Comparison of plasma concentrations of thromboxane B₂ in prinzmetal's variant angina and classical angina pectoris

Abstract

We have reported that thromboxane B2 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 A2 (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 B2 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 B2 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 B2 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 B2 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 B2, although the latter responses are smaller. The role of these phenomena in the pathogenesis of coronary artery spasm and ischemia remains to be clarified.

Prostaglandins and Coronary Circulation

“…Elevated levels of thromboxane B, have been found in the peripheral blood in Prinzmetal's variant angina (60) and in coronary sinus blood in patients with vasotonic angina (61). Robertson et al (62) reported a five-fold increase in the concentration of coronary sinus thromboxane B, in spontaneous ischaemia.…”

Molecular Markers of Platelet Activation

“…Myocardial ischemia associated with coronary vasospasm as seen in Prinzmetal's angina is associ ated with increased levels of TxB 2 when measured during or within 5 to 10 minutes postangina. 44 Stable angina pectoris is associated with little or no elevation of platelet markers in the blood, but if a myocardial infarction in the past has resulted in left ventricular dysfunction there is an elevation of BTG. 22,59 Acute myocardial infarction results in an eleva tion of both PF4 and BTG but the PF4 levels are near normal and return to normal soon, whereas levels of BTG may remain elevated for a month or more.…”

Current Trends in Hemostatic Testing

“…Although measurement of the clot formation or dissolution has provided a means to screen hemostasis and monitor anticoagulant therapy for over a quarter of a century, it suffers from many drawbacks. 8,9,11,19,26,[35][36][37][38]43,59,61,68,69,73,78,81,85,86,93,116 Most assays only identify bleeding problems and do not necessarily provide an overall hemostatic picture for a given patient, since the individual para metric alterations vary widely (for example, activa tion of factors or consumption of inhibitors). Table 5 depicts various methods that can be used to quantitate the molecular markers of hemostatic activation.…”