Spinal cord stimulation reduces ventricular arrhythmias during acute ischemia by attenuation of regional myocardial excitability
Spinal cord stimulation reduces ventricular arrhythmias during acute ischemia by attenuation of regional myocardial excitability
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DOI：
10.1152/ajpheart.00129.2017
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发表时间：
2017-08-01
影响因子：
4.8
通讯作者：
Mahajan, Aman
中科院分区：
文献类型：
--
作者：
Howard-Quijano, Kimberly;Takamiya, Tatsuo;Mahajan, Aman
心肌缺血造成自主神经系统失衡，并可引发心律失常。我们假设，脊髓刺激（SCS）的神经调节将减弱局部心脏交感神经兴奋缺血诱导的传入信号的增加，减少室性心律失常，并改善急性缺血期间的心肌功能。将约克郡猪（n = 20）随机分为SCS组（50 Hz，持续时间200 μ s，电流90%运动阈值）或假手术组（假手术），在缺血前30 min。在硬膜外腔（T-1-T-4）中放置一根四极SCS电极导线，并在心脏上放置一个56电极网，以进行高分辨率电生理记录，包括激动恢复间期（阿里斯）、激动时间、复极时间和复极离散度。在基线、SCS/假手术后、急性缺血（300-s冠状动脉结扎）期间和整个再灌注期间记录电生理和血流动力学测量。SCS 1）减少缺血心肌中交感神经兴奋诱导的ARI和复极时间缩短; 2）减弱复极离散度的增加; 3）减少室性心动过速[非持续性室性心动过速：24起事件（3只假手术动物）vs. 1起事件（1只SCS动物），P < 0.001];和4）改善心肌功能（从基线到缺血的dP/dt：假手术组为1，814 +/- 213至1，596 +/- 282 mmHg/s，SCS组为1，422 +/- 299至1，380 +/- 299 mmHg/s，P < 0.01）。在无心肌应力或非缺血心肌的基线条件下，心室电生理学无变化。总之，在猪急性心室缺血模型中，SCS降低了局部心肌交感兴奋，减少了室性心律失常，并改善了心肌功能。SCS局部降低了缺血心肌中的交感神经激活，而在正常心肌中没有观察到影响，从而提供了对SCS的抗心律失常和心肌保护作用的机理认识。这表明脊髓刺激的抗心律失常作用可能是由于缺血心肌中局部交感神经兴奋的衰减而不是整体心肌电生理学的变化。
Myocardial ischemia creates autonomic nervous system imbalance and can trigger cardiac arrhythmias. We hypothesized that neuromodulation by spinal cord stimulation (SCS) will attenuate local cardiac sympathoexcitation from ischemia-induced increases in afferent signaling, reduce ventricular arrhythmias, and improve myocardial function during acute ischemia. Yorkshire pigs (n = 20) were randomized to SCS (50 Hz at 200-mu s duration, current 90% motor threshold) or sham operation (sham) for 30 min before ischemia. A four-pole SCS lead was placed percutaneously in the epidural space (T-1-T-4), and a 56-electrode mesh was placed over the heart for high-resolution electrophysiological recordings, including activation recovery intervals (ARIs), activation time, repolarization time, and dispersion of repolarization. Electrophysiological and hemodynamic measures were recorded at baseline, after SCS/sham, during acute ischemia (300-s coronary artery ligation), and throughout reperfusion. SCS 1) reduced sympathoexcitation-induced ARI and repolarization time shortening in the ischemic myocardium; 2) attenuated increases in the dispersion of repolarization; 3) reduced ventricular tachyarrythmias [nonsustained ventricular tachycardias: 24 events (3 sham animals) vs. 1 event (1 SCS animal), P < 0.001]; and 4) improved myocardial function (dP/dt from baseline to ischemia: 1,814 +/- 213 to 1,596 +/- 282 mmHg/s in sham vs. 1,422 +/- 299 to 1,380 +/- 299 mmHg/s in SCS, P < 0.01). There was no change in ventricular electrophysiology during baseline conditions without myocardial stress or in the nonischemic myocardium. In conclusion, in a porcine model of acute ventricular ischemia, SCS reduced regional myocardial sympathoexcitation, decreased ventricular arrhythmias, and improved myocardial function. SCS decreased sympathetic nerve activation locally in the ischemic myocardium with no effect observed in the normal myocardium, thus providing mechanistic insights into the antiarrhythmic and myocardial protective effects of SCS.NEW & NOTEWORTHY In a porcine model of ventricular ischemia, spinal cord stimulation decreased sympathetic nerve activation regionally in ischemic myocardium with no effect on normal myocardium, demonstrating that the antiarrhythmic effects of spinal cord stimulation are likely due to attenuation of local sympathoexcitation in the ischemic myocardium and not changes in global myocardial electrophysiology.