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The characteristics of cardiac rupture associated with thrombolytic therapy for acute myocardial infarction (MI) were studied in the hearts of 10 autopsy patients, 7 men and 3 women aged 41-80 years (mean 59.9 +/- 13.2 years), who died of rupture of the free wall of the left ventricle following acute MI. The site of rupture was examined histologically and the percentage areas of living myocytes, the processes of organization, necrosis and degeneration, and hemorrhage were compared in four patients who received thrombolytic therapy (group R) and six patients without thrombolytic therapy (group N). There were four pathological findings at the site of rupture: necrosis, neutrophil infiltration, hemorrhage, and evidence of the process of absorption. Group R consisted of two patients with hemorrhage, one with absorption, and one with unsuccessful reperfusion and neutrophilic infiltration. Group N included three patients with necrosis, two with neutrophilic infiltration, and one with hemorrhage. The percentage area involved by necrosis and degeneration was significantly lower in group R than in group N. Therefore, local stress produced by more surviving myocardium around the smaller necrosis area and the weakness of myocardium due to hemorrhage and absorption may provoke cardiac rupture in acute MI patients receiving thrombolytic agent.

The effects of residual stenosis after intracoronary thrombolysis (ICT) on the hospital course and on left ventricular function were investigated in 94 patients with acute myocardial infarction. The in-patient hospital events including death, post-infarction angina, and re-infarction occurred in 6 of 24 (25%) patients with 100-99% residual stenosis (Group I), 18 of 55 (32.7%) patients with 95-90% stenosis (Group II) and one of 15 (7%) patients with 75% or less stenosis (Group III), suggesting that the presence of severe residual stenosis could be associated with the occurrence of in-patient hospital events. However, re-infarction occurred in only 3.6% of Group II patients. In an analysis of left ventricular function, global and regional wall motion was significantly improved in this group of patients, compared with patients who had no reperfusion (Group I). What is more, the degree of the improvement in wall motion in Group II, despite the severe stenosis, was the same as that in Group III with 75% or less stenosis. It was concluded that further intervention following thrombolysis may not be necessarily required for patients who underwent reperfusion without filling delay, even if the residual stenosis is greater than 90%.

Among 144 patients with hypertrophic cardiomyopathy, eight (58.3 +/- 7.0 years, M:F = 7:1) had complicating myocardial infarction, which was diagnosed clinically and by elevated cardiac enzymes or new Q-waves on electrocardiography. Coronary occlusion or stenosis evidenced by coronary angiography and nuclear cardiological findings were investigated. In six of the eight patients, coronary atherosclerosis caused infarction. These patients had many coronary risk factors compared to the other two patients. Sixteen of the 144 patients (11%) with hypertrophic cardiomyopathy had coronary atherosclerosis, the rate of which is reportedly 10 to 20%. Two of the eight patients had no coronary atherosclerosis. One patient had a diffusely spastic diathesis provoked by the intravenous administration of ergonovine maleate during coronary angiography, suggesting that coronary spasm caused myocardial infarction. The other patient had recurrent episodes of supraventricular tachyarrhythmia and no evidence of spasm during coronary angiography, suggesting coronary embolism as a cause of myocardial infarction. Myocardial infarction in patients with hypertrophic cardiomyopathy and normal coronary arteries as advocated by Maron et al. may have such pathogenesis. We conclude that coronary angiography may be mandatory in patients with hypertrophic cardiomyopathy, especially those who have many coronary risk factors and anginal symptoms. In these patients, ST-T changes and abnormal Q-waves on electrocardiography sometimes may be misleading when diagnosing the occurrence of acute myocardial infarction by electrocardiography alone. In such cases, infarct-avid scintigraphy with 99 m-Tc pyrophosphate is preferable.