To clarify the role of thromboxane A
2 (TXA
2) in evoking coronary spasm, we compared coronary arterial spasticity induced by ergonovine maleate (EM) with coronary sinus thromboxane B
2 (TXB
2: a stable catabolite of TXA
2) in 34 patients with documented variant angina and 11 patients with chest pain syndrome (CPS). We also examined the effect of OKY-1581 ( 8 mg/kg, i.v), a TXA
2 synthetase inhibitor, on the coronary arterial spasticity of these patients. When blood samples were taken from coronary sinus just before EM test, all patients with variant angina exhibiting markedly augmented TXB
2 levels (424±138 pg/ml), had positive EM test results, while CPS exhibiting lower TXB
2 levels (223±38 pg/m), had negative EM test. We found that the amounts of EM needed to induce coronary spasm were inversely correlated with TXB
2 levels in coronary sinus. In 7 out of these 8 patients, OKY-1581 was found to attenuate the increased spasticity with reduction of coronary sinus TXB
2 levels. In 3 patients, an EM rechanllenge at symptomatically quiescent stage resulted in negative test with augmented TXB
2 levels being markedly decreased. These findings indicate that increased TXA
2 in circulating plasma is closely correlated with the hypersensitivity of coronary arteries to EM in patients with variant angina, suggesting a possible role of augmented TXA
2 production in the enhancement of coronary vascular spasticity.
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