Autopsy-proved coronary atherosclerosis in marathon runners.
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Biomedical subjects
Publications and source records attributed to A G Rose.
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The changes of myospherulosis were observed in masses from the buttocks of three patients. Ultrastructural examination of parent bodies and spherules from two patients revealed some spherules to contain dense bodies and filaments. Spherules had a double electron dense wall: the outer layer had a thickness corresponding to that of a cell membrane. Incubation of packed red blood cells with tetracycline ointment produced a similar electron dense deposit on the inner aspect of the cell membrane of the erythrocytes. No filaments or parent bodies were seen. Our findings support the hypothesis that myospherulosis represents altered red blood cells. The filaments seen in our patients may represent polymers of haemoglobin. It is suggested that parent bodies may be derived from histiocytes.
An experienced marathon runner died suddenly during a competitive race. At necropsy, ventricular hypertrophy but no asymmetrical septal hypertrophy was found. Histological studies showed features of hypertrophic cardiomyopathy. The coronary arteries were normal. We propose that the runner died from myocardial ischaemia, precipitated by marathon running on a background of hypertrophic cardiomyopathy. Excess cardiac work, induced by marathon running in the presence of mild congenital cardiac defects, could have contributed to the development of the cardiomyopathy.
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So-called varicosities of the fossa ovalis are rare, venous malformations, which have also been previously labeled angiomas. In four cases encountered as incidental autopsy findings, the microscopic appearance was that of dilated venous channels. Veins larger than 100 micrometer in diameter were found close to the posteroinferior rim of the fossa ovalis in 18 of 21 consecutive, routine autopsy cases. The pathogenesis of the venous dilation is unknown but it may be related to the development of the interatrial septim. The term venous malformation seems preferable to varix for such lesions.
Primary sarcoma of the gallbladder was encountered in only 1 patient in a 5-year period during which primary carcinoma of the gallbladder was diagnosed in 1,8% of 954 surgically resected gallbladders and in 0,5% of 2 230 autopsies. The autopsy findings of the patient are described.
The pathological alterations in 34 patients with infective endocarditis complicating congenital heart defects were studied. The overall incidence of infective endocarditis in patients with major congenital cardiac defects was 4,7%. Most patients were under 31 years of age and males predominated. The infection was associated with Fallot's tetralogy in 10 patients (17%), ventricular septal defect in 7 (4%), bicuspid aortic valve in 7 (16%), coarctation of the aorta in 6 (8%), atrial septal defects in 2 (1%), and patent ductus arteriosus and pulmonary artery branch stenosis in 1 patient each. The causative micro-organisms were successfully cultured from only 29% of patients. Fourteen of the 34 patients had infection of an associated 'jet' lesion. Patients with isolated ventricular septal defect showed tricuspid valve endocarditis more commonly than did patients with Fallot's tetralogy. The infection had been missed clinically in 34,8% of patients, 50% of whom were aged 3 years or younger.
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The reliability of endomyocardial bioptome samples in detecting cardiac rejection was assessed in 26 formalin-fixed previously transplanted hearts. Thirteen human donor hearts (mean postoperative survival 128 days) and 13 baboon donor hearts (mean survival 16.5 days) were studied. Twenty samples were taken under direct vision from the endomyocardium of each heart with an Olympus bioptome catheter. A total of 397 tissue samples was examined "blindly" histologically (177 human and 220 baboon). The bioptome samples were assigned a histological rejection score and then compared with the score accorded multiple tissue sections from the same heart. Sample scores agreed with tissue section scores as follows: humans 86% (samples showed more severe alterations in 5% and less severe in 9%) and baboons 57% (samples more severe in 40% and less severe in 3%). Only 2 false-negative samples were encountered among 285 tissue samples from hearts showing rejection. Changes of rejection were equally distributed between the left and right ventricles. Endomyocardial sampling proved an accurate means of detecting the presence of rejection. In the baboon hearts the endomyocardium tended to show more severe changes than the rest of the myocardium.
The clinical and light and electron microscopic findings are reported in a 14-year-old patient who died 12 months after mitral valve replacement with a Hancock prosthesis. Severe cusp calcification had led to immobilisation of the valve and stenosis. Calcification involved the substance of the valve cusps. The cause of the calcification in this patient is unknown.
A patient who died of Whipple's disease had moderate mitral stenosis with large firm yellow vegetations on the contact area of the mitral leaflets. Light microsocopy showed PAS positive macrophages within the thickened cusps and overlying vegetations. Negative images of rod-shaped bodies were visible in the cytoplasm of the histiocytes. No Aschoff bodies were seen, and there was no history of rheumatic fever. The findings in this patient lend support to the concept that chronic rheumatic type valvar deformity may result from a persistent intrinsic infectious agent.
A 62-year-old man who died suddenly was found at autopsy to have multiple coronary arteriosystemic fistulae involving all three major coronary arteries and both ventricles. This is the second such case reported and the first with biventricular involvement and autopsy findings. A congenital bicuspid valve was also present. Numerous small blood vessels opened onto the endocardial surface of both ventricles and there were microscopic foci of persistent embryonic spongy myocardium.
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Surgical replacement of the mitral valve by a prosthetic valve may lead to localized disruption of atrioventricular continuity resulting from direct surgical trauma or from delayed rupture of the weakened annulus. Such disruption leads to subepicardial hematoma formation that may remain localized if pericardial adhesions are present. Of two patients who suffered this complication, the first died of rupture of the epicardial hematoma. The hemorrhage in the second patient was contained by pericardial adhesions and had organized, thus resulting in a subannular left ventricular false aneurysm. The aneurysm was found incidentally at autopsy after the patient died of cerebral embolism from prosthetic valve thrombi.
The autopsy findings in 41 patients with University of Cape Town aortic valve prostheses were studied. Twenty patients died within 1 month of operation and 21 patients died later, up to 141 months after operation. The most important postoperative complications which were common to both groups of patients were arrhythmias, myocardial failure and infection. Systemic embolism was the most important late complication. The type of coronary arterial perfusion or ventricular rhythm during bypass did not influence the myocardial pathology. Patients who died of myocardial failure did not show more severe myocardial alterations than did those who died of other causes.
The relationship between alterations in myocardial fibrinolytic activity and the degree of graft tolerance or rejection was studied in 22 nonimmunosuppressed heterotopic cardiac transplants in chacma baboons. Fibrinolysis was evaluated on tissue sections and tissue extracts. Fibrinolytic activity was compared with electrocardiographic voltage alterations and multiple myocardial biopsies and terminal heart specimens were examined by light and electron microscopy. Histopathology and reduction in fibrinolytic activity proved superior to electrocardiographic voltage reductions in assessing early cardiac rejection. The two former modalities correlated well with one another. Myocardial histology showed rejection change earlier than fibrinolytic activity reduction.
A young woman with unexplained radiographic calcification of the ascending aorta was found at necropsy to have healed idiopathic aorititis. Calcification also involved the aortic valve which was stenosed and the mitral valve. Death was the result of infective endocarditis of these valves with aortic ring abscess, rupture of aortic root, and cardiac tamponade.
Light microscopical criteria of early experimental myocardial infarction were compared with biochemical changes in glycogen content and the tissue K+/Na+ ratio in 19 mongrel dogs. Five sham-operated dogs served as controls, and seven of the 14 dogs with experimentally induced infarcts received infusions of glucose, insulin, and potassium (GIK). Infarcts were diagnosed by a scoring system based on edema formation, congestion, waviness of myofibers, myofibrillar degeneration, polymorphonucleosis, glycogen depletion, and fuchsinorrhagia. Significant histologic scores were associated with tissue K+/Na+ ratios of less than 1.2, with 30% depletion of biochemical glycogen, and with epicardial ST-segment elevation. Progression of the infarction zone to involve the surrounding border zone was prevented by GIK infusions. Routine light microscopy used in conjunction with tissue K+/Na+ ratios enabled early infarction to be diagnosed with a high degree of accuracy.