Munsif A N, Saksena S
Division of Cardiology, University of Medicine and Dentistry of New Jersey, Newark.
Pacing Clin Electrophysiol. 1989 Nov;12(11):1816-26. doi: 10.1111/j.1540-8159.1989.tb01868.x.
We examined the clinical efficacy and safety of intravenous nadolol acutely, as well as chronic nadolol alone or combined with a type IA antiarrhythmic drug in 19 patients with sustained ventricular tachycardia and heart disease, mean age 62 +/- 15 years, and mean left ventricular ejection fraction 39 +/- 8%. Patients underwent electrophysiological studies in the drug-free state (control), after intravenous nadolol (dose = 0.05 mg/kg), and oral nadolol (dose = 80 mg/day) for 5 days alone or in combination with a type IA antiarrhythmic drug. Electrocardiographic and electrophysiological effects as well as ventricular tachycardia induction at electrophysiological study were analyzed. Long-term therapy with oral nadolol alone or in combination with a type IA antiarrhythmic drug was evaluated in responders. Intravenous nadolol prolonged RR and QRS intervals but had no effect on PR and QTc intervals. Oral nadolol alone tended to prolong RR intervals (P = 0.08). Oral nadolol with type IA antiarrhythmic drug prolonged RR and QTc intervals (P less than 0.001). The mean right ventricular effective refractory period tended to prolong after intravenous nadolol alone (from 251 +/- 29 to 263 +/- 25 msec, P = 0.08). Oral nadolol and type IA antiarrhythmic drugs did not prolong right ventricular effective refractory period (P = 0.3). Eighteen patients had inducible sustained ventricular tachycardia at control electrophysiological study. After intravenous nadolol, ventricular tachycardia was no longer inducible in seven patients. Ventricular tachycardia did not recur and remained noninducible in two of six patients who tolerated oral nadolol alone. Mean right ventricular effective refractory period prolonged from baseline values (from 249 +/- 30 to 271 +/- 30 msec, P less than 0.02) in patients who became noninducible on intravenous nadolol. In patients who remained inducible, mean right ventricular effective refractory period remained unchanged (from 253 +/- 29 to 258 +/- 22 msec, P greater than 0.2). In nonresponders to intravenous or oral nadolol, oral nadolol, and type IA antiarrhythmic drug suppressed ventricular tachycardia induction in two of ten patients. During follow-up, three patients continued on oral nadolol alone (one patient) or oral nadolol and type IA antiarrhythmic drug (two patients). Adverse effects resulting in nadolol discontinuation occurred in five patients. Therefore, we concluded that intravenous nadolol is effective in acute suppression of inducible ventricular tachycardia in selected patients. Oral nadolol alone or in combination with type IA antiarrhythmic drug is infrequently effective and poorly tolerated by this patient population. In addition, electrophysiological studies on intravenous nadolol do not predict the outcome of oral nadolol therapy.
我们对19例持续性室性心动过速且患有心脏病的患者（平均年龄62±15岁，平均左心室射血分数39±8%），急性静脉注射纳多洛尔以及单独长期使用纳多洛尔或联合IA类抗心律失常药物的临床疗效和安全性进行了研究。患者在无药状态（对照）下、静脉注射纳多洛尔（剂量=0.05mg/kg）后、单独口服纳多洛尔（剂量=80mg/天）5天后或联合IA类抗心律失常药物进行了电生理研究。分析了心电图和电生理效应以及电生理研究时室性心动过速的诱发情况。对有反应者评估了单独口服纳多洛尔或联合IA类抗心律失常药物的长期治疗效果。静脉注射纳多洛尔可延长RR和QRS间期，但对PR和QTc间期无影响。单独口服纳多洛尔有延长RR间期的趋势（P=0.08）。口服纳多洛尔联合IA类抗心律失常药物可延长RR和QTc间期（P<0.001）。单独静脉注射纳多洛尔后平均右心室有效不应期有延长趋势（从251±29毫秒延长至263±25毫秒，P=0.08）。口服纳多洛尔和IA类抗心律失常药物未延长右心室有效不应期（P=0.3）。18例患者在对照电生理研究时有可诱发的持续性室性心动过速。静脉注射纳多洛尔后，7例患者的室性心动过速不再能被诱发。单独耐受口服纳多洛尔的6例患者中有2例室性心动过速未复发且仍不能被诱发。静脉注射纳多洛尔后不能被诱发的患者，平均右心室有效不应期从基线值延长（从249±30毫秒延长至271±30毫秒，P<0.02）。仍能被诱发的患者，平均右心室有效不应期无变化（从253±29毫秒至258±22毫秒，P>0.2）。对静脉或口服纳多洛尔无反应者中，口服纳多洛尔和IA类抗心律失常药物在10例患者中有2例抑制了室性心动过速的诱发。在随访期间，3例患者继续单独口服纳多洛尔（1例患者）或口服纳多洛尔联合IA类抗心律失常药物（2例患者）。5例患者出现导致停用纳多洛尔的不良反应。因此，我们得出结论，静脉注射纳多洛尔对特定患者急性抑制可诱发的室性心动过速有效。单独口服纳多洛尔或联合IA类抗心律失常药物对此类患者疗效不佳且耐受性差。此外，静脉注射纳多洛尔的电生理研究不能预测口服纳多洛尔治疗的结果。
