Coltorti F, Bardy G H, Reichenbach D, Greene H L, Thomas R, Breazeale D G, Alferness C, Ivey T D
Circulation. 1985 Sep;72(3):612-22. doi: 10.1161/01.cir.72.3.612.
In a series of 12 dogs, the electrophysiologic and histologic effects of a single damped sine-wave shock delivered via standard electrocatheters to the region of the coronary sinus orifice were investigated. Six dogs received 200 J and six received 360 J of stored energy. The shock was delivered to two consecutive proximal poles of a standard quadripolar catheter positioned at the coronary sinus orifice and connected to the positive output (anode) of a defibrillator. A disc electrode positioned on the anterior chest wall served as the cathode (negative pole). During the shock, voltage and current were recorded. Electrophysiologic testing was done before and 4 weeks after the shock. At 4 weeks, animals were killed and serial sections of the atrioventricular groove and conduction system were performed. No significant long-term change in atrioventricular conduction, spontaneous or induced atrial or ventricular arrhythmias was observed. However, transient atrioventricular block was seen in five and idioventricular rhythms in six animals in the short term. No persistent electrocardiographic changes were observed, and no sudden deaths occurred. Microscopically, transmural injury at the anulus proper or basilar ventricular epicardium was inconstant and infrequent. However, transmural atrial injury at the level of the coronary sinus was produced over a 10 +/- 5 mm length with the 200 J shock and a 21 +/- 6 mm length with the 360 J shock. Neither coronary artery injury nor damage to the conduction system was seen and cardiac tamponade did not occur. However, localized intramural atrial rupture of the coronary sinus wall (on the endocardial aspect only) was observed in each dog, consistent with barotrauma. With the present technique, atrial injury potentially capable of blocking the effects of accessory pathway conduction could be produced without other electrophysiologic alterations or complications. Injury to the anulus proper (and therefore to any accessory pathway per se) is probably unlikely. Barotrauma may play a significant role in the type of injury observed in this study.
在一组12只犬中，研究了通过标准电导管向冠状窦口区域施加单次阻尼正弦波电击的电生理和组织学效应。6只犬接受200焦耳的储能，6只接受360焦耳的储能。电击施加于位于冠状窦口的标准四极导管的两个连续近端电极，并连接到除颤器的正输出端（阳极）。置于前胸壁的盘状电极作为阴极（负极）。电击期间记录电压和电流。在电击前和电击后4周进行电生理测试。4周时，处死动物并对房室沟和传导系统进行连续切片。未观察到房室传导、自发或诱发的房性或室性心律失常有明显的长期变化。然而，短期内5只动物出现短暂性房室传导阻滞，6只动物出现心室自主节律。未观察到持续的心电图变化，也未发生猝死。显微镜下，瓣环本身或基底心室心外膜的透壁损伤不恒定且不常见。然而，200焦耳电击时，冠状窦水平的透壁心房损伤长度为10±5毫米，360焦耳电击时为21±6毫米。未观察到冠状动脉损伤或传导系统损伤，也未发生心脏压塞。然而，在每只犬中均观察到冠状窦壁的局限性壁内心房破裂（仅在心内膜面），符合气压伤。采用本技术，可产生可能能够阻断旁路传导效应的心房损伤，而无其他电生理改变或并发症。瓣环本身（以及因此任何旁路本身）可能不太可能受到损伤。气压伤可能在本研究观察到的损伤类型中起重要作用。
