- Thromboxane release in coronary artery disease: Spontaneous versus pacing-induced angina To determine thromboxane A2 release in coronary artery disease, we measured its stable metabolite thromboxane B2 by radioimmunoassay in 20 patients. In 15 patients with stable disease (last angina episode >96 hours before study), coronary venous thromboxane Bz concentrations were lower than in aortic blood (mean 109 f 36 vs 194 t- 40 pg/ml, p < 0.001). In contrast, in five other patients with spontaneous angina, coronary venous thromboxane B2 concentrations were higher than aortic thromboxane B2 concentrations during the angina episode (mean 1716 f 316 vs 875 f 388 pg/ml, p < 0.02). Plasma thromboxane Bz levels were in the normal range (mean 175 f 35 pg/ml) in patients with stable angina but significantly (p < 0.02) higher in patients with spontaneous angina. With atrial pacing to the point of chest pain and/or ECG changes in patients with stable coronary artery disease, aortic thromboxane B, concentrations increased in 10 of 13 patients (mean 283 f 70 pg/ml, p < 0.02). Coronary venous thromboxane Bz concentrations increased in seven patients at peak pacing rates (mean 223 + 76 pg/ml) and in three other patients after termination of pacing. These data indicate that release of thromboxane A2 is much greater during spontaneous angina than with pacing stress in patients with coronary artery disease. Thromboxane A2 released during spontaneous or pacing-induced angina may modulate coronary and systemic vascular tone. Enhanced thromboxane A2 activity may either precede or follow myocardial ischemia and could be a factor in the initiation and propagation of the ischemic episode. (AM HEART J 107:286, 1984.) Jawahar Mehta, M.D., Paulette Mehta, M.D., Robert L. Feldman, M.D., and Christine Horalek. Gainesville, Fla. Evidence has been accumulating that platelets may play a role in the propagation and manifestations of coronary heart disease. l-4 It is believed that certain prostaglandins of platelet and vessel wall origin are of importance in maintenance of vascular tone and platelet homeostasis. 3-6 Platelet-derived thrombo- xane AZ, a very potent vasoconstrictor and platelet proaggregant, has been reported to be increased in patients with stable coronary artery disease.7-8 Inap- propriate increase in thromboxane A, in peripheral and coronary venous blood has been described dur- ing exercise-induced, pacing-induced, and at times spontaneous myocardial ischemia in certain patients8-” However, whether increases in thrombo- From the Departments of Medicine and Pediatrics, University of Florida College of Medicine, and the Veterans Administration Medical Center. Supported in part by grants from the American Heart Association, Florida Affiliate, and by a National Institutes of Health Research Career Award (Dr. Feldman). Received for publication Oct. 1, 1982; accepted Nov. 3, 1982. Reprint requests: Jawahar Mehta, M.D., JHM Health Center, Box J-277, University of Florida, Gainesville, FL 32610. xane A2 precede myocardial ischemia or occur as a result of myocardial ischemia is much debated. The purpose of this study was to determine thromboxane A, concentrations in aortic and coro- nary venous blood in a variety of patients with coronary artery disease. The alterations in thrombo- xane A, release under the influence of atrial pacing stress were compared to those during spontaneous angina to define relative coronary and noncoronary contributions. The observations made from this study indicate that release of thromboxane A2 may be of more significance in the pathogenesis of spon- taneous angina than in stable angina. METHODS Patients. Twenty male patients, aged 32 to 70 years (mean 55 2 5), undergoing routine cardiac catheterization were included in this study. All patients gave informed consent before the study, which was approved by the Institutional Review Committees. None of the patients included had taken aspirin, dipyridamole, sulfinpyrazone, or other pro&&din-active drugs in the preceding 7 days. Thirteen patients were taking beta-adrenergic blockers. Eight patients were also receiving long-acting nitrate therapy. The last dose of beta blockers or nitrates 286