Cardiovascular Center, Taichung Veterans General Hospital, Taichung and Department of Internal Medicine, Institute of Clinical Medicine, National Yang-Ming University School of Medicine, Taipei, Taiwan.
Circ J. 2009 Dec;73(12):2214-22. doi: 10.1253/circj.cj-09-0432. Epub 2009 Sep 29.
Therapeutic hypothermia (TH, 30 degrees C) protects the brain from hypoxic injury. However, TH may potentiate the occurrence of lethal ventricular fibrillation (VF), although the mechanism remains unclear. The present study explored the hypothesis that TH enhances wavebreaks during VF and S(1) pacing, facilitates pacing-induced spatially discordant alternans (SDA), and increases the vulnerability of pacing-induced VF.
Using an optical mapping system, epicardial activations of VF were studied in 7 Langendorff-perfused isolated rabbit hearts at baseline (37 degrees C), TH (30 degrees C), and rewarming (37 degrees C). Action potential duration (APD)/conduction velocity (CV) restitution and APD alternans (n=6 hearts) were determined by S(1) pacing at these 3 stages. During TH, there was a higher percentage of VF duration containing epicardial repetitive activities (spatiotemporal periodicity) (P<0.001). However, TH increased phase singularity number (wavebreaks) during VF (P<0.05) and S(1) pacing (P<0.05). TH resulted in earlier onset of APD alternans (P<0.001), which was predominantly SDA (P<0.05), and increased pacing-induced VF episodes (P<0.05). TH also decreased CV, shortened wavelength, and enhanced APD dispersion and the spatial heterogeneity of CV restitution.
TH (30 degrees C) increased the vulnerability of pacing-induced VF by (1)facilitating wavebreaks during VF and S(1) pacing, and (2)enhancing proarrhythmic electrophysiological parameters, including promoting earlier onset of APD alternans (predominantly SDA) during S(1) pacing.
治疗性低温（30 摄氏度）可保护大脑免受缺氧损伤。然而，低温可能会增强致命性室颤（VF）的发生，尽管其机制尚不清楚。本研究旨在验证以下假说：低温增强VF 和 S1 起搏时的波破裂，促进起搏诱导的空间不同步交替（SDA），并增加起搏诱导的 VF 易感性。
本研究使用光学映射系统，在 7 只 Langendorff 灌注分离兔心的基线（37 摄氏度）、低温（30 摄氏度）和复温（37 摄氏度）时，研究了 VF 的心外膜激活。在这 3 个阶段，通过 S1 起搏测定动作电位时程（APD）/传导速度（CV） restitution 和 APD 交替（n=6 个心脏）。在低温时，VF 中含有心外膜重复活动（时空周期性）的持续时间百分比更高（P<0.001）。然而，低温增加了VF（P<0.05）和 S1 起搏（P<0.05）时的位相奇点数量（波破裂）。低温导致 APD 交替的更早出现（P<0.001），主要为 SDA（P<0.05），并增加了起搏诱导的 VF 发作（P<0.05）。低温还降低了 CV，缩短了波长，并增强了 APD 离散度和 CV restitution 的空间异质性。
低温（30 摄氏度）通过以下方式增加了起搏诱导的 VF 的易感性：（1）促进 VF 和 S1 起搏时的波破裂；（2）增强致心律失常的电生理参数，包括在 S1 起搏时更早出现 APD 交替（主要为 SDA）。
