Augmented Platelet Reactivity and Thromboxane A_2 Production Possible Aggravating Factors in Unstable Angina : SYMPOSIUM ON PATHOGENESIS OF MYOCARDIAL INFARCTION : 49th Annual Scientific Session of Japanese Circulation Society

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We examined platelet aggregation and plasma levels of thromboxane B_2, a stable metabolite of thromboxane A_2, in patients with unstable angina and correlated these platelet indices with the response to antianginal conventional therapy such as isosorbide dinitrate and calcium channel blocker. Eight of 36 patients exhibited anginal attacks more than 5 times/week in spite of the therapy, designated refractory unstable angina, associated with augmented platelet aggregation induced by arachidonate (0.3 mM, 71 ± 3%, mean ± SEM) and collagen (2 μg/ml, 72 ± 5%), and elevated plasma levels of thromboxane B_2 (350 ± 19 pg/ml). In the remainder of the patients whose anginal attacks were effectively subsided by the therapy, platelet aggregation was much lower (arachidonate: 34 ± 9%, collagen: 31 ± 8%, p < 0.01) and plasma levels of thromboxane B_2 were also lower (295 ± 12 pg/ml, p < 0.05). To evaluate the effect of selective thromboxane A_2 blockade on clinical findings and platelet reactivity in refractory unstable angina, OKY-046 (600 mg/day, p.o.) was administered to another 14 patients with refractory unstable angina in addition to the conventional therapy. We found that platelet aggregation induced by arachidonate (71 ± 4%) and collagen (65 ± 8%) was markedly reduced (44 ± 7% and 24 ± 3%, respectively, p < 0.01) and plasma levels of thromboxane B_2 (358 ± 31 pg/ml) and thromboxane B_2 production in serum (29 ± 5 ng/ml) were also significantly reduced after OKY-046 treatment (262 ± 21 pg/ml, p < 0.05, and 1.4 ± 0.2 ng/ml, p < 0.001). In accordance with these findings, frequency of anginal attacks (8.4 ± 1.1 times/week) was markedly decreased to less than one half (3.6 ± 1.1 times/week, p < 0.01). Under these conditions, during the first month of admission occurrence of myocardial infarction in refractory unstable angina treated with OKY-046 was effectively decreased (7%) compared with that in controls (50%, p < 0.05). These results suggest that augmented platelet reactivity and thromboxane A_2 production by platelets play a key role in the pathogenesis of refractory unstable angina.
社団法人日本循環器学会の論文
1986-02-20

Augmented Platelet Reactivity and Thromboxane A_2 Production Possible Aggravating Factors in Unstable Angina : SYMPOSIUM ON PATHOGENESIS OF MYOCARDIAL INFARCTION : 49th Annual Scientific Session of Japanese Circulation Society

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