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The cardioprotective benefits of low-dose aspirin therapy are due largely to aspirin's irreversible and almost complete inhibition of thromboxane produced by blood platelets. Inhibition of thromboxane, which is a potent inducer of platelet aggregation, helps prevent blood thickening. Many nonaspirin, nonsteroidal antiinflammatory agents (NANSAIDs) inhibit the production of thromboxane and thus also inhibit platelet aggregation. However, this inhibition is reversible and appears to be less complete than that of aspirin. For example, naproxen, the most efficient NANSAID studied, suppresses the production of thromboxane and inhibits platelet aggregation by 88 percent for up to 8 hours.
On the basis of currently limited data, it would be inappropriate to withhold aspirin from patients who would otherwise qualify for NANSAID use, according to a study supported in part by the Agency for Healthcare Research and Quality (HS07768). The benefits of aspirin for secondary prevention have been confirmed in large rigorous randomized controlled trials with protection shown both for deaths related to cardiovascular disease and for all-cause mortality. Data of equal rigor would be necessary to confirm NANSAIDs as an acceptable substitute, assert Wayne A. Ray, Ph.D., and Katherine T. Murray, M.D., of Vanderbilt University School of Medicine, in a recent commentary.
The researchers point out that NANSAIDs used in higher doses inhibit synthesis of prostacyclin, a potent endogenous platelet inhibitor. This theoretically could increase the risk of coronary heart disease, as could other dose-related effects of NANSAIDs, such as hypertension. They cite several case-control studies which suggest that the protective effect of NANSAIDs—if there is one—is not as large as that for aspirin, for which a large protective effect was apparent in observational studies.
See "Aspirin: Redundant in users of nonaspirin, nonsteroidal antiinflammatory agents?" by Drs. Ray and Murray, in the March 2002 American Heart Journal 143(3), p. 381-382.
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