Hemodynamic and electrophysiologic effects of verapamil and nifedipine in patients on propranolol.
Hemodynamic and electrophysiologic effects of verapamil and nifedipine in patients on propranolol.
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维拉帕米和硝苯地平对普萘洛尔患者的血流动力学和电生理影响。
DOI：
10.1016/0002-9149(82)91222-x
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Hillis,LD
中科院分区：
文献类型：
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作者：
Winniford,MD;MarkhamJr,RV;Firth,BG;Nicod,P;Hillis,LD
由于β-肾上腺素能阻滞剂和钙拮抗剂的联合使用可能对严重心绞痛患者有益，我们评估了维拉帕米或硝苯地平对口服普萘洛尔患者的血流动力学和电生理学影响。26例稳定型心绞痛患者口服心得安（234 ± 230 mg/d，平均值±标准差），进行心导管检查，并在基线和（1）静脉注射生理盐水10 ml（n = 6），（2）静脉注射维拉帕米0.15 mg/kg体重至最大剂量10 mg（n = 10），（3）静脉注射生理盐水10 ml（n = 10），（4）静脉注射维拉帕米0.15 mg/kg体重至最大剂量10 mg（n = 10）后5 - 10分钟测量变量。舌下含服硝苯地平10 mg（n = 10）。心输出量（热稀释法）在生理盐水和维拉帕米后无变化，但在硝苯地平后增加（4.3 ± 1.1至5.0 ± 1.4升/分，p < 0.05）。平均动脉压没有改变与生理盐水或硝苯地平，但降低与维拉帕米。仅维拉帕米可降低峰值阳性dP/dt（从1，086 ± 175降至926 ± 167 mm Hg/s，p < 0.05）。冠状静脉窦血流量（热稀释法）不受生理盐水、硝苯地平或维拉帕米的影响。维拉帕米使心率从63 ± 8次/分降低到60 ± 9次/分（p < 0.05），A-H间期从108 ± 14 ms增加到129 ± 23 ms（p < 0.05）。与此相反，硝苯地平增加心率（从65 ± 8到71 ± 8次/分，p < 0.05），但不改变A-H间期。左心室射血分数（放射性核素心室造影）在生理盐水或维拉帕米作用下无变化，但在硝苯地平作用下增加（从0.52 ± 0.13增加到0.57 ± 0.13，p < 0.05）。总之，当给予左心室功能正常或仅轻度抑制的患者口服普萘洛尔时，硝苯地平可改善心输出量和左心室射血分数，而不影响心内充盈压或房室传导。与此相反，维拉帕米减少左心室收缩力和减缓房室传导。因此，维拉帕米和普萘洛尔的组合必须谨慎使用潜在的左心室功能障碍或传导系统疾病的患者。
Because the combined use of a beta-adrenergic blocking agent and a calcium antagonist may be beneficial in patients with severe angina, we assessed the hemodynamic and electrophysiologic effects of verapamil or nifedipine in patients receiving oral propranolol. In 26 patients with stable angina receiving oral propranolol (234 ± 230 mg/day, mean ± standard deviation), cardiac catheterization was performed, and variables were measured at baseline and 5 to 10 minutes after (1) intravenous saline solution, 10 ml (n = 6); (2) intravenous verapamil, 0.15 mg/kg body weight to a maximal dose of 10 mg (n = 10); and (3) sublingual nifedipine, 10 mg (n = 10). Cardiac output (by thermodilution) was unchanged after saline solution and verapamil but increased with nifedipine (4.3 ± 1.1 to 5.0 ± 1.4 liters/min, p < 0.05). Mean arterial pressure did not change with saline solution or nifedipine but decreased with verapamil. Peak-positive dP/dt was reduced only by verapamil (from 1,086 ± 175 to 926 ± 167 mm Hg/s, p < 0.05). Coronary sinus blood flow (by thermodilution) was not altered by saline solution, nifedipine, or verapamil. Verapamil reduced the heart rate (from 63 ± 8 to 60 ± 9 beats/min, p < 0.05) and increased the A-H interval (from 108 ± 14 to 129 ± 23 ms, p < 0.05). In contrast, nifedipine increased the heart rate (from 65 ± 8 to 71 ± 8 beats/min, p < 0.05) but did not change the A-H interval. Left ventricular ejection fraction (by radionuclide ventriculography) was unaltered by saline solution or verapamil but increased with nifedipine (from 0.52 ± 0.13 to 0.57 ± 0.13, p < 0.05). In summary, when administered to patients with normal or only mildly depressed left ventricular function who are receiving oral propranolol, nifedipine improves cardiac output and left ventricular ejection fraction without affecting intracardiac filling pressure or atrioventricular conduction. In contrast, verapamil diminishes left ventricular contractility and slows atrioventricular conduction. Thus, the combination of verapamil and propranolol must be used with caution in patients with underlying left ventricular dysfunction or conduction system disease.