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

Abstract

Aims Acute myocardial ischaemia 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 ischaemia. The role of right stellate ganglion stimulation (RSGS) in arrhythmogenesis is unclear. We hypothesized that RSGS is proarrhythmic during left lateral ventricular wall ischaemia. Methods and results In 11 anaesthetized female pigs, ventricular repolarization was measured in unipolar epicardial electrograms from the left lateral ventricular wall. Seven subsequent episodes of acute ischaemia (5 min) were produced by occlusion of the circumflex coronary artery (CX), separated by 20 min of reperfusion. The second occlusion served as a control. After 3 min of ischaemia during the third occlusion, LSGS was initiated for 30 s. 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 occlusions). RSGS during ischaemia was more arrhythmogenic than LSGS or control with more spontaneous ventricular premature beats (3-5 min of ischaemia) and two instances of ventricular fibrillation. The LSGS-induced effect on repolarization was absent in myocardium that had been ischaemic for 3 min by CX occlusion. Conclusions LSGS-induced repolarization shortening is absent in ischaemic 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 ischaemic zone supporting the clinical findings that bilateral sympathectomy is superior to left sympathectomy alone.