Wietholt D, Alberty J, Hindricks G, Vogt B, Haverkamp W, Blasius S, Gülker H, Breithardt G
Hospital of the Westfälische Wilhelms University of Münster, Department of Cardiology and Angiology, Federal Republic of Germany.
Pacing Clin Electrophysiol. 1992 Jan;15(1):52-9. doi: 10.1111/j.1540-8159.1992.tb02901.x.
Laser-photocoagulation (LPC) of arrhythmogenic myocardium has been reported to successfully ablate ventricular tachycardia. The purpose of this study was to investigate the acute hemodynamic and electrophysiological effect of continuous laser energy (Nd:YAG, 1060 nm) applied via a 0.4-mm quartz fiberoptic on the epicardial surface of the heart in nine dogs. A total of 51 +/- 2.3 pulses was delivered in each animal to induce homogeneous tissue necrosis. Applied energy was 12.3 +/- 2.7 J/mm2, irradiated surface measured 12.6 +/- 3.0 cm2, lesion depth was 6.3 +/- 1.2 mm (range: 5.0-8.1 mm), lesion volume was 8.1 +/- 2.8 cm3 (6.8% of left ventricular [LV] mass). After LPC, epicardial stimulation threshold significantly rose from 1.0 +/- 0.3 to 10.2 +/- 4.9 mA in the border zone to nontreated tissue and from 0.9 +/- 0.4 to 32 +/- 15.7 mA in the center of the lesions. Loss of epicardial activation in the irradiated areas could be demonstrated by epicardial mapping. Ventricular extrasystoles during LPC were seen in all dogs, ventricular tachycardia in seven, and ventricular fibrillation in two dogs. After LPC, cardiac output and LV dP/dtmax significantly decreased by 14.2% and 11.2%. LPC induced predictable homogeneous tissue edema, eosinophilic staining, contraction band necrosis, and sharp demarcated hemorrhagic border zones with a sharp electrical border zone to nontreated tissue and loss of epicardial activation. During LPC, various arrhythmogenic effects could be observed. However, no persistent arrhythmic activity developed after LPC. The results confirm the feasibility of epicardial LPC of the myocardium. Although not rested in this study, LPC of arrhythmogenic tissue may also be feasible as a treatment modality of ventricular tachycardia.
据报道，对致心律失常心肌进行激光光凝术（LPC）可成功消融室性心动过速。本研究的目的是探讨通过0.4毫米石英光纤将连续激光能量（Nd:YAG，1060纳米）施加于9只犬心脏的心外膜表面的急性血流动力学和电生理效应。每只动物共输送51±2.3个脉冲以诱导均匀的组织坏死。施加的能量为12.3±2.7焦耳/平方毫米，照射面积为12.6±3.0平方厘米，病变深度为6.3±1.2毫米（范围：5.0 - 8.1毫米），病变体积为8.1±2.8立方厘米（占左心室[LV]质量的6.8%）。LPC后，在心外膜刺激阈值方面，病变边缘至未处理组织区域显著从1.0±0.3毫安升至10.2±4.9毫安，病变中心则从0.9±0.4毫安升至32±15.7毫安。通过心外膜标测可证明照射区域的心外膜激活丧失。所有犬在LPC期间均出现室性期前收缩，7只出现室性心动过速，2只出现心室颤动。LPC后，心输出量和LV dP/dtmax显著降低14.2%和11.2%。LPC诱导出可预测的均匀组织水肿、嗜酸性染色、收缩带坏死以及界限清晰的出血性边缘区，与未处理组织有明显的电边界区且心外膜激活丧失。在LPC期间，可观察到各种致心律失常效应。然而，LPC后未出现持续性心律失常活动。结果证实了心外膜心肌LPC的可行性。尽管本研究未对此进行验证，但对致心律失常组织进行LPC作为室性心动过速的一种治疗方式可能也是可行的。
