Abnormal cardiocoronary thromboxane A₂ production in patients with unstable angina

Thromboxane B₂ (TXB₂), the stable metabolite of thromboxane A₂ (TXA₂), was measured in the coronary sinus and in aortic blood before and after cold pressor test (CPT) in 21 patients suffering from ischemic heart disease (7 affected by stable effort angina and 14 by unstable angina) and in 12 patients not suffering from myocardial ischemia (control group) during coronary angiography. Aspirin (10 mg/kg intravenously) was administered before catheterization in order to prevent platelet and leukocyte TXA₂ formation. Control subjects and patients with effort angina had TXB₂ resting levels lower than unstable angina patients without a transcardiac gradient which, on the contrary, was found in unstable angina patients. Only in these patients CPT resulted in a significant TXB₂ increase more marked in the coronary sinus (from 50.0 ± 18.9 pg/ml to 73.0 ± 35.1 pg/ml, p <0.001) than in the aorta (from 33.4 ± 17.1 pg/ml to 42.6 ± 24.0 pg/ml, p <0.05), so that the transcardiac TXB₂ gradient significantly increased. In all but two unstable angina patients, TXB₂ elevation was not associated with a fall of cardiac lactate extraction. The resting and CPT-induced TXB₂ gradients were unrelated to the presence and severity of coronary angiographic lesions. These results indicate that unstable angina patients show an abnormal cardiocoronary capacity to synthesize TXA₂, which seems not to be elicited by the occurrence of myocardial ischemia.