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How to study the effects of platelet aggregation and thrombosis on coronary vasomotion and their clinical relevance.

Following arterial injury, platelets may activate and adhere to the damaged vessel wall, release vasoactive products, and produce vasoconstriction or even vasospasm. In the last few years the hypothesis of intracoronary thrombosis, triggered by plaque ulceration or fissuration, has gained wide acceptance as one of the key events in the pathophysiology of acute coronary syndromes. Following arterial injury, platelets readily adhere to the subendothelium and release a variety of chemical mediators which, apart from recruiting additional platelets from the circulation, are also powerful vasoactive substances. Platelet-induced coronary vasoconstriction may therefore contribute to the occurrence of myocardial ischemia in patients with acute coronary syndromes. Several studies have also focused on some components of the vessel wall and indicate that endothelial dysfunction in atherosclerosis plays a key role in altered vascular responses. We and others have suggested that augmented constrictor responses of atherosclerotic coronary arteries to platelet-derived substances, such as serotonin and thromboxane A2, perhaps combined with an impaired release of endothelium-derived relaxing factor, may contribute to vasoconstricting responses to aggregating platelets. The purpose of this article is to summarize recent development in knowledge relating to alteration in coronary tone associated with intracoronary platelet activation.