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eBook details

• Title: Aspirin Responsiveness in Healthy Volunteers Measured with Multiple Assay Platforms.
• Author : Clinical Chemistry
• Release Date : January 01, 2008
• Genre: Chemistry,Books,Science & Nature,
• Pages : * pages
• Size : 188 KB

Description

Platelet inhibition induced by treatment with aspirin is a cornerstone of preventive therapy for arterial thrombotic events, reducing the risk of acute arterial thrombotic events by at least 25% in high-risk patients (1, 2). In patients with acute myocardial infarction, it also reduces mortality (3). The mechanism of the aspirin effect on platelet function is well defined. Aspirin acts through irreversible inhibition of cyclooxygenase enzyme activity in platelets and therefore reduces levels of the platelet activator thromboxane [A.sub.2] (1, 2). Many patients, however, still have acute arterial thrombotic events despite treatment with aspirin, a situation that some consider to be due to "aspirin resistance" or "aspirin nonresponsiveness." Several definitions of aspirin resistance have been proposed, including (1) a clinical definition of aspirin resistance applied to a patient that has an acute arterial thrombotic event despite aspirin therapy; (2) a definition based on ex vitro assessment of platelet activation, i.e., failure of platelets to be inhibited after aspirin therapy as measured by various platelet function tests in the clinical laboratory; and (3) a definition predicated on the failure of aspirin to inhibit thromboxane [A.sub.2] production in vivo (1, 2). Over the past decade, multiple efforts have been made to develop clinical laboratory tests that provide more meaningful measurements of aspirin effects on platelet function and thromboxane generation to study and define aspirin resistance or nonresponsiveness. The most commonly used tests include light transmittance aggregometry in response to arachidonic acid (AA LTA), the Dade Behring PFA-100 platelet function analyzer, and the VerifyNow Rapid Platelet Function Assay (Accumetrics Inc.). The most common measurements of the aspirin effect on thromboxane generation are serum thromboxane [B.sub.2] and urinary 11-dehydrothromboxane [B.sub.2] (d-Tx[B.sub.2]), [2] both metabolites of thromboxane [A.sub.2] (1, 2). Numerous studies on both normal individuals and various at-risk patient populations have led to vastly different estimates of the prevalence of aspirin nonresponsiveness, in part depending on what laboratory measure is used to define the syndrome. However, no study has evaluated all 4 of the commonly used tests for aspirin effect under well-controlled conditions so that all laboratory and clinical variables affecting test performance could be accounted for. The lack of consistency among studies has impeded the ability to define a gold standard test or method for assessing aspirin response, or even to understand whether laboratory assessment of aspirin effect is warranted (1, 2).

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