Aortic Stenosis

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Aortic Stenosis “Senile” calcific aortic stenosis. Degeneration and calcification of bicuspid aortic valve. Chronic Rheumatic Heart Disease Endocardium Fibrosa Spongiosa Elastic fibers in black Aortic valve structure Ventricular side 1 Calcification 2 3 Aortic insufficiency due to aortic dissection • Hypertension • Connective tissue disorders Marfan’s: 1 in 5000. 70-85% familial (Autosomal dominant) Fibrillin-1 (15q21) ~ 500 distinct mutations 4 Medial degeneration without atherosclerosis Mitral Stenosis • Chronic Rheumatic Heart Disease • (Rare) Mitral annular calcification Myxoma 5 Acute Rheumatic Fever Immunologically mediated, following 1-6 weeks after pharyngitis with Group A Streptococcus in 3% of those infected. ?Antibodies ? Hypersensitivity reaction induced by streptococcal M proteins with cross-reaction with similar antigenic determinants in joints, heart, skin, CNS. Clinical Diagnosis: revised Jones criteria Acute Rheumatic Fever Pancarditis Pericarditis Myocarditis (Aschoff body) Endocarditis with sterile vegetations Death in acute rheumatic fever is very rare (<1%) and due to cardiac involvement 6 Aschoff body of acute rheumatic carditis: a cardiac granuloma Acute rheumatic fever: involvement of mitral chordae tendineae 7 Native chordae bound together by fibrous tissue in chronic rheumatic mitral valve disease Chronic Rheumatic Heart Disease Follows Acute Rheumatic Heart Disease by decades. MV involved in 65-70% MV & AV in 25% Mitral stenosis, aortic stenosis. Arrhythmias (A. fib. with left atrial enlargement). Heart failure. Predisposed to infective endocarditis. 8 9 Chronic Rheumatic Heart Disease: “Fishmouth” deformity of the mitral valve Mitral Valve Prolapse • 2 populations: women in 20s; men in 40-50s; the gross and microscopic appearances of the valves are the same. • Most are asymptomatic • Mid-systolic click • Rarely: chest pain, dyspnea, fatigue, or psychiatric manifestations • ~3% have complications: Infective endocarditis Mitral insufficiency Thrombus formation with embolization Arrhythmia/sudden death (unknown mechanism) 10 Normal (aortic) valve structure Myxomatous, prolapsing mitral valve 11 “Myxomatous” mitral valve 12 Acute endocarditis of mitral valve 13 Rupture of MV papillary muscle with inferior wall MI The following 6 slides on valve prostheses were not presented in the lecture on 1-4-06 14 Heart Valve Prostheses: Complications • Mechanical: component failure • Bioprostheses: degeneration with calcification • Both: Paravalvular leak, endocarditis. Thrombosis and tissue overgrowth are less common in bioprostheses than in mechanical valves. Bioprosthetic (Hancock)valve: Degeneration and tissue overgrowth 15 Thrombus occluding AV prosthesis 16 Thrombus covering mitral valve prosthesis (viewed from opened left atrium Endocarditis (arrows on vegetations) of ball valve prosthesis (Starr-Edwards) 17.

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Heart Pathology in Rheumatic Heart Disease
University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1941 Heart pathology in rheumatic heart disease Jacob J. Brenneman University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Brenneman, Jacob J., "Heart pathology in rheumatic heart disease" (1941). MD Theses. 846. https://digitalcommons.unmc.edu/mdtheses/846 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. HEART PATHOLOGY IN RHEUMATIC HEART DISEASE J. James Brenneman Senior Thesis The College ot Medicine University of Nebraska Omaha, Nebraska CONTENTS Definition ............................ Page 1 Introduction and History .............. 2 General Pathology . ..... g The Typical Lesion -- The Aschoff Body 17 Specific Lesions - ·········~·~,~···· 25 Myocardial . .......... 25 Endocardial and Valvular .. 32 Per1cardial ................ 37 Conduction Mechanism ........ 4-2 s~~mary and Conclusion~ . ............ 52 481211 1. DEFINITION Cecil, (1). "Rheumatic fever is a disease, orobably infectious, and apparently closely associated with invasion of the body by hemolytic streptococci; it is characterized by febrile and toxic states7 by the presence in various parts or the cardiovascular system and joints or multiple disseminated focal inflammatory lesions and at times by serof1brinous inflammation or some or the great mesothe11al lined body cavities and joints; it is further characterized by a tendency for the febrile, toxio and arthritic signs to disappear following the exhibition of certain antipyretio drugs in sufficient doses." 2.
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Rheumatic Carditis Treated with High Doses of Pulsetherapy Methylprednisolone
Herdy et al OriginalArq Bras Article Cardiol Rheumatic carditis treated with metilprednisolone volume 72, (nº 5), 1999 Rheumatic Carditis Treated with High Doses of Pulsetherapy Methylprednisolone. Results in 70 Children Over 12 Years Gesmar Volga Haddad Herdy, Carlos Alberto Pinto, Maria Cecilia Olivaes, Elisabeth Amabile Carvalho, Hsu Tchou, Raquel Cosendey, Raquel Ribeiro, Fabiano Azeredo, Debora de Souza, Artur H. Herdy, Vania Glória S. Lopes Niterói, RJ - Brazil Purpose - To report the result of patients treated with Data from the World Health Organization reveal that IV methylprednisolone divided into three groups and 3% of the children experiencing infection of the upper compare their follow-up during the last 12 years. respiratory tract by group A β-hemolytic streptococci develop rheumatic fever, of whom, 30% have carditis 1. 30% Methods - Seventy children with active rheumatic to 70% of the patients with rheumatic sequelae do not carditis (76 episodes) in heart failure Class III and IV report previous oropharynx infection 2,3. Some of these (NYHA) were studied. The diagnosis was based on modi- children of preschool age might have severe congestive fied Jones’ criteria. After ruling out infections and stron- heart failure (CHF) due to severe carditis and rupture of gyloidiasis, treatment with IV methylprednisolone bolus mitral chordae tendineae, as already previously reported 4. was started three times a week until the laboratory tests In such cases, treatment with intravenous methylpre- became negative. Patients were divided into 3 groups, dnisolone proved efficient 5,6. This study aims to report the according to the time of hospital admittance: Groups 1, 2 and 3, comprising of 40, 18 and 12 children, respectively.
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Rheumatic Heart Disease
RHEUMATIC HEART DISEASE Rheumatic fever is an acute immunologically mediated multisystem inflammatory disease that occurs few weeks after an attack of group A beta- hemolytic streptococcal pharyngitis. It is not an infective disease. The most commonly affected age group is children between the ages of 5-15 yearsQ. The disease is a type II hypersensitivity reaction in which antibodies against ‘M’ protein of some streptococcal strains (1, 3, 5, 6, and 18) cross-react with the glycoprotein antigens in the heart, joints and other tissues (molecular mimicry). CLINICAL FEATURES It presents with fever, anorexia, lethargy and joint pain 2-3 WEEKS after an episode of Streptococcal Infection is required for diagnosis Migratory Polyarthritis is the commonest major manifestation. Q Salient feature`s of the major criteria Carditis All the layers of the heart namely pericardium, myocardium and endocardium are involved, so this is called pancarditis. The pericarditis is associated with fibrinous/serofibrinous exudate and is called as ‘bread and butter’ pericarditis. It may manifest as breathlessness (due to heart failure or pericardial effusion), palpitations or chest pain (usually due to pericarditis or pancarditis). Other features include tachycardia, cardiac enlargement and new or changed murmurs. A soft mid-diastolic murmur (the Carey Coombs murmur) is typically due to valvulitis, with nodules forming on the mitral valve leaflets. Aortic regurgitation occurs in 50% of cases but the tricuspid and pulmonary valves are rarely involved. Pericarditis may cause chest pain, a pericardial friction rub and precordial tenderness. Cardiac failure may be due to myocardial dysfunction or valvular regurgitation. Valvular involvement is common in rheumatic heart disease.
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Rheumatic Endocarditis
University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1938 Rheumatic endocarditis Roy F. Pierson University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Pierson, Roy F., "Rheumatic endocarditis" (1938). MD Theses. 690. https://digitalcommons.unmc.edu/mdtheses/690 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. .RHEUKATIC ENDOCARDITIS Boy :r. Pieraon SENIOR THESIS PRESENTED TO - THE UNIVERSITY OF NEBR. COLLEGE OF llmDICINE Olt:AHA, 1938 INDEX· DEFINITION 1 I NT RODUCTI ON 2 HISTORY 3 INCIDENCE 15 ETIOLOGY 26 PATHOLOGY 36 SYMPTOMS AND DIAGNOSIS 59 TREATMENT 70 BIBLIOGRAPHY 80 480967 DEFINITION Bbeumatic Endocarditis is an inflammat ory disease of the endoeardium associated with :Rheumatic Fever. The disease process is charact erized by its indefinitely prolonged febrile course, a tendeney toward relapses, arthritic and nervous manifestations, •ubcutaneous nodules and changes in the endoeardium and myoeardium which are dependent upon the extensiveness of involvement. -l- .......... INTRODUCTION Rb.eumatie Endoearditia and its innocent counterpart, Hleuma.tic Fever have been associated since Piteairn first described this condition in 1788. Since that time they have been a most consp icuous thorn in the palm of the medical hand. For to this day, their origin has been concealed from the most discriminating minds of the profession.
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Kow2 Observed These Myocardial Changes in Reaction to Celloidin Con- Taining Foreign Bodies
OCCURRENCE OF CATERPILLAR NUCLEI WITHIN NORMAL IMMATURE AND NORMAL APPEARING AND ALTERED MATURE HEART MUSCLE CELLS AND THE EVOLUTION OF ANITSCHKOW CELLS FROM THE LATTER GEORGE E. MuRPiHY, M.D., and Cma G. BECKE, M.D. From the Department of Pathology, The New York Hospital-CorneU Medical Center, New York, N.Y. In I9OI von Oppell reported changes that occurred in rabbit myo- cardium in reaction to implantation of a sewing needle. Twenty-four hours after the implantation frank necrosis of muscle fibers was evident in the puncture canal. A little distant, less altered muscle fibers had lost striations and were coarsely granular. In their enlarged elliptic nuclei the chromatin had become distributed in granules or clusters of granules or condensed in a "single thread running in the long axis" of the nucleus. Among these degenerating muscle fibers, cells ("free cells") appeared with nuclei like those in the altered muscle fibers. Subsequently Anitsch- kow2 observed these myocardial changes in reaction to celloidin con- taining foreign bodies. He emphasized the condensation of chromatin into a "serrated stripe" in nuclei of some of the altered muscle fibers at a distance from the puncture canal and in nuclei of some of the cells ("myocytes") that appeared among the altered muscle fibers. These "free cells" or "myocytes" have come to be known as Anitschkow cells or myocytes. Because such elements are often prominent components of Aschoff bodies, the myocardial lesions characteristic of rheumatic heart disease, they are sometimes referred to as Aschoff cells. The chromatin structure of Anitschkow cells is known to occur in embryonic and postembryonic hearts in members of all classes of verte- brates,3'4 and is one of the most distinctive nuclear forms.
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Sudden Cardiac Death in Children
FACTA UNIVERSITATIS Series: Medicine and Biology Vol.12, No 2, 2005, pp. 85 - 88 UC 616.12-008.315-053.2 SUDDEN CARDIAC DEATH IN CHILDREN Lidija Kostić-Banović1, Radovan Karadžić1, Jovan Stojanović1, Goran Ilić1, Tatjana Stanković2 1The Institute for Forensic Medicine, Faculty of Medicine Niš, Serbia and Montenegro 2Paediatric Clinic, Clinical Center Niš, Serbia and Montenegro Summary. Sudden cardiac death is defined as unexpected death from cardiac causes early after or without the onset of symptoms. Having in mind that acute myocarditis may be a rare cause of sudden cardiac death in children, we have undertaken the following study: clinical, macroscopical and histopathological characteristics of the myocardium of two autopsied children who died suddenly. A number of myocardial tissue specimens were fixed in formalin and embedded in paraffin. Laboratory sections were stained with HE, Van Gieson and PAS methods. The pathohistological features of viral and acute rheumatic myocarditis were found. Coronary arteries and valves were normal. Viruses are difficult to culture from myocardial tissue, but lymphocytic and monocytic infiltrates are histological markers of viral etiology and acute Aschoff bodies of rheumatic fever. Key words: Viral myocarditis, rheumatoid myocarditis, children, morphology Introduction of viral myocarditis may give a history of a recent upper respiratory tract viral syndrome. The pathogenesis of viral Sudden cardiac death (SCD) is most commonly de- myocarditis is believed to involve direct viral cytotoxicity fined as an unexpected death from cardiac causes early or cellular mediated immune reactions directed against after or without the onset of symptoms. In a vast major- infested myocytes (1-6). ity of cases in children, SCD is caused by a congenital structural abnormality, hereditary or acquired abnor- Rheumatic myocarditis malities of the cardiac conduction system, myocarditis, or idiopathic dilated or hypertrophic cardiomyopathy (1- Rheumatic heart disease may be manifested as an 5).
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Ring More Frequently in the Left Ventricle, Particularly Under the Auriculoventricular Ring
STUDIES ON THE MYOCARDIAL ASCHOFF BODY * I. DESCRIPTIVE CLASSIFICATION OF LESIONS Louis GROSS, M.D., AND JOSEPH C. ECH, M.D. (From the Laboratories of the Mount Sinai Hospital, New York, N. Y.) Although Romberg1 in I894 is generally considered the first to have described the inflammatory lesions in the myocardium now known as Aschoff bodies, it would appear that they were really first reported by Goodhart 2 in I879. This author observed inter- stitial cell growth around vessels and between myocardial fasciculi in a typical case of rheumatic fever that showed at autopsy verrucous endocarditis (hempseed size) of the mitral and aortic valves, and in all probability a fibrinous pericarditis. As is well known, the asso- ciation between rheumatic fever and cardiac injury was suspected and noted long before this. However, this short introductory review will deal only with the historical development of our knowledge of the myocardial Aschoff body and will accordingly be limited to those workers whose contributions in this field marked a definite advance. In I887 Cadet de Gassicourt3 suggested that the inflammatory process in "rheumatism" starts in the depth of the muscular sub- stance and is made evident by proliferation of interstitial tissue. In I890 Krehl 4 made the significant observation that in a case of acute verrucous endocarditis there were present in the heart perivascular infiltration, increase in connective tissue and changes in the coronary arterioles which were, in all probability, the lesions at present receiv- ing considerable recognition. Krehl observed these processes occur- ring more frequently in the left ventricle, particularly under the auriculoventricular ring.
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How Rare Is Isolated Rheumatic Tricuspid Valve Disease?
Journal of Mind and Medical Sciences Volume 7 Issue 1 Article 21 2020 How rare is isolated rheumatic tricuspid valve disease? Edme R. Mustafa CRAIOVA UNIVERSITY OF MEDICINE AND PHARMACY, DEPARTMENT OF CARDIOLOGY, CRAIOVA, ROMANIA Octavian Istrătoaie CRAIOVA UNIVERSITY OF MEDICINE AND PHARMACY, DEPARTMENT OF CARDIOLOGY, CRAIOVA, ROMANIA Roxana Mandia CRAIOVA EMERGENCY HOSPITAL, CRAIOVA, ROMANIA Georgică C. Târtea CRAIOVA UNIVERSITY OF MEDICINE AND PHARMACY, DEPARTMENT OF PHYSIOLOGY, CRAIOVA, ROMANIA Cristina Florescu CRAIOVA UNIVERSITY OF MEDICINE AND PHARMACY, DEPARTMENT OF CARDIOLOGY, CRAIOVA, ROMANIA Follow this and additional works at: https://scholar.valpo.edu/jmms Part of the Cardiology Commons, Internal Medicine Commons, and the Rheumatology Commons Recommended Citation Mustafa, Edme R.; Istrătoaie, Octavian; Mandia, Roxana; Târtea, Georgică C.; and Florescu, Cristina (2020) "How rare is isolated rheumatic tricuspid valve disease?," Journal of Mind and Medical Sciences: Vol. 7 : Iss. 1 , Article 21. DOI: 10.22543/7674.71.P128132 Available at: https://scholar.valpo.edu/jmms/vol7/iss1/21 This Case Presentation is brought to you for free and open access by ValpoScholar. It has been accepted for inclusion in Journal of Mind and Medical Sciences by an authorized administrator of ValpoScholar. For more information, please contact a ValpoScholar staff member at [email protected]. Journal of Mind and Medical Sciences https://scholar.valpo.edu/jmms/ https://proscholar.org/jmms/ I S S N : 2 3 9 2 - 7 6 7 4 How rare is isolated rheumatic tricuspid
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The Induction of Rheumatic-Like Cardiac Lesions in Rabbits by Repeated Focal Infections with Group a Streptococci
THE INDUCTION OF RHEUMATIC-LIKE CARDIAC LESIONS IN RABBITS BY REPEATED FOCAL INFECTIONS WITH GROUP A STREPTOCOCCI COMPARISON WITH THE CARDIAC LESIONS OF SERUM DISEASE BY GEORGE E. MURPHY, M.D.,* AND HOMER F. SWIFT, M.D. (From the Hospital of The Rockefeller Institute/or Medical Research) PIRATES21 TO 35 (Received for publication, November 26, 1949) Downloaded from http://rupress.org/jem/article-pdf/91/5/485/1184315/485.pdf by guest on 29 September 2021 In a previous communication (1) we presented data indicating that cardiac lesions, closely resembling those characteristic of rheumatic fever in man, had been induced in a small proportion of rabbits that had undergone multiple, successive skin infections with group A streptococci of several serological types. How the hypothesis leading to those experiments evolved is described elsewhere (2). The purpose of this report is to submit additional examples of the rabbit cardiac lesions, together with representative human cardiac lesions from sev- eral fatal cases of active rheumatic fever; to describe them and their apparent evolution; and to compare and characterize the two groups, both as to their morphology and pathogenesis. Methods, Materials, and Specimens Procured Details of the group A streptococci employed, preparation of cultures, the cutaneous areas infected, the character of the local skin response to the first and succeeding inocula, variations in the intervals between inoculations, the methods employed to document the course of in- fection, and the techniques employed in preparing the tissues for microscopic study are all given in the first communication (1). The streptococci had undergone many mouse passages, and in the case of some strains sev- eral rabbit passages in addition.
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Revisiting the Pathogenesis of Rheumatic Fever and Carditis
PERSPECTIVES OPINION result from insufficient sensitivity of clinical auscultatory examination. Revisiting the pathogenesis of rheumatic Rheumatic carditis typically occurs as a pancarditis that involves the pericardium, fever and carditis myocardium, and endocardium.6 Whereas the occurrence of fibrinous pericarditis and Rajendra Tandon, Meenakshi Sharma, Y. Chandrashekhar, Malak Kotb, verrucous endocarditis or valvulitis is well Magdi H. Yacoub and Jagat Narula characterized, the term ‘myocarditis’ has been used rather loosely, predominantly on Abstract | Rheumatic fever is one of the most-neglected ailments, and its the basis of the presence of interstitial gran pathogenesis remains poorly understood. The major thrust of research has been ulomas. The landmark manuscripts describ directed towards cross-reactivity between streptococcal M protein and myocardial ing the histopathology of rheumatic carditis, α‑helical coiled-coil proteins. M protein has also been the focus of vaccine published in the 20th century, defined rheu development. The characteristic pathological findings suggest that the primary site of matic myocarditis by the characteristic rheumatic-fever-related damage is subendothelial and perivascular connective tissue presence of focal interstitial inflammation, 8,9 matrix and overlying endothelium. Over the past 5 years, a streptococcal M protein referred to as Aschoff bodies. N‑terminus domain has been shown to bind to the CB3 region in collagen type IV. This In that latter part of the 20th century, binding seems to initiate an antibody response to the collagen and result in ground streptococcal M proteins were widely substance inflammation. These antibodies do not cross-react with M proteins, and reported to have a pivotal role in the patho genesis of rheumatic fever,10 and certain we believe that no failure of immune system and, possibly, no molecular mimicry M serotypes of group A streptococcus— occur in rheumatic fever.
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Mitral Stenosis
Valvular heart diseases METHODIC MATERIALS FOR INTERNATIONAL STUDENTS (IV-VI year) Author: N.A.Filippova, assistant professor Published: 2004 Valvular heart disease with mitral valve affection Normal mitral valve Anatomy The normal mitral valve is a complex structure, consisting of leaflets, annulus, chordae tendineae, and papillary muscles. Its anatomy as studied at autopsy shows an unusual degree of variation between normal subjects. Of the two leaflets, the anterior one is the larger, both from base to margin, and also in its perimeter. It is attached to the root of the aorta and the membranous septum at the base of the heart, and is continuous with the chordae peripherally. It thus passes across the centre of the left ventricular cavity, dividing the inlet from the outlet portion. The posterior cusp is attached to the mitral ring and to the anterior cusp at both commissures. It is continuous with the posterior wall of the left atrium, and is divided into three portions by two scallops. The chordae arise from the ventricular margins of both cusps, and are inserted into the heads of the papillary muscles. There are multiple subdivisions in the chordae as they pass from papillary muscles to the cusps, which form an effective secondary pathway, additional to the main one between the cusps, for blood to enter the ventricle. There are two papillary muscles, one anteromedial and the other posterolateral. In general, the former is larger, and has a more uniform structure than the latter which may be double. Both may have up to six heads, giving rise to chordae.
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Origin of the Aschoff Body
Ann Rheum Dis: first published as 10.1136/ard.22.3.127 on 1 May 1963. Downloaded from Ann. rheum. Dis. (1963), 22, 127. ORIGIN OF THE ASCHOFF BODY BY BERNICE G. WEDUM Rheumatic Fever Study, Frederick, Maryland AND JOHN W. McGUIRE Photography Section, Medical Arts and Photography Branch, Division of Research Services, National Institutes of Health, Bethesda, Md. Rheumatic fever has been compared with tuber- students of rheumatic fever for the next 150 years. culosis (Thorel, 1910; Fahr, 1930), Hodgkin's Ludwig Aschoff directed his attention to this disease (Aschoff and Tawara, 1906; Gross, Loewe, problem in his first paper (1904), seeking for evidence and Eliasoph, 1929), and hypersensitivity reactions that the conduction system of the heart was affected (Swift, 1924; Klinge, 1933). The ultimate, com- in acute rheumatism and was responsible for the plete explanation of its pathogenesis must explain functional disorder, an idea previously advanced by why it has presented such varying aspects to such Peter (1891). Aschoff found no evidence to support profound students of the disease. The present study such a theory in the three cases which were the concerns the nature of its most specific pathological subject of his first paper, but Aschoff and Tawara manifestations, the Aschoff body of the heart. (1906), in their monograph on the failing heart, copyright. Evidence is presented that the Aschoff body is described one case with considerable involvement of derived from the larger lymphatic vessels of the the bundle of Hiss. They came to the conclusion heart; the central core, which may be present, is that the basic disorder was an anaemic necrosis of composed of precipitated lymph and necrotic the myocardium caused by perivasculitis of the protoplasm.
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