Plaque rupture with thrombus formation is the primary pathophysiologic mechanism behind acute coronary syndromes (1-5). This process is complex and starts with exposure of subendothelial constituents like collagen, von Willebrand factor, fibronectin, and vitronectin. These elements are recognized by platelet surface receptor glycoprotein Ib and lead to platelet activation and adhesion to the vessel wall. Activated platelets release from their a-granules substances such as thromboxane A2, thrombin, adenosine diphosphate, and serotonin. These are vasoconstrictor substances, and they cause a physiological obstruction superimposed on the mechanical disruption. More important, they lead to further platelet activation and aggregation. The final common pathway of platelet aggregation involves activation of the GP IIb/IIIa surface receptors, which cross-link platelets via fibrinogen bridges. Aggregated platelets facilitate the conversion of pro-thrombin to thrombin, and this leads to increased thrombin formation, which in turn is a potent agonist for further platelet activation. Finally, the thrombus is stabilized by thrombin-mediated conversion of fibrinogen to fibrin.
Angioscopy studies have confirmed these findings and demonstrated intracoronary thrombus or complex plaques in 90-100% of patients presenting with unstable angina (6,7) Angiography studies, on the other hand, are limited by a low sensitivity for detecting intracoronary thrombus and have revealed its presence in only about 30-40% of patients (8,9). Moreover, the demonstration of improved clinical outcomes with the administration of aspirin and heparin has provided indirect evidence that coronary thrombosis plays a central role in acute coronary syndromes (10,11).
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