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The rare case of a 58 years old male patient with a combination of Ebstein's disease and coarctation of the aorta is reported. The patient presented and died with manifestations of cardiac and respiratory failure. The post mortem examination revealed the combination of Ebstein's disease and coarctation of the aorta. The analysis of the clinical and paraclinical data points to an atypical course of the disease probably due to the opposite hemodynamic characteristics of the two congenital heart diseases.

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Forty eight cases with infections endocarditis (IE) are analyzed--27 males and 21 females (75% at the age of 31-60). Only in 12.5% IE has developed on intact valvular apparatus. In 83.4% the preceding valvular pathology is rheumatic heart defect (RHD), and congenital cardiac malformations and valvular dysplasia--8.3% each. The mitral-aortic valvular defects predominate in RHD, followed by aortic, tricuspid and mitral ones. In 83.3% X IE is with valvular localization, in 4.2%--parietal and in 12.5%--on valvular prostheses. Vegetations are highly specific for valvular IE (100%) as well as ulcerations (90%) and perforations (45%). Ruptures of extra-valvular structures are established in 8.3%. The inflammatory alterations in myocardium are in 62.5%. The pericardial changes are found in 14.6%, mainly in the cases with valvular prosthesis. Septic changes are established in all cases in the spleen and regeneration of bone marrow, and vascular changes--in 85.4%. The cases with embolism and infarctions predominate in the kidneys (79.1%), followed by the cases with Löhlein's focal nephritis (18.6%). The inflammatory changes in liver are rare--6.9%. In 37.5% changes in brain were established, embolism according to incidence being first, followed by cerebral hemorrhages, cerebral abscesses and purulent leptomeningitis Staphylococcus aureus proved to be most frequent causative infectious agent established et necropsy.

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The course of idiopathic congestive cardiomyopathy in two full brothers is described. The diagnosis was made on the base of the existing cardiomegaly, gallop rhythm and congestive cardiac insufficiency, in the absence of any connection with some of the well known causes for hypertrophy and dilation of the heart. It was confirmed at necropsy in one of the brothers. A similarity was established in their case history, namely: considerable physical activity until the first signs of cardiac insufficiency, advancement of decompensation at the same age (20 years) with an already existing cardiomegaly, identical complaints--rhythm disturbances and pulmonary thromboembolism, similar electrocardiographic changes with formation of "pseudoinfarct" image, ventricular flutter--immediate cause for the death of one of the brothers, sudden death--for the other. The origination of the disease cannot be associated with the effect of exogenous morbid factors. There are no data on advancing of autoimmune process. With the genealogical study, covering four generations, the family was established to have a stillborn child, no other sick members of the family, no data about multiple deaths. The cytogenetic analysis showed no chromosomal aberrations. The possibility the disease to be transmitted via autosomal recessive mode or via autosomal-dominant gene with a low penetration is discussed.

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Analysis was made to 270 deceased with acute myocardial infarction. The signs discussed were: type of coronary circulation, sex and age, nosological belonging, atherosclerosis affection and allocation of thrombosis in coronary arteries. The acute infarction lesions were characterized according to site, layers involved, left ventricular mass engaged mural thrombosis and acute aneurysms ruptures. Consideration was given to myocardiosclerosis, postinfarction cicatrices and chronic aneurysms, hypertrophic rate, duration of recent infarction, thromboembolic complications and death causes. Essential discrepancies were found for the separate coronary types as regards stenosis distribution, predominating affection of separate coronary vessels, site of coronary thrombosis, infarction, resp., infarction extent (layer and mass), rupture incidence, acute aneurysms and postinfarction cicatrices. The study revealed that left coronary type was the most unfavourable terrain for acute myocardial infarction.

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Analysis was performed on 220 cases--decreased with acute myocardial infarction, subdivided into two groups--not hypertonics and hypertonics. The average age of the decreased with acute myocardial infarction with arterial hypertension is higher. Substantial differences are absent in the carriers of coronary type, degree of atherosclerotic affection and coronaries myocardiosclerosis and past infarctions, preceding the development of the acute myocardial infarction, being the cause of the death. Coronary thrombosis, mural thrombosis, acute aneurysms, and embolic complications in the systemic and pulmonary circulation proved to be more frequent among hypertonic. Discrepancies are absent as regards the localization of the necrotic zone and involvment of the ventricular muscles. Rupture incidence in both groups is very high and almost the same--over 25 per cent. External ruptures are found to be more frequent, being most often posterior in hypertonics. Parillary ruptures are characteristic for them. No difference is established concerning the exitus. Left ventricle insufficiency ranks first for both groups--over 67 per cent; second to follow are the heart ruptures with tamponade--about 20 per cent; and third--the arterial embolias in systemic circulation--9--10 per cent.

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