Detection of reversible platelet aggregates in the blood of smokers and ex-smokers with peripheral vascular disease.

Abstract

To demonstrate that smoking increases platelet aggregation in vivo, that smoking cessation reverses platelet aggregation and that this explains, in part, why smoking perpetuates the development of peripheral vascular disease. Prospective case-control study involving three groups of patients: smokers with peripheral vascular disease, ex-smokers with peripheral vascular disease and smokers with peripheral vascular disease who quit smoking during the study. Fourteen smokers and seven ex-smokers, new patients with confirmed peripheral vascular disease, attending the vascular clinic at Fremantle Hospital between February and November, 1988. Blood samples taken weekly from all subjects for five weeks. Week 1 was taken as the baseline before smoking cessation in the six smokers who were assigned to stop smoking during the study. Platelet aggregate ratio, an indicator of in-vivo platelet aggregability where an increase in platelet aggregate ratio suggests a decrease in platelet function. Only three of six smokers stopped smoking for the duration of the study. Median platelet aggregate ratios were: smokers = 0.85 (range, 0.79-0.92) v. non-smokers = 0.93 (range, 0.91-1.00). The difference was statistically significant P less than 0.0002. The difference in platelet aggregate ratios between smokers and quitters was not statistically significant. This study demonstrated an increase in platelet aggregability in smokers compared to ex-smokers but there was no clear evidence that platelet function was fully reversed after only four weeks cessation of smoking. The data suggested that platelet function of the ex-smokers had fully reversed to normal over a longer period. This could explain the decreased incidence of complications of peripheral vascular disease in ex-smokers. The small number of patients able to quit smoking impeded this study.