Low-Dose Aspirin for the Prevention of Atherothrombosis.
N Engl J Med 2005;353:2373-83.
ABSTRACT
Atherosclerosis, the major cause of ischemic coronary artery disease and cerebrovascular disease, is a chronic inflammatory disorder in which immune mechanisms interact with metabolic risk factors to initiate, propagate, and activate vascular lesions. Arterial thrombosis, an acute complication that develops on the surface of a ruptured atheromatous plaque or as a consequence of endothelial erosion, may cause myocardial infarction or ischemic stroke. Platelets are key cellular components of arterial occlusive thrombi and may participate in the devel- opment and progression of atheromatous plaques. Platelets are also vital components of hemostasis, the physiologic process that arrests hemorrhage after tissue trauma and vascular injury. Although the adhesion and activation of platelets can be viewed as a repair-oriented response to sudden fissuring or rupture of an atheromatous plaque, uncontrolled progression of such a process through a series of self-sustaining amplification loops may lead to the intraluminal formation of thrombus, vascular occlusion, and transient ischemia or infarction. The ability of platelets to participate in both normal hemostasis and atherothrombosis depends on their adhesive properties and their capacity to become activated very quickly in response to various stimuli.