EFFECTS OF OXYFEDRINE ON REGIONAL MYOCARDIAL BLOOD-FLOW IN PATIENTS WITH CORONARY-ARTERY DISEASE

Medical treatment of angina pectoris is largely based on the use of beta-blocking agents, calcium antagonists, and nitrates. Oxyfedrine, an amino ketone derivative and partial agonist at beta receptors, has been shown to have potent antianginal properties and to increase coronary blood flow in normal and ischemic myocardial regions in experimental studies. We assessed the effects of intravenous oxyfedrine on regional myocardial blood flow, using positron emission tomography (15-oxygen water), in six patients with chronic stable angina, positive exercise tests, and documented coronary artery disease. Myocardial blood flow was measured in all patients before (baseline) and 10 minutes after the intravenous administration of a single bolus (0.11-0.13 mg/kg) of oxyfedrine. Compared to baseline, heart rate and systolic blood pressure remained almost unchanged after the administration of oxyfedrine. Mean baseline myocardial blood flow was 0.90 +/- 0.15 ml/g/min in areas supplied by arteries with significant coronary stenosis and 1.08 +/- 0.19 ml/g/min in areas supplied by nonstenotic coronary vessels (p < 0.05). After the administration of oxyfedrine, myocardial blood flow increased significantly in both the regions supplied by stenotic vessels (by 25%; from 0.90 +/- 0.15 to 1.20 +/- 0.31 ml/g/min; p = 0.002) and in areas supplied by angiographically normal coronary vessels (by 22%; from 1.08 +/- 0.19 to 1.38 +/-0.49 ml/g/min; p < 0.05). The results of this study indicate that in patients with coronary artery disease, intravenous oxyfedrine significantly increases regional myocardial blood flow, both in areas supplied by critically obstructed vessels and in areas supplied by normal or less severely narrowed coronary arteries.