Elvan A, Pride H P, Eble J N, Zipes D P
Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis 46202-4800, USA.
Circulation. 1995 Apr 15;91(8):2235-44. doi: 10.1161/01.cir.91.8.2235.
The purpose of this study was to prevent induction of sustained atrial fibrillation (AF) by radiofrequency catheter ablation (RFCA) of the atria in an open-chest canine model.
In dogs randomized to acute studies, RFCA of the atria was performed after reproducible induction of sustained AF (lasting > 30 minutes) with burst stimulation or premature atrial pacing and perpetuation by low level cervical vagal stimulation or IV infusion of methacholine. Additionally, in four dogs, the long-term effectiveness of RFCA was assessed 7 to 21 days after ablation. Continuous discrete transmural lesions were produced with radiofrequency energy pulses (20 to 40 W for 60 seconds) delivered to five atrial epicardial sites and endovascularly to the coronary sinus wall. RFCA electrically isolated regions of the atria that became dissociated from the nonisolated parts. Atrial RFCA markedly attenuated vagally induced shortening of effective refractory period (ERP) at both isolated and nonisolated test sites located in the left and right atria (P < .001, n = 5). RFCA rendered noninducible sustained AF maintained by cervical vagal stimulation. The dose-response curve relating the dose of methacholine required to maintain AF was shifted down and to the right. AF was only inducible with high doses of methacholine. Atrial RFCA reduced the maximal sinus rate and prolonged the corrected sinus-node recovery time (P < .001, n = 6). However, RFCA did not affect atrial contractile function, AV-nodal ERP, or AV-nodal or His-Purkinje conduction times. In dogs in the chronic group, normal sinus rhythm and normal AV conduction were preserved and AF was only inducible with a high dose of methacholine. No atrial perforations resulted.
RFCA in open-chest dogs produces partial vagal denervation and reduces the inducibility of AF.
本研究的目的是在开胸犬模型中通过心房射频导管消融术（RFCA）预防持续性心房颤动（AF）的诱发。
在随机分组进行急性研究的犬中，在通过短阵刺激或房性早搏起搏可重复诱发持续性AF（持续>30分钟）并通过低水平颈迷走神经刺激或静脉注射乙酰甲胆碱使其持续存在后，进行心房RFCA。此外，在4只犬中，在消融后7至21天评估RFCA的长期有效性。通过将射频能量脉冲（20至40瓦，持续60秒）传递至五个心房心外膜部位并经血管内传递至冠状窦壁，产生连续的离散透壁损伤。RFCA使心房的电隔离区域与未隔离部分分离。心房RFCA显著减弱了位于左、右心房的隔离和未隔离测试部位的迷走神经诱导的有效不应期（ERP）缩短（P<.001，n = 5）。RFCA使由颈迷走神经刺激维持的持续性AF不能被诱发。维持AF所需的乙酰甲胆碱剂量的剂量反应曲线向下和向右移动。仅在高剂量乙酰甲胆碱时AF才可诱发。心房RFCA降低了最大窦性心率并延长了校正的窦房结恢复时间（P<.001，n = 6）。然而，RFCA不影响心房收缩功能、房室结ERP或房室结或希氏-浦肯野传导时间。在慢性组犬中，窦性心律和正常房室传导得以保留，仅在高剂量乙酰甲胆碱时AF才可诱发。未发生心房穿孔。
开胸犬的RFCA产生部分迷走神经去神经支配并降低AF的诱发性。
