Cardiac rupture following recent myocardial infarction is strongly associated with early thrombotic occlusion and transmural necrosis in previously unscarred myocardium.
Suggests heightened early post-MI monitoring for rupture; hypothesis-generating for transmural necrosis mechanisms, needing prospective validation.
A prospective, randomized autopsy study of possible pathogenetic factors involved in the mechanism of cardiac rupture following recent myocardial infarction is reported. The series consists of 508 cases (279 men and 229 women). Fourteen out of 122 cases with recent myocardial infarction had cardiac rupture. This corresponds to a 11.5 per cent frequency of rupture in the infarction group and 2.8 per cent in the total autopsy group. Rupture was more common in men than in women, and tended to occur early in the infarction period; 64 per cent of the rupture cases died within 3 days after infarction. Attempts at resuscitation was not found to have caused rupture in any case. No difference was found in the frequency of diabetes mellitus, hypertension, angina pectoris, psychiatric disease or anticoagulant treatment in the ruptured and the non‐ruptured cases. The most characteristic finding in the rupture cases was a thrombotic occlusion of a coronary artery and transmural necrosis in a heart without myocardial scars.
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Ø Havig (1973) studied this question.
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