Bunch T Jared, Bruce G Keith, Mahapatra Srijoy, Johnson Susan B, Miller Dylan V, Sarabanda Alvaro V, Milton Mark A, Packer Douglas L
Division of Cardiovascular disease, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, USA.
J Cardiovasc Electrophysiol. 2005 Dec;16(12):1318-25. doi: 10.1111/j.1540-8167.2005.00216.x.
The phrenic nerve can be injured with radiofrequency energy delivery. Nevertheless, the mechanisms of injury are unknown. This study was undertaken to examine phrenic nerve tissue temperatures during ablation at the pulmonary vein (PV) orifice, assess the temperature dependence of injury, and to delineate the possible mechanisms of untoward nerve effects.
Ten dogs underwent ablation at the right superior PV (RSPV) orifice. Phrenic nerve temperatures were assessed with implanted thermocouples overlying the endocardial ablation site. Using an 8-mm ablation catheter tip, energy was titrated to 50 degrees C and incremented by 5 degrees C for 120 seconds.
Phrenic nerve capture was achieved in nine (90%) dogs after thermocouple implantation. A RSPV orifice tissue temperature >60 degrees C occurred in 32 (84%) of energy deliveries with a power of 34 +/- 22 W. In three (33%) dogs, this resulted in nerve dysfunction (maximum nerve temperature: 41 degrees C, 41 degrees C, and 91 degrees C) with histology consistent with acute thermal injury. In four additional dogs, 17 energy deliveries were made directly to the phrenic nerve using a novel in situ model. In 5 (29%) energy deliveries, nerve function was impacted immediately by the generated current, with resolution simultaneous with discontinuing radiofrequency. Transient phrenic nerve injury occurred in all dogs at a temperature of 47 +/- 3 degrees C (range: 43-53 degrees C) after 38 +/- 32 seconds (range: 20-120 seconds). After termination of the energy delivery, nerve function returned in 15(88%) during 30 seconds of postablation pacing. In two (12%) ablation attempts, nerve recovery was delayed (>3 minutes). Permanent injury occurred in all dogs after 92 +/- 83 seconds (range: 20-280 seconds) of additional energy delivery at a temperature of 51 +/- 6 degrees C (range: 45-65 degrees C).
Phrenic nerve injury can be more common than anticipated with RF ablation at the RSPV orifice. Relatively low tissue temperatures can injure the nerve. Immediate nerve effects suggest a second mechanism of nerve dysfunction related to electrical current. Transient nerve effects occur prior to permanent damage, providing an opportunity to discontinue energy delivery before permanent injury.
射频能量传递可导致膈神经损伤。然而，损伤机制尚不清楚。本研究旨在检测肺静脉（PV）口部消融过程中膈神经组织的温度，评估损伤的温度依赖性，并阐明神经不良效应的可能机制。
对10只犬进行右上肺静脉（RSPV）口部消融。使用植入于心内膜消融部位上方的热电偶评估膈神经温度。使用8毫米消融导管尖端，将能量滴定至50℃，并以5℃递增，持续120秒。
植入热电偶后，9只（90%）犬实现了膈神经捕获。在34±22瓦功率的能量传递中，32次（84%）出现RSPV口部组织温度>60℃。在3只（33%）犬中，这导致神经功能障碍（最高神经温度分别为41℃、41℃和91℃），组织学检查结果与急性热损伤一致。在另外4只犬中，使用一种新的原位模型直接对膈神经进行了17次能量传递。在5次（29%）能量传递中，神经功能立即受到产生的电流影响，在停止射频时恢复。所有犬在38±32秒（范围：20 - 120秒）后，温度为47±3℃（范围：43 - 53℃）时均出现短暂性膈神经损伤。能量传递终止后，15只（88%）犬在消融后起搏30秒内神经功能恢复。在2次（12%）消融尝试中，神经恢复延迟（>3分钟）。在温度为51±6℃（范围：45 - 65℃）的情况下，额外进行92±83秒（范围：20 - 280秒）的能量传递后，所有犬均发生永久性损伤。
RSPV口部射频消融导致膈神经损伤可能比预期更常见。相对较低的组织温度即可损伤神经。即刻神经效应提示与电流相关的神经功能障碍的第二种机制。短暂性神经效应发生在永久性损伤之前，为在永久性损伤前停止能量传递提供了机会。
