INCREASED NUMBER OF THROMBOXANE A(2)-PROSTAGLANDIN H-2 PLATELET RECEPTORS IN ACTIVE UNSTABLE ANGINA AND CAUSATIVE ROLE OF ENHANCED THROMBIN

The current study was designed to investigate the number and affinity of platelet thromboxane A(2)/prostaglandin H-2 (TxA(2)/PGH(2)) receptors in patients with unstable angina and, if any, the role played by the increased thrombin formation that is a common finding in these patients. Measurements taken during active unstable angina but not those taken during inactive angina showed an increased number (p < 0.001), without changes in affinity, of platelet TxA(2)/PGH(2) receptors, evaluated as the binding capacity of iodine 125-PTA-OH, a stable TxA2 analogue. Moreover patients with active angina had higher plasma concentrations of fibrinopeptide A (FPA) (p < 0.0001), which were significantly related to the number of platelet TxA(2)/PGH(2) receptors (r = 0.76; p < 0.01). Heparin infusion but not aspirin treatment promptly normalized the number of TxA(2)/PGH(2) receptors and significantly reduced plasma FPA concentrations. In an in-vitro study thrombin in a concentration similar to that found in vivo significantly increased the number of platelet TxA(2)/PGH(2) receptors (p < 0.01), whereas heparin did not affect TxA(2)/PGH(2) receptors. These results have important therapeutic implications and indicate the preferential use of heparin rather than aspirin during the acute phase of unstable angina.