Abstract：
UNASSIGNED: Thoracic epidural anesthesia (TEA) has been shown to reduce the burden of ventricular tachycardia in small case series of patients with refractory ventricular tachycardia 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.
UNASSIGNED: Myocardial infarction was created in Yorkshire pigs (N=22) by left anterior descending coronary artery occlusion. 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: Myocardial infarction was created in Yorkshire pigs (N=22) by left anterior descending coronary artery occlusion. 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
摘要：
■胸部硬膜外麻醉（TEA）已被证明可以减轻小病例系列难治性室性心动过速和心肌病患者的室性心动过速的负担。然而,它在患病心脏中的电生理和自主神经作用尚不清楚，由于担心潜在的右心室功能障碍，其在心肌梗死后的使用受到限制。
■在约克郡猪（N=22）中，左冠状动脉前降支闭塞导致心肌梗塞。心肌梗塞后6周,在C7-T1椎体水平放置硬膜外导管,用于注射2%利多卡因.使用Millar压力传导导管记录右心室和左心室血流动力学,和心室激动恢复间隔（ARIs），动作电位持续时间的替代，通过56电极袜子和64电极篮式导管。血流动力学和ARIs,压力反射敏感性和内在心脏神经活动，在TEA前后评估心室有效不应期和恢复斜率（Smax）。通过编程电刺激评估室性快速性心律失常的诱导性。
■TEA将室性快速性心律失常的诱导性降低了70％。TEA不影响右心室收缩压或收缩力，尽管左心室收缩压和收缩力略有下降。全球和区域性心室ARIs增加，包括TEA后的疤痕和边界区域。TEA减少了ARI色散，特别是在边界区域。在心律失常发生的关键部位，心室有效不应期明显延长，Smax降低了。有趣的是,TEA显著改善心脏迷走神经功能，通过压力反射敏感性和内在心脏神经活动来测量。
■TEA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增加心室有效不应期和ARIs介导的，Smax降低，边界区电生理异质性的减少。TEA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。
■在约克郡猪（N=22）中，左冠状动脉前降支闭塞导致心肌梗塞。心肌梗塞后6周,在C7-T1椎体水平放置硬膜外导管,用于注射2%利多卡因.使用Millar压力传导导管记录右心室和左心室血流动力学,和心室激动恢复间隔（ARIs），动作电位持续时间的替代，通过56电极袜子和64电极篮式导管。血流动力学和ARIs,压力反射敏感性和内在心脏神经活动，在TEA前后评估心室有效不应期和恢复斜率（Smax）。通过编程电刺激评估室性快速性心律失常的诱导性。
■TEA将室性快速性心律失常的诱导性降低了70％。TEA不影响右心室收缩压或收缩力，尽管左心室收缩压和收缩力略有下降。全球和区域性心室ARIs增加，包括TEA后的疤痕和边界区域。TEA减少了ARI色散，特别是在边界区域。在心律失常发生的关键部位，心室有效不应期明显延长，Smax降低了。有趣的是,TEA显著改善心脏迷走神经功能，通过压力反射敏感性和内在心脏神经活动来测量。
■TEA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增加心室有效不应期和ARIs介导的，Smax降低，边界区电生理异质性的减少。TEA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。
