Effects of chronic smoking on platelet function.

Platelet function was investigated in 20 healthy cigarette smokers and 23 nonsmokers. Cigarette consumption was 1.4 +/- 0.5 packs/day (mean +/- SD) and the duration of smoking was 19 +/- 12 years. Platelet surface activation in vitro, aggregation in vivo and in vitro, as well as the release of platelet-specific proteins in vivo were evaluated. The mean number of platelet aggregates counted on an activating surface (Formvar film) was higher in smokers (80 +/- 59) than in nonsmokers (43 +/- 27) (P less than .01), indicating enhanced activity following exposure to an activating surface. Smokers who were 50 years of age or older showed an enhanced platelet aggregation following an in vitro stimulation in comparison to younger smokers (105 +/- 54 vs 54 +/- 55 aggregates) (P less than .05). Those who smoked 20 years or more also showed enhanced aggregation in comparison to those who smoked less than 20 years (112 +/- 60 vs 53 +/- 45 aggregates) (P = .02). Circulating platelets showed no significant difference among smokers and nonsmokers in the following tests: platelet aggregate ratio (0.67 +/- 0.30 vs 0.86 +/- 0.76), platelet count per mm3, (310,000 +/- 82,000 vs 278,000 +/- 78,000/mm3), levels of platelet factor 4 (9.8 +/- 5.2 vs 9.4 +/- 5.3 ng/ml), and plasma concentrations of beta-thromboglobulin (53.9 +/- 23.5 vs 49.1 +/- 25.5 ng/ml). The data suggest that chronic smoking primes platelets, causing them to aggregate more readily when exposed to an activating stimulus in vitro.