Comparison of plasma concentrations of thromboxane B 2 in prinzmetal's variant angina and classical angina pectoris

Abstract We have reported that thromboxane B 2 is present in plasma of Prinzmetal's angina patients measured by radioimmunoassay but is below detection limits, <0.5 pmol/ml, in normals. To determine whether this metabolite of thromboxane A 2 (a coronary vasoconstrictor) is present in the peripheral blood in classical angina pectoris, we studied 14 patients with fixed obstructive coronary artery disease (2.5 lesions per patient) in whom angina was induced by atrial pacing. Thromboxane B 2 at rest was barely detectable (0.537±0.16 pmol/ml), but rose during pacing (0.747±0.18 pmol/ml) and was maximal (p<0.05) 5–10 min after pacing (1.237±0.36 pmol/ml). In eight variant angina patients, resting levels of thromboxane B 2 were not statistically different during spontaneous angina and angina‐free intervals (2.837±0.56 and 1.577±0.34 pmol/ml), but the mean 5–10 min after angina was higher than during angina (6.41 7±1.46 pmol). The means of preanginal, anginal, and postanginal samples were all higher than the corresponding means of the classical angina group, and thromboxane B 2 levels in variant angina patients in the absence of angina, during angina, and 5–10 min after angina were all significantly higher (p<0.025) compared to the classical angina group measured prior to pacing. Unlike the case with variant angina, thromboxane B 2 is indetectable in classical angina pectoris patients at rest. Furthermore, spontaneous angina in variant angina or pacing‐induced angina in classical angina pectoris are both followed by increased thromboxane B 2 , although the latter responses are smaller. The role of these phenomena in the pathogenesis of coronary artery spasm and ischemia remains to be clarified.