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Electron microscopic investigation was carried out to confirm our hypothesis, derived from a large number of macroscopic and light-microscopic observations, that impairment of the peripheral circulation of the myocardium, and not the presence of coronary thrombi, plays the fundamental role in the development of acute myocardial infarction. The peripheral coronary vessels of 5 human hearts obtained at autopsy showed severe histolytic impairment of the endothelial cells and of the tunica media muscle cells, even though no myocardial necrosis was observed either macroscopically or microscopically. An additional experimental study using 12 rabbits was performed to ascertain the induction of myocardial necrosis without coronary occlusion, by intravenous administration of either epinephrine or endotoxin alone or a combination of both. One-third of the epinephrine group and all of the combined treatment group developed myocardial necrosis. The intramyocardial vessels of these rabbits showed similar hystolytic changes to those observed in human cases. These findings support our concept that derangement of the peripheral circulation precedes the development of a coronary thrombus in cases of acute myocardial infarction.

Ultrastructural observation in clinical and experimental myocardial infarction, with reference to pathogensis.