An imbalance between the excretion of thromboxane and prostacyclin metabolites in women after the menopause.

An increase in the incidence of cardiovascular disease has generally been observed in postmenopausal women. Because thromboxane A2 is both vasoconstrictor and a potent stimulus for platelet aggregation, it may be an important mediator of atherosclerosis. Its effects are antagonized by prostacyclin. We tested the hypothesis that there may be an imbalance between the release of thromboxane A2 and prostacyclin in women after menopause. We used radioimmunoassays to measure the 24-hour urinary excretion of two stable metabolites of thromboxane A2 and a metabolite of prostacyclin in 106 postmenopausal women and in 105 premenopausal women, both aged 45 to 55 years. The 24-hour excretion of 11-dehydro-thromboxane B2 (a stable metabolite of thromboxane A2) was increased in postmenopausal women whereas the 24-hour excretion of 2,3-dinor-6-keto-prostaglandin F1 alpha (a stable metabolite of prostacyclin) was decreased. Whether the imbalance in the release of these mediators is a cause or a result of atherosclerosis is unknown, but it may play a part in the development of this disorder.