Ultrastructural observation in clinical and experimental myocardial infarction, with reference to pathogenesis
Related Experiment Videos
1First Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.
Abstract:
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.
Insights
Peripheral circulation impairment, not coronary thrombi, fundamentally causes acute myocardial infarction. Electron microscopy revealed histolytic damage in human and rabbit coronary vessels, supporting this hypothesis.
Area of Science:
- Cardiovascular Pathology
- Myocardial Infarction Research
Background:
- Acute myocardial infarction (AMI) is traditionally linked to coronary thrombi.
- Previous observations suggested peripheral circulation issues might be primary.
Purpose of the Study:
- To investigate the role of peripheral coronary circulation impairment in AMI development.
- To test the hypothesis that vascular damage precedes thrombus formation.
Main Methods:
- Electron microscopic examination of human autopsy hearts (n=5).
- Experimental induction of myocardial necrosis in rabbits (n=12) using epinephrine and/or endotoxin.
- Histological analysis of intramyocardial vessels.
Main Results:
- Human coronary vessels showed severe histolytic impairment of endothelial and muscle cells without necrosis.
- Rabbits treated with epinephrine or combined agents developed myocardial necrosis.
- Intramyocardial vessels in affected rabbits exhibited similar histolytic changes.
Conclusions:
- Peripheral coronary circulation derangement is a fundamental factor in AMI.
- Histolytic vascular damage precedes myocardial necrosis and potential thrombus formation.
- Findings challenge the sole focus on coronary thrombi in AMI etiology.