Kus T, Dubuc M, Lambert C, Shenasa M
Clinical Electrophysiology Laboratory, Hôpital du Sacré-Coeur, Montreal, Quebec, Canada.
J Am Coll Cardiol. 1990 Nov;16(5):1229-37. doi: 10.1016/0735-1097(90)90558-7.
The efficacy of propafenone in preventing induction of ventricular tachycardia was evaluated in 25 consecutive patients (mean age 62 +/- 8 years) with remote myocardial infarction who underwent programmed electrical stimulation for ventricular arrhythmia using up to three extra-stimuli after basic drive at the right ventricular apex. In nine patients (Group A), propafenone prevented induction of sustained ventricular tachycardia (noninducible in four, nonsustained [less than 30 s] in five). In the other 16 patients (Group B), sustained ventricular tachycardia was still inducible; in 11 of the 16, the tachycardia configuration was unchanged but the cycle length was significantly longer (431 +/- 99 versus 284 +/- 44 ms, p less than 0.001). Propafenone did not significantly affect either sinus cycle length or AH and HV intervals. However, it prolonged QRS duration during sinus rhythm equally in both groups of patients. With ventricular pacing, propafenone also prolonged right ventricular effective and functional refractory periods and surface QRS duration. There was greater lengthening of the paced surface QRS duration when drug therapy was ineffective (for example, +35 +/- 12 ms in Group A versus +69 +/- 23 ms in Group B at a basic drive of 400 ms, p less than 0.01). Drug-induced prolongation of a paced QRS complex greater than 40 ms had a 94% positive predictive value for drug failure to prevent induction of ventricular tachycardia. Drug-induced percent prolongation of ventricular tachycardia cycle length in Group B did not correlate well with percent QRS prolongation.(ABSTRACT TRUNCATED AT 250 WORDS)
在25例有陈旧性心肌梗死的连续患者(平均年龄62±8岁)中,评估了普罗帕酮预防室性心动过速诱发的疗效。这些患者因室性心律失常接受了程控电刺激,在右心室尖部基础驱动后使用多达三个额外刺激。在9例患者(A组)中,普罗帕酮预防了持续性室性心动过速的诱发(4例不能诱发,5例为非持续性[小于30秒])。在另外16例患者(B组)中,持续性室性心动过速仍可诱发;在这16例中的11例中,心动过速形态未改变,但周长显著延长(431±99对284±44毫秒,p<0.001)。普罗帕酮对窦性周期长度或AH及HV间期均无显著影响。然而,它在两组患者的窦性心律期间均同样延长了QRS时限。在心室起搏时,普罗帕酮也延长了右心室有效和功能不应期以及体表QRS时限。当药物治疗无效时,起搏体表QRS时限延长更明显(例如,在400毫秒基础驱动时,A组为+35±12毫秒,B组为+69±23毫秒,p<0.01)。药物诱发的起搏QRS波群延长大于40毫秒对药物预防室性心动过速诱发失败有94%的阳性预测价值。B组中药物诱发的室性心动过速周长延长百分比与QRS延长百分比相关性不佳。(摘要截短于250字)