Teichman S L, Waspe L E, Matos J A, Kim S G, Fisher J D
J Am Coll Cardiol. 1985 Sep;6(3):510-7. doi: 10.1016/s0735-1097(85)80106-6.
Twelve cardiac electrophysiology centers conducted an open label prospective trial of bethanidine sulfate, an oral bretylium analog, for the prevention of ventricular tachyarrhythmias during programmed electrical stimulation. The study group included 56 patients (44 men, 12 women; mean age 60 years; 55 with structural heart disease). Sixteen patients had both ventricular tachycardia and fibrillation, 30 had ventricular tachycardia alone and 10 had ventricular fibrillation alone. Programmed stimulation on no antiarrhythmic drugs induced sustained ventricular tachycardia in 46 patients, nonsustained ventricular tachycardia in 4 patients and ventricular fibrillation in 6 patients. During programmed ventricular stimulation after 59 trials of 20 to 30 mg/kg body weight of oral bethanidine (acute dosing in 40 patients, and divided dosing over 24 hours in 19 patients), no ventricular tachyarrhythmias were inducible in 6 patients (11%), sustained ventricular tachycardia was converted to nonsustained ventricular tachycardia in 3 patients (5%), ventricular tachyarrhythmias remained inducible in 39 patients (70%) and spontaneous ventricular tachyarrhythmias occurred more frequently in 4 patients (7%). Side effects prevented repeat testing in four patients. The 10 patients presenting with only ventricular fibrillation appeared to have a higher response rate: no ventricular tachyarrhythmias were inducible in 2 patients and sustained ventricular tachycardia was converted to nonsustained ventricular tachycardia in 2 patients. Despite protriptyline administration in 54 of 59 bethanidine trials, symptomatic hypotension occurred in 30 trials (51%). In conclusion, the efficacy of bethanidine for preventing ventricular tachyarrhythmias as assessed by programmed stimulation is low. Patients presenting with only ventricular fibrillation may have a more favorable response to bethanidine sulfate. Symptomatic hypotension occurs frequently despite concomitant use of protriptyline.
12个心脏电生理中心开展了一项关于硫酸苄乙铵（一种口服的溴苄铵类似物）预防程序性电刺激期间室性快速性心律失常的开放标签前瞻性试验。研究组包括56例患者（44例男性，12例女性；平均年龄60岁；55例有结构性心脏病）。16例患者既有室性心动过速又有室颤，30例仅有室性心动过速，10例仅有室颤。在未使用抗心律失常药物的情况下，程序性刺激诱发出持续性室性心动过速46例，非持续性室性心动过速4例，室颤6例。在给予20至30mg/kg体重口服硫酸苄乙铵进行59次试验性心室刺激期间（40例患者急性给药，19例患者24小时分次给药），6例患者（11%）未诱发出室性快速性心律失常，3例患者（5%）持续性室性心动过速转变为非持续性室性心动过速，39例患者（70%）仍可诱发出室性快速性心律失常，4例患者（7%）自发性室性快速性心律失常更频繁发作。副作用导致4例患者无法重复检测。仅表现为室颤的10例患者似乎有更高的反应率：2例患者未诱发出室性快速性心律失常，2例患者持续性室性心动过速转变为非持续性室性心动过速。尽管在59次硫酸苄乙铵试验中的54次使用了丙咪嗪，但仍有30次试验（51%）出现症状性低血压。总之，通过程序性刺激评估，硫酸苄乙铵预防室性快速性心律失常的疗效较低。仅表现为室颤的患者可能对硫酸苄乙铵反应更佳。尽管同时使用丙咪嗪，症状性低血压仍频繁发生。
