LOW-DOSE ASPIRIN DOES NOT LOWER IN-VIVO PLATELET ACTIVATION IN HEALTHY SMOKERS

Smoking causes atherosclerosis, and smelters have increased thromboxan e (TXA(2)) formation. As aspirin inhibits TXA(2) production we specula ted that smokers would preferentially profit from inhibition of the TX A(2) pathway by aspirin. Increased expression of P-selectin, a constit uent of the alpha-granules of platelets, and increased levels of circu lating (c)P-selectin in plasma are markers for platelet activation. Th e aim of this study was to compare P-selectin expression on platelets between smelters and nonsmokers, and to compare with placebo the effec t of 2 weeks administration of 100 mg/d aspirin on platelet activation in smokers. Smokers exhibited higher P-selectin expression on platele ts than nonsmokers (2.7 +/- 1.8% v 1.6 +/- 0.6%, P = 0.018), thus conf irming increased platelet activation. Aspirin did not reduce platelet activation as demonstrated by unchanged P-selectin expression on plate lets and cP-selectin plasma levels.