Summary
Smoking is a risk factor for the development of atherosclerotic cardiovascular disease,
in men as well as in women. An increased urinary excretion of the thromboxane metabolite
2,3-dinor-thromboxane B2 (Tx-M) has been observed in smokers of both genders, suggesting that cigarette smoking
may facilitate cardiovascular disease via an action on the platelets. The present
study addressed the hypothesis that the increased Tx-M excretion in female smokers
reflects a true facilitation of platelet reactivity in vivo, rather than an increased
destruction of the platelets. In healthy female volunteers (aged 20–46 years, 18 smokers
and 17 non-smokers) platelet life-span and indices of platelet activity were determined,
together with plasma levels of plasminogen activator inhibitor-1 (PAI-1), fibrinogen,
peripheral blood cell counts and hematocrit. The urinary excretion of Tx-M was higher
in smokers than in non-smokers (361 vs. 204 pg/mg creatinine, respectively, p <0.05), while plasma and urinary β-thromboglobulin, plasma platelet factor 4, platelet
mean life-span and platelet production rate did not differ between the groups. PAI-1
activity, white blood cell count and hematocrit were higher in smokers than in non-smokers
(p <0.05). These data indicate that smoking facilitates platelet formation of thromboxane
A2 without affecting platelet survival; i.e. it increases the activity of platelets
without affecting their viability to a measurable extent. Such an increase in platelet
activity, operating in parallel to a reduced fibrinolytic activity and a higher hematocrit
and white blood cell count, may play an etiological role in smoking-induced cardiovascular
disease in women.
