Inhibition of platelet aggregation by prostacyclin is attenuated after exercise in patients with angina pectoris

Abstract

We tested whether alteration of platelet sensitivity to prostacyclin (PGI 2) is involved in the activation of platelets induced by exercise in patients with stable angina. Twenty patients and 20 control subjects underwent treadmill testing. Blood samples were obtained before and immediately after exercise for plasma thromboxane B 2 (TXB 2) and 6-keto-PGF 1α (6kP) assays and platelet aggregation studies. Dose-response curves for platelet aggregation to coliagen were obtained in the presence and absence of 1 nmol/L PGI 2 to quantify the antiaggregation effects of PGI 2. At rest, platelet aggregation by collagen was enhanced in the patients. However, platelets were more sensitive to exogenous PGI 2, apparently associated with lower plasma 6kP levels in the patients. After exercise, plasma TXB 2 levels increased in the patients but not in the control subjects. Plasma 6kP levels remained unchanged and platelet sensitivity to PGI 2 decreased in the patients whereas these values increased in the control subjects. The exercise-induced changes in platelet sensitivity to PGI 2 correlated with those of platelet adenylate cyclase activity in response to 1 nmol/L PGI 2 ( r = 0.787, p < 0.01). Thus impaired sensitivity of platelets to PGI 2, in addition to the reduced response of prostanoid secretion, might be relevant to the platelet activation associated with exercise in patients with stable angina.