Right stellate ganglion stimulation modulates arrhythmogenesis in acute left lateral ventricular ischemia

Aim Acute myocardial ischemia causes fatal arrhythmias as result of a flow of ‘injury current’. Left stellate ganglion stimulation (LSGS) modulates the injury current and is arrhythmogenic during left anterior ventricular wall ischemia. The role of right stellate ganglion stimulation (RSGS) in arrhythmogenesis is unclear. We hypothesized, that RSGS is proarrhythmic during left lateral ventricular wall ischemia. Methods and results In 11 anesthetized female pigs, ventricular repolarization was measured in unipolar epicardial electrograms from the left lateral ventricular wall. Seven subsequent episodes of acute ischemia (5 minutes) were produced by occlusion of the circumflex coronary artery (CX), separated by 20 minutes of reperfusion. The second occlusion served as a control. After 3 minutes of ischemia during the third occlusion, LSGS was initiated for 30 seconds. In the 4th occlusion, RSGS was performed. After decentralization of both left and right stellate ganglia and vagal nerves, LSGS and RSGS were initiated (6th and 7th occlusion). RSGS during ischemia was more arrhythmogenic than LSGS or control with more spontaneous ventricular premature beats (3-5 minutes of ischemia) and 2 instances of ventricular fibrillation. The LSGS-induced effect on repolarization was absent in myocardium that had been ischemic for 3 minutes by CX occlusion. Conclusions LSGS-induced repolarization shortening is absent in ischemic myocardium. RSGS was more arrhythmogenic following CX-occlusion than LSGS or control. These data demonstrate that the arrhythmogenic influence of RSGS or LSGS is contingent on the location of ischemic zone supporting the clinical findings that bilateral sympathectomy is superior to left sympathectomy alone.