Abstract
Nitroglycerin (NTG) and nifedipine (NIF) have the potential to augment coronary blood flow in addition to reducing peripheral determinants of myocardial oxygen demand as a synergistic protective mechanism during ischemia. To examine these effects, systemic and coronary hemodynamic responses were measured continuously before and during brief periods of myocardial ischemia induced by left anterior descending coronary balloon occlusion in 26 patients undergoing angioplasty (PTCA). Data were compared for two matched occlusion periods, one control and one “drug” occlusion. In 17 patients (NTG group), 200 μg of intracoronary NTG was given immediately before coronary occlusion. In nine patients (NIF group), 10 mg of sublingual NIF was given 15 minutes before the “drug” occlusion. NTG significantly but transiently reduced mean arterial pressure (91 ± 11 to 82 ± 15 mm Hg, p < 0.05) and augmented basal coronary blood flow (95 ± 38 to 127 ± 54 ml/min, p < 0.05) but did not alter great vein blood flow (59 ± 29 vs 61 ± 29 ml/min) or coronary occlusion pressure (25 ± 7 to 24 ± 7 mm Hg) during ischemia. NIF significantly reduced systolic, diastolic, and mean arterial pressure (119 ± 21 to 95 ± 8 mm Hg, p < 0.001) and heart rate-pressure product from control. NIF maintained basal great vein blood flow (125 ± 41 to 106 ± 57 ml/min) during reduced myocardial oxygen demand, but did not affect great vein blood flow (73 ± 29 to 79 ± 37 ml/min) or coronary occlusion pressures during ischemia. Neither agent prolonged the time to ischemic ST segment alteration after the 50 to 60 second coronary flow occlusion periods. These data suggest that during the initial minutes of myocardial ischemia due to coronary occlusion, neither the coronary nor peripheral hemodynamic effects of the two vasodilators significantly improved regional coronary blood flow responses of ECG signs of myocardial ischemia. During PTCA, the beneficial effects of these agents most likely occur through mechanisms such as spasmolytic action, or indirectly by reduction of myocardial oxygen demand, more than directly augmenting coronary blood flow or collateral supply.
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