Mechanism of Ventricular Premature Beats Elicited by Left Stellate Ganglion Stimulation During Acute Ischemia of the Anterior Left Ventricle.

AIMS Enhanced sympathetic activity during acute ischemia is arrhythmogenic, but the underlying mechanism is unknown. During ischemia, a diastolic current flows from the ischemic to the non-ischemic myocardium. This "injury" current can cause ventricular premature beats originating in the non-ischemic myocardium, especially during a deeply negative T wave in the ischemic zone. We reasoned that shortening of repolarization in myocardium adjacent to ischemic myocardium increases the "injury" current and causes earlier deeply negative T waves in the ischemic zone, and re-excitation of the normal myocardium. We tested this hypothesis by activation and repolarization mapping during stimulation of the left stellate ganglion (LSGS) during left anterior descending coronary artery (LAD) occlusion. METHODS AND RESULTS In 9 pigs, five subsequent episodes of acute ischemia, separated by 20 min of reperfusion, were produced by occlusion of the LAD and 121 epicardial local unipolar electrograms were recorded. During the third occlusion, LSGS was initiated after 3 min for a 30-sec period, causing a shortening of repolarization in the normal myocardium by about 100 msec. This resulted in more negative T waves in the ischemic zone and more ventricular premature beats (VPBs) than during the second, control, occlusion. Following decentralization of the LSG (including removal of the right stellate ganglion and bilateral cervical vagotomy), fewer VPBs occurred during ischemia without LSGS. During LSGS, the number of VPBs was similar to that recorded before decentralization. CONCLUSION LSGS, by virtue of shortening of repolarization in the non-ischemic myocardium by about 100 msec, causes deeply negative T waves in the ischemic tissue and VPBs originating from the normal tissue adjacent to the ischemic border. In this setting, decentralization of the LSG is antiarrhythmic. TRANSLATIONAL PERSPECTIVE Cardiac sympathetic denervation is a promising therapy for reducing arrhythmias during acute ischemia. Currently it is not clear which patients with ischemic heart disease would benefit from cardiac sympathetic denervation and for which patients it is unlikely to have an effect. This is important because cardiac sympathetic denervation by removing the stellate ganglia often results in severe side effects and morbidity. Our results indicate that left stellate ganglion activity is pro-arrhythmic and that left stellectomy is beneficial for the prevention of arrhythmias during anterior wall ischemia. When the ischemic zone is in the lateral and posterior wall, the effects of LSGS will be different because it will directly affect the ischemic myocardium, and might even be antiarrhythmic. Thus, the effect of left stellate stimulation can be pro or antiarrhythmic, depending on the location of myocardial ischemia.