Engel T R, del Gonzalez A, Meister S G, Franki W S
Clin Pharmacol Ther. 1978 Sep;24(3):274-82. doi: 10.1002/cpt1978243274.
Ventricular extrastimulation was performed in 11 patients evaluated for chronic recurrent ventricular tachycardia, before and after a 1-gm procainamide infusion. Extrastimulation caused only nonsustained extra beats (less than 4) in 3 patients. Sustained tachycardia was induced in 7 patients in the basal state, of which 6 continued to have inducible tachycardia after procainamide was given (5.2 to 9.8 mg/L). The zone of coupling intervals that initiated tachycardia was unchanged or widened in these 6 patients because ventricular refractoriness was unchanged or because the tachycardia zone shifted to later diastole by an interval at least equivalent to the prolongation of ventricular refractoriness. Post-procainamide tachycardia cycle length was prolonged in all patients, by an average 51 msec. The one patient who responded to procainamide had a shortened ventricular refractory period, but the greatest slowing of tachycardia. Finally, sustained ventricular tachycardia could be induced in the eleventh patient only following procainamide administration, consistent with his clinical history. These results suggest that procainamide often may be ineffective in preventing sustained ventricular tachycardia, and that slowed conduction, rather than prolonged refractoriness, is the basis for the procainamide antiarrhythmic effect. Our data emphasize that antiarrhythmic drug effectiveness be evaluated in terms of effect on sustained arrhythmia rather than suppression of isolated ectopic beats.
对11例因慢性复发性室性心动过速而接受评估的患者,在静脉输注1克普鲁卡因胺前后进行心室额外刺激。额外刺激仅在3例患者中引发了非持续性额外心搏(少于4次)。在基础状态下,7例患者诱发了持续性心动过速,其中6例在给予普鲁卡因胺(5.2至9.8毫克/升)后仍可诱发心动过速。在这6例患者中,引发心动过速的配对间期区域未改变或增宽,这是因为心室不应期未改变,或者是因为心动过速区域转移至舒张晚期,其间隔至少相当于心室不应期的延长。所有患者在给予普鲁卡因胺后的心动过速周期长度均延长,平均延长51毫秒。对普鲁卡因胺有反应的那例患者心室不应期缩短,但心动过速减慢最为明显。最后,第11例患者仅在给予普鲁卡因胺后才诱发了持续性室性心动过速,这与他的临床病史相符。这些结果表明,普鲁卡因胺在预防持续性室性心动过速方面通常可能无效,并且传导减慢而非不应期延长是普鲁卡因胺抗心律失常作用的基础。我们的数据强调,抗心律失常药物的有效性应根据其对持续性心律失常的影响而非对孤立性异位搏动的抑制来评估。