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Transmural myocardial infarct begins with a sudden reduction of flow in the distribution of a major epicardial coronary artery. This process of reversible injury, progressing to necrosis, correlates with characteristic electrocardiographic and enzyme changes. The relationship of these changes to the coronary anatomy has remained a matter of controversy because coronary angiography has seldom been performed during the early phase of myocardial infarct. Without angiographic studies, our understanding of the interrelationships between the degree of luminal narrowing, the intensity and duration of myocardial injury, and the response to therapy is limited.

This paper focuses on the findings in the major epicardial coronary arteries in acute myocardial infarction (AMI).

The current understanding of the pathogenesis of myocardial ischemia is primarily based either on the concept of a high-grade ‘fixed’ coronary artery obstruction or a spastic vasoconstriction of an epicardial coronary artery. Both of these mechanism do not sufficiently explain the variable clinical syndromes of angina pectoris, particularly not the variation in anginal threshold experienced by many patients. Therefore, the concept of a variable vasoconstriction (‘functional component’) superimposed on an atherosclerotic lesion (‘organic component’) constitutes a plausible hypothesis connecting both pathogenic mechanisms.

To evaluate the vasodilatory potency of the new dihydropyridine nisoldipine on epicardial coronary arteries in 18 patients, coronary angiograms were performed before and 2, 4, 7, 10 and 15 minutes (min) after onset of an intravenous 4-min infusion of either 0.5 mg (n = 8, group A) or 1 mg nisoldipine (n = 10, group B). Percentage diameter changes (Δ D) of normal epicardial coronary arteries were quantitatively analyzed- using an automated contour detection system — and correlated to nisoldipine plasma levels and aortic pressure.

From March 1 (1983) to June 15 (1984) 127 patients with evolving myocardial infarction (MI) entered a randomized clinical trial at the II. Medizinische Klinik, Johannes Gutenberg-Universitat, Mainz.