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The role of platelets in coronary heart disease

Jane E Freedman, MD
Section Editor
Freek Verheugt, MD, FACC, FESC
Deputy Editor
Gordon M Saperia, MD, FACC


Platelets play an important role in cardiovascular disease both in the pathogenesis of atherosclerosis and in the development of acute thrombotic events. Their importance in coronary disease and in acute coronary syndromes is indirectly confirmed by the benefit of antiplatelet agents (particularly aspirin, clopidogrel, and the glycoprotein IIb/IIIa inhibitors) in these disorders. (See "Antiplatelet agents in acute non-ST elevation acute coronary syndromes" and "Antiplatelet agents in acute ST elevation myocardial infarction" and "Aspirin in the primary prevention of cardiovascular disease and cancer".)


Both superficial and deep intimal injury disrupt the intact endothelium, which normally prevents the adherence of platelets by the production of the antiplatelet agents nitric oxide and prostacyclin. Disruption of the endothelium also exposes collagen. These factors lead to the adherence of platelets to the subendothelium, both directly and via von Willebrand factor, and, subsequently, to platelet activation (figure 1) [1].

The following is a brief summary of platelet adhesion and aggregation. These processes are discussed in detail separately. (See "Platelet biology".)

Adhesion — Platelet adhesion is mediated by the binding of platelet receptors to a number of arterial wall receptors, including subendothelial collagen (whose corresponding platelet receptor is glycoprotein [GP] Ia/IIa), von Willebrand factor (GP Ib/IX and GP IIb/III), and fibrinogen (GP IIb/IIIa).

Activation — Binding of platelets to these structural proteins in concert with the action of soluble receptor-mediated stimulants, such as thrombin, adenosine diphosphate (ADP), and thromboxane A2 (TxA2), induces platelet activation. This process involves the mobilization of calcium from intracellular stores, the activation of several intracellular kinases, and the release of arachidonic acid from membrane phospholipids, resulting in the generation of TxA2 (figure 2) [2]. Platelet activation produced in vivo is enhanced by circulating catecholamines [3].

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Literature review current through: Oct 2017. | This topic last updated: Nov 01, 2017.
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