Modulation of thrombotic responses in moderately stenosed arteries by cigarette smoking and aspirin ingestion.

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Abstract
Cigarette smoking is a known risk factor for cardiovascular disease in men and women, and it has been suggested that this risk is linked to enhanced formation of platelet thromboxane A2 (TxA2). This led us to investigate the effect of cigarette smoking and TxA2 formation on collagen-induced thrombogenesis in flowing nonanticoagulated human blood. Thrombus formation in blood from smokers and nonsmokers was compared before and 2 hours after ingestion of a single oral dose of 990 mg aspirin, which is sufficient to block platelet TxA2 formation. Nonanticogulated blood was drawn directly from an antecubital vein over collagen fibrils in a parallel-plate perfusion chamber by a peristaltic roller pump placed distally to the chamber. Wall shear rates at the collagen surface were characteristic for medium-sized (650 s-1) and moderately stenosed (2600 s-1) arteries. Blood-collagen interactions were morphologically quantified, and markers of platelet release, beta-thromboglobulin (beta-TG), and activation of coagulation, fibrinopeptide A (FPA), were measured immediately distal to the perfusion chamber. The thrombus volume in blood from cigarette-smoking individuals was nearly twofold larger than in blood from nonsmokers at 2600 s-1 (37.4 and 19.4 microns 3/microns 2; P < .03). However, ingestion of aspirin reduced the thrombus volume in blood from smokers by 61.8% (P < .01), which was substantially more than the 37.6% reduction in blood from nonsmokers (P < .03). Neither cigarette smoking nor aspirin ingestion affected thrombus formation at 650 s-1. The plasma levels of FPA and beta-TG were slightly lower in nonsmokers and after aspirin ingestion.(ABSTRACT TRUNCATED AT 250 WORDS)