Key result
Intravenous propranolol (0.1 mg/kg) neither potentiated nor attenuated nitroglycerin-induced increases in regional coronary blood flow in patients with normal or diseased coronary arteries.
Why the study?
Does intravenous propranolol affect nitroglycerin-induced augmentation of regional coronary blood flow in patients with or without severe coronary artery disease?
Does intravenous propranolol affect nitroglycerin-induced augmentation of regional coronary blood flow in patients with or without severe coronary artery disease?
Concomitant use of beta blockade does not limit nitroglycerin-induced vasodilatory responses in regions supplied by normal or diseased coronary arteries.
May support combined beta-blocker and nitroglycerin use; hypothesis-generating pending larger trials.
Although beta‐adrenergic blockade may increase coronary vascular resistance in some patients with severe ischemic heart disease, the effects of beta blockade on the nitroglycerin (NTG)‐induced augmentation of coronary blood flow have not been elucidated. Therefore, systemic hemodynamic and anterior left ventricular regional coronary bloodflow (thermodilution) data were measured during administration of NTG into the left coronary artery, before and 10 min after intravenous propranolol (0.1 mg/kg) in 22 patients. Six patients (Group 1) had normal left coronary arteries and nine (Group 2) had severe coronary artery disease with at least >70% narrowing of the left anterior descending artery. In seven additional patients (three without and four with >70% left anterior descending coronary artery disease), measurements were obtained with constant‐paced heart rates (Group 3). Before beta blockade, NTG (200 mcg) significantly increased anterior regional great‐vein flow [for Group 1, 84 ± 38% (81 ± 20 to 140 ± 60 ml/min); Group 2, 39 ± 41% (61 ± 26 to 83 ± 38 ml/min); and Group 3, 87 ± 55% (75 ± 36 to 144 ± 86 ml/min)]. In Groups 1 and 2, beta‐adrenergic blockade reduced heart rate 10% (p<0.01) but did not affect mean arterial or pulmonary artery pressures. After beta blockade, although control great cardiac vein flow was reduced only for Group 2 (58 ± 23 to 50 ± 15 ml/min, p<0.05), the hyperemic responses to NTG were unaffected (99 ± 47% 46 ± 23%, and 83 ± 73% for the three groups, respectively). These findings indicate that beta‐adrenergic blockade neither potentiates nor attenuates NTG‐induced increases in coronary blood flow and that the concomitant use of beta blockade does not appear to limit NTG‐induced vasodilatory responses in regions supplied by normal or diseased coronary arteries
No takes yet. Share an insight, caveat, or question.
Miller et al. (1988) studied Ischemic heart disease (n=22). Propranolol and Nitroglycerin vs. Baseline (before beta blockade) was evaluated on Nitroglycerin-induced augmentation of regional coronary blood flow. Intravenous propranolol (0.1 mg/kg) neither potentiated nor attenuated nitroglycerin-induced increases in regional coronary blood flow in patients with normal or diseased coronary arteries.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: