CLINICAL AND PATHOLOGIC FEATURES OF POSTINFARCTION CARDIAC RUPTURE

In a 15 year period 106 instances of myocardial rupture after myocardial infarction were observed at autopsy, an incidence of 8.6 per cent of fatal acute myocardial infarcts. This complication occurred most frequently in the seventh and eighth decades and was slightly more common in women. Clinically, rupture occurred most frequently during the first week after infarction. Historical evidence of previous coronary artery disease was uncommon. Hypertension had been present in 70 percent of the patients, but it persisted after the infarct in less than a third. Pathogenetic factors were sought in the clinical aspects of the patients. No definite role could be ascribed to anticoagulant or sympathomimetic drugs or digitalis. Physical activity after infarction may be a predisposing factor in some instances. Sudden death without antecedent change in symptoms most often occurred. Cardiac tamponade or vascular collapse was documented in a few instances prior to death. In most instances no physical findings, laboratory tests, or electrocardiographic features that indicated cardiac rupture could be ascertained. Based on histologie data, 90 per cent of the ruptures occurred during the first two weeks after infarction, at an average time of five days; 22 per cent were in the first 24 hours, and 69 per cent were in the first week. All of the infarcts were transmural and involved large areas of the left ventricle. Ruptures presented as distinct tears (79 per cent) or large areas of hemorrhagic dissection (9 per cent), or both (12 per cent). The most common site of rupture was through the anterior wall of the left ventricle; commonly, ruptures were near the septum or near the base of papillary muscle. The areas of rupture were more common in the basal two thirds of the ventricle than in the apical portion. The ruptures varied greatly in size. Most were situated within the area of infarction rather than at the junction between the infarcted and the normal myocardium. Unusual accumulations of polymorphonuclear leukocytes were not found in most specimens. Most hearts had severe coronary artery disease, but myocardial scarring was present in only a fourth. Cardiac hypertrophy was usually present. The amount of hemopericardium varied widely and was the apparent mechanism responsible for death in some patients. Mural hemorrhage, hypertension, degree of polymorphonuclear infiltration, degree of myocardial fibrosis and location of the infarct may all be of pathogenetic significance in post-infarction rupture in different situations, but these considerations did not have universal applicability. The only common morphologic features among the infarcts that ruptured were their large size and transmural extent. The major pathogenetic considerations probably are loss of tensile strength of the infarcted segment, increased tension in this area, and, in some cases, divergent vector forces. © 1969.