Previous Abstract | Next Abstract
Printable Version
October 25, 2015
10:00:00 AM - 11:30:00 AM
Room Upper 11A
Thoracic Epidural Anesthesia Suppresses Cardiac Excitability Induced by Acute Myocardial Ischemia
Kimberly J. Howard-Quijano, M.D., M.S., Kentaro Yamakawa, M.D., Tatsuo Takamiya, M.D., Wei Zhou, Ph.D., Jeffrey Ardell, Ph.D., Kalyanam Shivkumar, M.D.,Ph.D., Aman Mahajan, M.D.,Ph.D.
University of California, Los Angeles, Los Angeles, California, United States
Disclosures: K.J. Howard-Quijano: None. K. Yamakawa: None. T. Takamiya: None. W. Zhou: None. J. Ardell: None. K. Shivkumar: None. A. Mahajan: None.
Introduction: Sudden cardiac death (SCD) due to ventricular arrhythmias is the leading cause of mortality in the USA. Autonomic nervous system imbalances are fundamental to progression of cardiac pathology, including the potential of SCD. Myocardial ischemia reflexly induces increases in sympathetic tone with a corresponding reduction in central parasympathetic inputs. Selective neuraxial intervention at the spinal level, namely thoracic epidural anesthesia (TEA) has been used as a therapeutic approach for control of cardiac arrhythmias. However, cardiac electrophysiological effects of modulation of sympathetic activity at this spinal level during acute myocardial ischemia are not well understood. The goal of this study is to understand the mechanism of therapeutic benefits of TEA in a porcine model when cardiac neural afferents are altered by acute ischemia.

Methods: Yorkshire pigs (n=8, weight 41 ± 4 kg) were anesthetized, underwent placement of a thoracic epidural catheter at the T1 level, and median thoracotomy to expose the heart and left stellate ganglion. A 56-electrode sock was placed over ventricles to obtain cardiac electrograms for measurement of activation recovery intervals (ARIs). (Figure 1A,B) ARI is the duration between activation time and repolarization time and is a surrogate marker for action potential duration. Increased sympathetic tone leads to shortening of ARI duration. Acute ischemia was induced with 45 sec ligation of the 2nd diagonal branch of the left anterior descending coronary artery (LAD). ARI was recorded at baseline, with acute ischemia, and ischemia + left stellate ganglion stimulation (LSGS) to augment sympathetic tone. TEA was induced by 0.5% bupivacaine (0.4mg/kg) and measurements were taken again post-TEA at baseline, acute ischemia, and ischemia + LSGS. Regional ARIs were assessed in 2 regions (left ventricular ischemic: apex/anterior and non-ischemic: lateral and posterior).

Results: There was no significant difference between baseline global ARI duration or the magnitude of ARI shortening with left stellate ganglion stimulation before or after TEA administration (pre-TEA baseline 380ms, LSGS 358 ms, LAD occlusion post-TEA baseline 360ms, LSGS 352ms p=0.5). Acute ischemia was associated with an expected reduction in regional ARI, however this reduction was attenuated post TEA in the ischemic zone with no difference observed in non-ischemic myocardium. Ischemic control: 392ms - 384ms LAD occlusion vs. post-TEA: 397 ms - 391ms LAD occlusion, p < 0.01. Non-ischemic control: 360 - 355ms LAD occlusion vs. TEA 364 - 359ms, p = 0.6. (Figure 1C,D) With LSG stimulation, which increases sympathetic tone and augments ischemia induced autonomic imbalance, TEA again attenuated afferent sympathetic output and reduced magnitude of ARI shortening in ischemic areas. (% change baseline to ischemia/LSGS: control -7% vs. TEA -4%, p <0.01 and non-ischemic: control -21% vs. -25%, p = 0.3, Figure 1C,D).

Conclusions: The results of this study show that thoracic epidural anesthesia reduces cardiac excitability from acute myocardial ischemia induced autonomic imbalance. Through neuromodulation of the dorsal (afferent) and ventral (efferent) roots at the thoracic level, TEA suppressed ischemia induced sympathoexcitation. Lethal ventricular arrhythmias are often associated with focal reentrant circuits in the ischemic and border zones, thus these findings provide important mechanistic evidence supporting treatment of ventricular arrhythmias using thoracic epidural anesthesia.
Figure 1

Copyright © 2015 American Society of Anesthesiologists