Kwan Y Y, Fan W, Hough D, Lee J J, Fishbein M C, Karagueuzian H S, Chen P S
Department of Medicine, Cedars-Sinai Medical Center and University of California, Los Angeles, School of Medicine, 90048, USA.
Circulation. 1998 May 12;97(18):1828-36. doi: 10.1161/01.cir.97.18.1828.
There is increasing evidence that both functional reentrant wave fronts and multiple wavelets are present during ventricular fibrillation (VF). However, the effects of procainamide on the characteristics of activation waves during VF are poorly understood.
Seven dogs were studied; six underwent subendocardial chemical ablation procedures. A plaque with 317 to 480 bipolar electrodes was sutured to the right ventricular free wall, and the patterns of activation were registered with a computerized mapping system. VF was electrically induced, and the patterns of activation were registered at baseline and during procainamide infusion (serum concentration, 9.3+/-1.9 microg/mL). Among the six dogs that had their subendocardium ablated, reentrant wave fronts were present in 6 of the 108 runs of VF at baseline and in 6 of the 100 runs of VF during procainamide infusion. By analyzing the wave fronts, we found that the cycle length, refractory period, conduction velocity, and wavelength at baseline were 101+/-9 ms, 54+/-5 ms, 0.93+/-0.21 mm/ms, and 51+/-16 mm, respectively, and during procainamide infusion, values became 125+/-11 ms (P<.001), 119+/-7 ms (P<.001), 0.42+/-0.02 mm/ms (P<.001), and 50+/-4 mm (P=.8), respectively. The vast majority of the activation waves do not form organized reentry. These activation waves broke up more frequently at baseline than during procainamide administration. The number of activation waves was 7.25+/-1.39 s(-1) x cm(-2) at baseline and 4.45+/-1.80 s(-1) x cm(-2) during procainamide administration (P<.001). The dog without subendocardial ablation had similar results.
Procainamide decreases the number of wavelets during VF by preventing spontaneous wave breaks. This represents a novel mechanism of antiarrhythmic drug action.
越来越多的证据表明，心室颤动（VF）期间存在功能性折返波前和多个小波。然而，普鲁卡因胺对VF期间激活波特征的影响尚不清楚。
对7只犬进行了研究；6只接受了心内膜下化学消融手术。将带有317至480个双极电极的斑块缝合到右心室游离壁，并使用计算机映射系统记录激活模式。电诱导VF，并在基线和普鲁卡因胺输注期间（血清浓度，9.3±1.9μg/mL）记录激活模式。在6只接受心内膜下消融的犬中，基线时108次VF发作中有6次存在折返波前，普鲁卡因胺输注期间100次VF发作中有6次存在折返波前。通过分析波前，我们发现基线时的周期长度、不应期、传导速度和波长分别为101±9毫秒、54±5毫秒、0.93±0.21毫米/毫秒和51±16毫米，普鲁卡因胺输注期间，这些值分别变为125±11毫秒（P<0.001）、119±7毫秒（P<0.001）、0.42±0.02毫米/毫秒（P<0.001）和50±4毫米（P=0.8）。绝大多数激活波未形成有组织的折返。这些激活波在基线时比普鲁卡因胺给药期间更频繁地破裂。基线时激活波的数量为7.25±1.39秒-1×厘米-2，普鲁卡因胺给药期间为4.45±1.80秒-1×厘米-2（P<0.001）。未进行心内膜下消融的犬也有类似结果。
普鲁卡因胺通过防止自发波破裂来减少VF期间的小波数量。这代表了抗心律失常药物作用的一种新机制。
