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Thromboxane A2 (TXA2), a vasoconstrictive prostanoid, causes intense spasm of isolated coronary vessels and increases platelet aggregability. To define the role of TXA2, in the pathogenesis of angina pectoris, plasma levels of thromboxane B2 (TXB2), a biologically inactive product of TXAs, were determined in the coronary sinus (CS), aorta (AO) and peripheral vein of 30 patients with angina pectoris. Determinations were made by radioimmunoassay using anti-TXB2 antisera and [3HJTXB2. Acidic lipids were extracted from plasma after treatment of samples with ethylenediamine tetraacetic acid (EDTA) and indomethacin. The 18 patients with effort angina and angiographically documented coronary stenosis (> = 75%) showed a marked increase in peripheral TXB, (mean ± SD 505 ± 178 pg/mI plasma) compared with 24 normal subjects (254 ± 89 pg/ml plasma; p < 0.01). When AO and CS TXB2 levels were determined in 10 cases with simultaneous measurements of CS blood flow during atrial pacing, calculated TXB% release in coronary circulation at rest (-2.3 ± 14.8 ng/min) markedly rose during pacing-induced myocardial ischemia (34.7 ± 50.6 ng/min; p < 0.01), while in four control subjects with normal coronary arteries the values at rest (-1.0 ± 5.0 ng/min) did not change significantly at peak pacing (-1.5 ± 10.9 ng/min). All 12 patients with variant angina had a marked increase in peripheral TXB2 (802 ± 249 pg/ml plasma;p < 0.01); two of five cases who were subjected to coronary sampling showed increased TXB2 levels both in CS and AO during a spontaneous attack or attacks induced by ergonovine or by atrial pacing, which were accompanied by coronary vasospasm and fluctuation of CS blood flow. These results indicate that increased TXA2 production in the coronary circulation may be at least partly responsible for coronary vasospasm and angina.

Elevation of thromboxane B2 levels in patients with classic and variant angina Pectoris.