Chorro F J, Sanchis J, Such L, García-Civera R, Llavador E, Mainar L, Cánoves J, Egea S, Cerdá M, López-Merino V
Service of Cardiology, Valencia University Clinic Hospital, Spain.
Pacing Clin Electrophysiol. 1998 Apr;21(4 Pt 1):659-68. doi: 10.1111/j.1540-8159.1998.tb00121.x.
The electrophysiological effects of RF ablation upon the areas in proximity to the lesioned zones have not yet been well characterized. An experimental model is used to investigate atrial conduction in the boundaries of RF damaged zones. In 11 isolated and perfused rabbit hearts, endocardial atrial electrograms were recorded using an 80-lead multiple electrode positioned in the left atrium. Both before and after the RF application (5 W, 8 s, 1-mm diameter unipolar epicardial electrode) in the mid-portion of the free left atrial wall, measurements were made of conduction time from the pacing zone (posterior wall of the left atrium) to three points between 7.5 and 7.9 mm distal to the damaged zone. Conduction velocity and the direction of the activation propagation vector were determined in ten groups of four electrodes positioned around the damaged zone, and at the left atrial appendage. The mean diameter (+/- SEM) of the transmural lesions produced by RF ablation and defined by macroscopic examination was 4.2 +/- 0.2 mm. The conduction times to the three points distal to the lesion site were significantly prolonged as a result of RF ablation; 7.6 +/- 0.4, 7.4 +/- 0.5, and 6.9 +/- 1.0 ms (control); and 11.3 +/- 1.0 (P < or = 0.01), 11.1 +/- 1.3 (P < 0.01), 10.6 +/- 1.4 ms (P < 0.05) (post-RF). The differences between the conduction velocities determined in the areas surrounding the lesion, before and after RF application, failed to reach statistical significance: 86.2 +/- 6.5 cm/s (control) versus 75.5 +/- 5.7 cm/s (post-RF) (NS). After RF, significant variations were only observed in the direction of impulse propagation in the proximal-inferior quadrant adjacent to the lesion site, the difference being -61 degrees +/- 18 degrees (P < 0.02). In 2 of 4 experiments in which the lesion size was increased by a second RF application (5 W, 16 s), tachycardias with activation sequence around the lesion could be induced, with cycle lengths of 56 and 50 ms, respectively. In the atrial wall, the conduction times to the regions distal to the RF lesion are significantly prolonged. No significant changes are observed in conduction velocity in the areas in proximity to the lesion. Prolonged conduction to the areas distal to the ablation site is due to the lengthened pathway traveled by the impulses in reaching these areas. Tachycardias with activation patterns that suggest reentry around the RF damaged zone may be induced.
射频消融对损伤区域附近区域的电生理效应尚未得到充分表征。采用实验模型研究射频损伤区域边界处的心房传导。在11个离体灌流兔心脏中,使用置于左心房的80导联多电极记录心内膜心房电图。在左心房游离壁中部施加射频(5W,8s,1mm直径单极心外膜电极)前后,均测量从起搏区(左心房后壁)到损伤区远端7.5至7.9mm之间三个点的传导时间。在围绕损伤区以及左心耳的十组四个电极处测定传导速度和激动传播向量的方向。通过宏观检查确定的射频消融产生的透壁损伤平均直径(±SEM)为4.2±0.2mm。由于射频消融,损伤部位远端三个点的传导时间显著延长;对照时分别为7.6±0.4、7.4±0.5和6.9±1.0ms;射频消融后分别为11.3±1.0(P≤0.01)、11.1±1.3(P<0.01)、10.6±1.4ms(P<0.05)。射频施加前后在损伤周围区域测定的传导速度差异未达到统计学显著性:对照时为86.2±6.5cm/s,射频消融后为75.5±5.7cm/s(无显著性差异)。射频消融后,仅在与损伤部位相邻的近下象限观察到冲动传播方向有显著变化,差异为-61°±18°(P<0.02)。在4个实验中的2个中,通过第二次施加射频(5W,16s)增大损伤大小,可诱发围绕损伤的激动顺序的心动过速,其心动周期长度分别为56和50ms。在心房壁中,到射频损伤远端区域的传导时间显著延长。在损伤附近区域未观察到传导速度有显著变化。到消融部位远端区域的传导延长是由于冲动到达这些区域所经过的路径延长所致。可能诱发具有提示围绕射频损伤区折返的激动模式的心动过速。