Failure of thromboxane A2 blockade to prevent attacks of vasospastic angina.
Thromboxane A2 (TxA2), released by aggregating platelets, has been proposed as a potential mediator of coronary vasospasm. We studied six patients with variant angina, a clinical syndrome due to coronary vasospasm, and one patient with frequent recurrent episodes of transient ST-segment depression at rest in whom the spasm was demonstrated angiographically. All patients underwent continuous ECG monitoring for 2 days before and 2 days after a single, low, i.v. dose of aspirin (2 mg/kg), which reduced TxB2 (the stable metabolite of TxA2) to less than 3% of the control values. There were 129 transient ischemic episodes during control and 146 after aspirin, when platelet TxB2 was reduced to negligible levels. The duration, severity and incidence of symptomatic episodes were not significantly affected by TxA2 blockade. We conclude that platelet TxA2 is probably not responsible for the initiation of coronary vasospasm.
D000328:Adult; D001241:Aspirin / Q000008:administration & dosage*; D003327:Coronary Disease / Q000175:diagnosis / Q000209:etiology*; D003329:Coronary Vasospasm / Q000175:diagnosis / Q000209:etiology*; D004562:Electrocardiography; D006801:Humans; D008297:Male; D008875:Middle Aged; D013928:Thromboxane A2 / Q000037:antagonists & inhibitors* / Q000097:blood; D013929:Thromboxane B2 / Q000097:blood; D013931:Thromboxanes / Q000037:antagonists & inhibitors*
D013931:Thromboxanes; D013929:Thromboxane B2; D013928:Thromboxane A2; D001241:Aspirin