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Coronary thrombosis is a fundamental event in the pathophysiology of atherosclerotic coronary artery disease, being involved in both the development of atheroma and its lethal complications. Without thrombus formation, the coronary plaque would be a cause of morbidity but not mortality. Pharmacological manipulation of the haemostatic system, with the aim of preventing or reducing the incidence of coronary thrombosis, is therefore of central importance in the treatment of patients with coronary artery disease.
PLATELETS AND ATHEROSCLEROSIS
Platelets, despite being the smallest of blood cells, have a crucial role in haemostasis and the development of arterial thrombosis. Inhibition of platelet function might be expected to have a beneficial effect in reducing the amount of thrombus consequent on the rupture of an intracoronary plaque, and hence reduce mortality and morbidity in patients with coronary artery disease. At the same time platelet inhibition may increase the risk of haemorrhage. The balance of effects and side effects are crucial to an understanding of the use of antiplatelet drugs in patients with stable coronary artery disease.
“Antiplatelet drug” is a generic term that does not fully allow an appreciation of the different effects of inhibition of one or more of the complex functions that the platelet fulfils. Platelets respond to disruption of the endothelial monolayer by changing from their resting discoid shape to a compact sphere with dendritic extensions that facilitate adhesion to the damaged endothelium (fig 1).1 Exposed collagen is a potent stimulus to platelet activation and results in the secretion of granule contents. The dense granules secrete ADP and calcium, which reinforce adhesion and aggregation, and the α granules secrete a wide range of vasoactive and proinflammatory compounds such as von Willebrand factor and platelet factor 4. Platelet activation also results in conformational changes in platelet surface glycoprotein receptors that mediate adhesion to the subendothelial …
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