Use of Antiplatelet Inhibitors in Peripheral Vascular Interventions

Abstract

In the past decade, a tremendous amount of information has been gathered about platelet function and its impact on percutaneous vascular interventions. Strategies for prevention of platelet aggregation have moved beyond aspirin administration. Powerful oral antiplatelet agents such as ticlopidine (Ticlid) and clopidogrel (Plavix) have been developed to prevent platelet aggregation and thrombosis. The discovery of the glycoprotein IIb/IIIa receptor, which is responsible for platelet aggregation, has led to the development of receptor antagonists. These drugs include abciximab (ReoPro), eptifibatide (Integrilin), and tirofiban (Aggrastat). Several large studies have demonstrated that these drugs can improve outcomes in coronary interventions. Because most of the data regarding antiplatelet agents in percutaneous interventions comes from studies of coronary interventions, knowledge of these studies is necessary before using the antiplatelet drugs in peripheral vascular interventions. This article reviews the use of these agents in percutaneous coronary artery interventions and discusses their potential use in peripheral interventions.KEYWORDS: Blood, platelets, arteries, transluminal angioplasty, thrombosis, drugsObjectives: Upon completion of this article, the reader will understand the use of antiplatelet agents in percutaneous coronary artery interventions and be able to discuss their potential use in peripheral interventions. Accreditation: Tufts University School of Medicine (TUSM) is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. Credit: TUSM designates this educational activity for a maximum of 1 Category 1 credit toward the AMA Physicians Recognition Award. Each physician should claim only those credits that he/she actually spent in the activity.Over the past decade, our understanding of the role of the platelet in acute vascular events including those associated with percutaneous interventions has increased dramatically. Although aspirin was introduced in the late 1890s, its antiplatelet effect was not discovered until the 1960s.1,2 Aspirin primarily affects the biosynthesis of cyclic prostanoids such as thromboxane A 2 (TXA 2 ) by irreversibly inhibiting both the function of cyclooxygenase (COX-1) in platelets and the vascular synthesis of prostacyclin. 3,4 Although the efficacy of aspirin in preventing thrombotic complications during percutaneous coronary interventions (PCIs) is well established, 5-8 aspirin is a relatively weak platelet antagonist and some patients may be resistant to its effects. Other non-TXA 2 -dependent activators of platelet aggregation such as thrombin, adenosine diphosphate (ADP), and collagen 3,4 are not affected by aspirin. The current general recommendation for 584-4662. 0739-9529,p;2005,22,02,080,087,ftx,en;sir00297x. 80 aspirin use during PCI is an empirical dose of aspirin, 80 to 325 mg, given at least 2 hours prior to an intervention. 9Pharmacologic therapy during peripheral vascu...

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