 
 pathogcneMlH, 182 
 
 DiSE.\SES of the aortic orifice, experimental, 
 58 
 unusual cases of, 58 
 
 Embolism in acute endocarditis, 10 
 
 in endocarditis, 27 
 Endocardial lesions, statistics, 46 
 Endocarditis, acute, 1 
 
 age of occurrence, 12 
 
 auricular thrombosis in, S, 185 
 
 bacteriology, 12, 13, 26 
 
 classification, 4 
 
 clinical considerations, 27 
 
 diagnosis, 30 
 
 embolism in, 10, 27 
 
 etiology, 1 
 
 gonococcus, 21 
 
 in chorea, 20 
 
 in congenital lesions, 211, 213 
 
 in malaria, 24 
 
 in pneumonia, 17 
 
 in tuberculosis, 22 
 
 in typhoid fever, 24 
 
 infarction in, 8 
 
 malignant, 8, 13 
 
 morbid anatomy, 6 
 
 pathogenesis, 12 
 
 pneumococcus, 20 
 
 predisposition, 10 
 
 rheumatic, 12, 14 
 
 simple, 8, 13 
 
 verrucose, 2 
 bacteriology of, 30 
 chronic, 39 
 
 clinical considerations, 44 
 
 duration of life in, 44 
 
 frequency of, 43 
 
 heredity of, 46 
 
 infective, 30 
 
 bacteriology of, .30 
 classification, 31 
 
 morphologic classification, 42 
 
 post-inort(!m frequency, 46 
 in domestic animals, 154 
 pni'umococcus, 13 
 
 !3I 
 
232 
 
 INDEX OF SUBJECTS 
 
 Endocarditis, subacute, 24 
 
 syphilitic, 32 
 
 trauma as a cause, 34 
 Experimental myocarditis, 168 
 
 production of pericarditis, 104 
 
 valvular lesions, 36, 58, 84, 77, 94 
 
 Fibrous hands in heart, 216 
 
 Heart, congenital lesions, anomalies of semi- 
 lunar valves, 218 
 fibrous bands, 216 
 
 imperforate ventricular septum, 206 
 of the auriculo-ventricular valves, 218 
 patulous ductus arteriosus, 212 
 
 foramen ovale, 214 
 transposition of the vessels, 212 
 dilatation of, 162 
 
 clinical considerations, 166 
 in rheumatic fever, 170 
 pathogenesis, 162 
 pathologic anatomy, 164 
 displacement of other organs, 146 
 foreign bodies in, 58, 60 
 hypertrophy, auriculo-ventricular bundle 
 in, 142 
 chemistry of, 158 
 ■ classification, 138 
 congenital, 156 
 from beer drinking, 154 
 idiopathic, 156 
 in nephritis, 148 
 in rheumatic fever, 170 
 in valvular disease, 152 
 Mtiller's method of estimating, 158 
 occurrence of, 137 
 pathogenesis, 140 
 normal dimensions of, 136 
 position of, in pericardial effusion, 123 
 rupture of, 194 
 
 frequency, 196 
 syphilis of, 200 
 thrombosis of, 192 
 tumors of, 19S 
 Hemopericardium, 110 
 Heredity and valvular disease, 46 
 Hydrothorax in valvular disease, 85 
 Hypertrophy of the heart. See Heart, 
 hypertrophy of 
 
 Left auricle, dilatation of, 70 
 
 size of, 68 
 Liver in tricuspid insufficiency, 94 
 
 Mitral insufficiency, 80 
 
 experimental, 84 
 frequency of, 80 
 
 pathogenesis, 80 
 
 pathologic anatomy of, 81 
 physiology, 82 
 leaflets, anterior, function of, 64 
 obstruction, 64 
 
 anatomy of, pathologic, 66 
 
 and congenital malformations, 78 
 
 and pulmonary tuberculosis, 68 
 
 classification, 64 
 
 clinical considerations, 77 
 
 congenital, 67 
 
 etiology of, 71 
 
 experimental, 77 
 
 functional, 64 
 
 in nephritis, 71 
 
 occurrence and frequency of, 71 
 
 operative possibilities, 77 
 
 pathologic physiology, 74 
 
 thrombosis in, 74, 194 
 
 varieties, 64 
 
 vocal paralysis in, 70 
 orifice, button-hole, 67 
 
 diseases of, 64 
 
 double, 218 
 
 embryology, 68 
 
 funnel-shaped, 66 
 
 size of, 64 
 sphincter, 86 
 
 valve, test of, efficiency of, 81 
 Myocardial lesions, statistics, 48 
 Myocarditis, acute, 166 
 chronic, 168 
 
 clinical considerations, 176 
 experimental, 168 
 in infections, 174 
 rheumatic, 170 
 suppurative, 174 
 toxic, 174 
 Myocardium, syphilis of, 200 
 
 Nephritis, in mitral obstruction, 71 
 
 Papillary muscles, rupture of, 196 
 Patulous ductus arteriosus, 212 
 
 interventricular septum, 206 
 Pericardial effusion, position of heart in, 123 
 
 "milk spots," 117 
 
 pseudo-cirrhosis of liver, 124 
 Pericarditis, acute, as a terminal infection, 116 
 bacteriology of, 106 
 
INDEX OF SUBJECTS 
 
 233 
 
 Pericarditis, acute, chemistry of, 104 
 
 classification and frequency, 105 
 
 in gonorrhea, 117 
 
 in nephritis, 116 
 
 in pneumonia, 112 
 
 in sypliihs, 117 
 
 occurrence and frequency, 100 
 
 pathogenesis, lOS 
 
 pathologic anatomy, 100 
 physiology, 120 
 
 statistics, 108 
 
 toxic, 116 
 
 trauma as cause of, 104 
 
 tuberculous, 113 
 chronic, 124 
 
 calcification in, 128 
 
 frequency of, 132 
 
 pathogenesis, 124 
 
 pathologic physiology, 130 
 
 varieties of, 126 
 chnical considerations, 134 
 in rheumatic fever, 110 
 maculae albidse, 117 
 mediastinitis in, 124 
 suppurative, 105 
 Pericardium, anthracosis of, 110 
 calcification of, 118 
 congenital defects of, 134 
 lymphatic circulation of, 106 
 normal capacity, 104 
 Pick's disease, 124 
 Pulmonary artery, disease of, 99 
 insufficiency, 98 
 
 pathogenesis, 98 
 
 pathologic anatomy, 99 
 
 relative, functional, 98 
 obstruction, and pulmonary tuberculosis, 97 
 
 pathogenesis, 96 
 
 pathologic anatomy, 97 
 physiology, 97 
 orifice, anatomic and physiologic pecu- 
 liarities, 96 
 
 diseases of, 96 
 
 Rheumatic fever, as cause of acute endocar- 
 ditis, 12, 14 
 of mitral obstruction, 71 
 pericarditis in, 110 
 
 Stromrinne, 66 
 
 Syphihs and angina pectoris, 186 
 aortitis in, 202 
 as cause of aortic disease, 62 
 of the aorta, 168, 184 
 of the heart, 200 
 frequency, 200 
 pathologic anatomy, 200 
 Syphilitic aortitis, 168, 186, 202 
 
 Thrombosis in mitral disease, 74 
 stenosis, 194 
 of the heart, 192 
 Transposition of the great vessels, 212 
 Trauma as a cause of endocarditis, 34 
 
 of pericarditis, 104, 108 
 Tricuspid insufficiency, clinical considera- 
 tions, 95 
 experimental, 94 
 fiver in, 94 
 pathologic anatomy, 92 
 
 physiology, 94 
 relative, 95 
 lesions, frequency of, 86 
 
 pathogenesis, 86 
 obstruction, congenital, 87, 90 
 frequency, 87 
 pathologic anatomy, 88 
 physiology, 92 
 orifice, diseases of, 86 
 Tuberculosis, pulmonary, effect of valvular 
 lesions upon, 68 
 
 Valvular aneurism, 43 
 
 lesions, experimental, 36, 58, 77, 84, 99 
 
 hydrothorax in, 85 
 
 of the right heart, 86 
 Vocal paralysis in mitral obstruction, 70 
 
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