Postinfarction cardiac rupture. A pathogenetic consideration in eight cases.
Eight fatalities due to cardiac rupture, of 40 consecutively autopsied myocardial infarctions, were clinicopathologically examined. Total duration of infarctions in 8 cases ranged from 9 hours to 14 days. The longer the period, the more the infarction extended, and aneurysmal dilatation of infarcted wall and tissue weakness were striking. The weakness was caused by the lack of replacement of necrotic muscle fibers by granulation, and was related to aneurysmal structure per se and also to its paradoxical pulsations. Postinfarction cardiac rupture occurring in relatively later phase was considered to be mainly due to weakness of infarcted wall, with less influence factors of mechanical stress such as physical exertion, hypertension, or intracardiac pressure. In the case where cardiac rupture took place in a relatively early stage of the episodes, infarction covered only a small range and aneurysmal change of the ventricle was slight, for which dynamic factors, represented by the degree of a localized strain elicited by myocardial contraction of non-infarcted site, seemed to play a significant role.
D000368:Aged; D005260:Female; D006341:Heart Rupture / Q000209:etiology / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology*; D009206:Myocardium / Q000473:pathology*