BACKGROUND Thoracic epidural anesthesia (TEA) has been shown to reduce the burden of ventricular tachycardia in small case series of patients with refractory ventricular tachyarrhythmias and cardiomyopathy. However, its electrophysiological and autonomic effects in diseased hearts remain unclear, and its use after myocardial infarction is limited by concerns for potential right ventricular dysfunction. METHODS Myocardial infarction was created in Yorkshire pigs (N=22) by left anterior descending coronary artery occlusion. Approximately, six weeks after myocardial infarction, an epidural catheter was placed at the C7-T1 vertebral level for injection of 2% lidocaine. Right and left ventricular hemodynamics were recorded using Millar pressure-conductance catheters, and ventricular activation recovery intervals (ARIs), a surrogate of action potential durations, by a 56-electrode sock and 64-electrode basket catheter. Hemodynamics and ARIs, baroreflex sensitivity and intrinsic cardiac neural activity, and ventricular effective refractory periods and slope of restitution (Smax) were assessed before and after TEA. Ventricular tachyarrhythmia inducibility was assessed by programmed electrical stimulation. RESULTS TEA reduced inducibility of ventricular tachyarrhythmias by 70%. TEA did not affect right ventricular-systolic pressure or contractility, although left ventricular-systolic pressure and contractility decreased modestly. Global and regional ventricular ARIs increased, including in scar and border zone regions post-TEA. TEA reduced ARI dispersion specifically in border zone regions. Ventricular effective refractory periods prolonged significantly at critical sites of arrhythmogenesis, and Smax was reduced. Interestingly, TEA significantly improved cardiac vagal function, as measured by both baroreflex sensitivity and intrinsic cardiac neural activity. CONCLUSIONS TEA does not compromise right ventricular function in infarcted hearts. Its antiarrhythmic mechanisms are mediated by increases in ventricular effective refractory period and ARIs, decreases in Smax, and reductions in border zone electrophysiological heterogeneities. TEA improves parasympathetic function, which may independently underlie some of its observed antiarrhythmic mechanisms. This study provides novel insights into the antiarrhythmic mechanisms of TEA while highlighting its applicability to the clinical setting.

中文翻译：

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心肌梗死后硬膜外阻滞的抗心律失常机制。


背景 胸段硬膜外麻醉 (TEA) 已被证明可以减轻难治性室性快速心律失常和心肌病患者的小病例系列中的室性心动过速负担。然而，其对患病心脏的电生理和自主神经作用仍不清楚，并且由于担心潜在的右心室功能障碍，其在心肌梗塞后的使用受到限制。方法通过左冠状动脉前降支闭塞在约克夏猪（N=22）中产生心肌梗塞。心肌梗塞后大约六周，将硬膜外导管置于 C7-T1 椎骨水平，注射 2% 利多卡因。使用 Millar 压力电导导管记录右心室和左心室血流动力学，并通过 56 电极短袜和 64 电极篮式导管记录心室激活恢复间隔 (ARIs)（动作电位持续时间的替代）。在 TEA 前后评估血流动力学和 ARI、压力反射敏感性和内在心脏神经活动、心室有效不应期和恢复斜率 (Smax)。通过程序化电刺激评估室性快速心律失常的诱发性。结果茶可将室性快速心律失常的诱发率降低 70%。 TEA 不影响右心室收缩压或收缩力，但左心室收缩压和收缩力略有下降。整体和局部心室 ARI 增加，包括 TEA 后疤痕和边界区区域。 TEA 减少了 ARI 的扩散，特别是在边境地区。在心律失常发生的关键部位，心室有效不应期显着延长，Smax 降低。 有趣的是，TEA 显着改善了心脏迷走神经功能，通过压力反射敏感性和内在心脏神经活动来测量。结论茶不会损害梗塞心脏的右心室功能。其抗心律失常机制是通过心室有效不应期和 ARI 的增加、Smax 的减少以及边界区电生理异质性的减少来介导的。 TEA 可改善副交感神经功能，这可能是其观察到的一些抗心律失常机制的独立基础。这项研究为 TEA 的抗心律失常机制提供了新的见解，同时强调了其在临床环境中的适用性。