Circulation, Vol 80, 198-205, Copyright © 1989 by American Heart Association
JT Willerson, P Golino, J Eidt, WB Campbell and LM Buja
We have speculated previously that the abrupt conversion from chronic
stable to unstable angina and the continuum to acute myocardial infarction
may result from myocardial ischemia caused by progressive platelet
aggregation and dynamic vasoconstriction themselves caused by local
increases in thromboxane and serotonin at sites of coronary artery stenosis
and endothelial injury. Platelet aggregation and dynamic coronary artery
vasoconstriction probably result from the local accumulation of thromboxane
and serotonin and also relative decreases in the local concentrations of
endothelially derived vasodilators and inhibitors of platelet aggregation,
such as endothelium-derived relaxing factor (EDRF) and prostacyclin. With
severe reductions in coronary blood flow caused by these mechanisms,
platelet aggregates may increase, and an occlusive thrombus composed of
platelets and white and red blood cells in a fibrin mesh may develop. When
coronary arteries are occluded or narrowed for a sufficient period of time
by these mechanisms, myocardial necrosis, electrical instability, or sudden
death may occur. We believe that unstable angina and acute myocardial
infarction are a continuum in relation to the process of coronary artery
thrombosis and vasoconstriction. When the period of platelet aggregation or
dynamic vasoconstriction at sites of endothelial injury and coronary artery
stenosis is brief, unstable angina or non-Q wave infarction may occur.
However, when the coronary artery obstruction by these mechanisms is
prolonged for several hours, Q wave myocardial infarction results. Chronic
endothelial injury and coronary artery stenosis are probably associated
with the accumulation of platelets, white and red blood cells, and a fibrin
mesh at the site of stenosis and endothelial injury.
ARTICLES
Specific platelet mediators and unstable coronary artery lesions. Experimental evidence and potential clinical implications
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-9047.
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