ABSTRACT
Platelets play a key role in thrombosis and in the pathophysiology of ischemic syndromes related to coronary artery disease (CAD) and atherosclerotic vascular disease including peripheral vascular disease and cerebrovascular disease (1). Inactivated platelets circulate in a resting state until encountering activating substances such as thrombin and collagen. With the binding of these messenger molecules, platelets become activated, resulting in two major processes: shape change, which exposes more surface area for binding messengers and interaction with other circulating cells including platelets and leukocytes, and degranulation, which results in the release of secondary messengers, which further activates circulating platelet in a paracrine fashion. In addition to further platelet activation, release of signaling molecules including serotonin results in local vasoconstriction. Activation of platelets also results in the exposure of activated glycoprotein (GP) IIb/IIIa receptors allowing for fibrin-mediated cross-links of multiple platelets and formation of aggregates leading to an early platelet monolayer, which seals an injured vessel. In the setting of bleeding, this physiologic process serves a protective role; however, in the setting of atherosclerotic plaque rupture-either spontaneously or following percutaneous coronary intervention (PCI)—this process is central to the transition from stable CAD to unstable coronary syndromes including unstable angina (UA), nonST-elevation myocardial infarction (NSTEMI), and ST-elevation MI (STEMI).
