Abstract

Ischemic heart disease (IHD) represents a pathophysiologic continuum consisting of stable angina, unstable angina, non-ST-segment elevation myocardial infarction, and ST-segment elevation myocardial infarction. Patients who develop a change in their usual stable pattern of ischemia are classified as having an acute coronary syndrome, which includes patients with unstable angina, non-ST-segment elevation myocardial infarction, and ST-segment elevation myocardial infarction. Such progression from a stable to an unstable state is believed to result from disruption of an atherosclerotic plaque with subsequent platelet aggregation and thrombus formation. This, in turn, leads to the clinical manifestations of unstable angina, MI or death. Because platelets play a central role in the thrombotic complications of atherosclerosis, antiplatelet agents have been the cornerstone of the therapy for IHD. Aspirin has been the traditional antiplatelet agent, and remains the mainstay of treatment for all forms of IHD. However, aspirin is a weak antiplatelet agent and is often poorly tolerated by many patients. Clopidogrel is a new antiplatelet agent of the thienopyridine class. Clopidogrel, when used alone, and especially in combination with aspirin, has been shown to improve outcomes in patients with IHD across a variety of syndromes. However, combination therapy with aspirin and clopidogrel has been associated with an increased risk of bleeding. Therefore, despite improved outcomes, further studies are required to determine the optimal duration and dosage regimen of such combination therapy to maximize its risk-benefit ratio.

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