Antiplatelet Therapy for Transient Ischemic Attack

Authors

  • Maria Czarina Acelajado MD,

    1. From the Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL
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  • Suzanne Oparil MD

    1. From the Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL
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Suzanne Oparil, MD, Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, University of Alabama at Birmingham, 1034 Zeigler Research Building, ZRB 1034, 1530 3rd Avenue South, Birmingham, AL 35294-0007
E-mail:suzanne.oparil@ccc.uab.edu

Abstract

J Clin Hypertens (Greenwich).****;**:**–**. ©2011 Wiley Periodicals, Inc.

Transient ischemic attack (TIA) is currently defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia without infarction. TIA is an important risk factor for stroke and other major vascular events. Risk factors for TIA or stroke need to be addressed effectively to reduce the risk for stroke in patients who have had a TIA. Aspirin (ASA) significantly reduces the risk for stroke when given after a TIA, stroke, or myocardial infarction in a dose of 50 mg/d to 325 mg/d. The role of ASA in the primary prevention of TIA or stroke, however, is less well-substantiated. Clopidogrel may be used in the secondary prevention of TIA or stroke, but its antiplatelet effect may be reduced in poor metabolizers of the drug. The combination of ASA and extended-release dipyridamole is effective in reducing risk for TIA and stroke, and may confer additional risk-lowering without an increased risk of bleeding compared with ASA alone. ASA monotherapy, clopidogrel alone, or the combination of ASA and extended-release dypiridamole are all acceptable options for initial therapy in patients with a TIA and stroke, and the combination of ASA plus extended-release dypiridamole is recommended over ASA alone.

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