Neuss H
Drugs. 1985;29 Suppl 4:21-5. doi: 10.2165/00003495-198500294-00005.
The acute effects of intravenous flecainide on electrically-induced paroxysmal supraventricular tachycardia and the safety and efficacy of long term prophylaxis with orally administered flecainide were assessed in 37 patients with paroxysmal supraventricular tachycardia refractory to treatment with 'conventional' antiarrhythmic drugs. Over a mean treatment period of 14.2 months, flecainide 200 to 400mg daily completely suppressed paroxysmal supraventricular tachycardia in 9 of 20 patients with paroxysmal supraventricular tachycardia due to Wolff-Parkinson-White syndrome, while 3 patients reported only transient episodes of paroxysmal supraventricular tachycardia, and 1 patient had a decreased ventricular response to chronic atrial fibrillation. Of 17 patients with paroxysmal supraventricular tachycardia due to atrioventricular nodal re-entry, flecainide 200 to 500mg daily for a mean period approaching 26 months totally prevented episodes of paroxysmal supraventricular tachycardia in 8, and reduced the frequency and duration of episodes of paroxysmal supraventricular tachycardia in 3 others. Flecainide prolonged action potential refractoriness in a few patients in each group; however, an increased frequency of occurrence of paroxysmal supraventricular tachycardia occurred due to a simultaneous decrease in the re-entry circuit conduction velocity. In both patient groups the acute electrophysiological effects of flecainide were often predictive of the long term efficacy of the drug in the prophylaxis of paroxysmal supraventricular tachycardia. Side effects usually involved the central nervous system and were most commonly manifested by disturbances in vision, balance, and taste and increased nervousness. These side effects generally subsided following 1 to 2 months' treatment with flecainide. No abnormal trends were observed in laboratory analysis of blood samples taken from patients during long term treatment with flecainide.(ABSTRACT TRUNCATED AT 250 WORDS)
对37例使用“传统”抗心律失常药物治疗无效的阵发性室上性心动过速患者，评估了静脉注射氟卡尼对电诱发的阵发性室上性心动过速的急性效应，以及口服氟卡尼进行长期预防的安全性和有效性。在平均14.2个月的治疗期内，对于20例因预激综合征导致阵发性室上性心动过速的患者，每日200至400毫克氟卡尼使9例患者的阵发性室上性心动过速完全得到抑制，3例患者仅报告有阵发性室上性心动过速的短暂发作，1例患者对慢性房颤的心室反应有所降低。在17例因房室结折返导致阵发性室上性心动过速的患者中，每日200至500毫克氟卡尼，平均治疗近26个月，8例患者的阵发性室上性心动过速发作完全得到预防，另外3例患者的阵发性室上性心动过速发作频率和持续时间有所降低。每组均有少数患者的氟卡尼使动作电位不应期延长；然而，由于折返环传导速度同时降低，阵发性室上性心动过速的发生率增加。在两组患者中，氟卡尼的急性电生理效应通常可预测该药物预防阵发性室上性心动过速的长期疗效。副作用通常累及中枢神经系统，最常见的表现为视力、平衡和味觉障碍以及紧张情绪增加。这些副作用在使用氟卡尼治疗1至2个月后通常会消退。在对长期接受氟卡尼治疗的患者采集的血样进行实验室分析时，未观察到异常趋势。（摘要截选至250词）
