I. MECHANISM OF ACTION
Coronary thrombosis is known to be the major cause of coronary artery occlusion resulting in fatal or nonfatal acute myocardial infarction. Antiplatelet agents are named this because they inhibit platelet aggregation, which plays a major role in coronary thrombosis, myo-cardial infarction, and cardiac death.
Platelets clump on to atherosclerotic plaques, causing occlusion of the artery, and/or embolize downstream. The occlusion of these vessels may induce fatal arrhyth¬mias and cardiac death. In patients with unstable angina, angioscopy has confirmed the presence of platelet clumps attached to the surface of eccentric atheromatous plaques that jut into the lumen of arteries causing partial to near complete occlusion. The atheromatous plaques may become fissured or rupture exposing a ‘‘porridge/gruel’’ like substance or substances that are highly thrombogenic. (See also the chapter Atherosclerosis/Atherothrombosis.) However, antiplatelet agents are not expected to prevent all forms of thrombotic events.
After plaque rupture the formation of a platelet-rich thrombus requires three essential steps:
1. Platelet adhesion: This occurs shortly after an ather-omatous plaque has ruptured and the process of adhesion is mediated by the platelet glycoprotein IIb receptor through its interaction with von Willebrand factor.
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