Modulation of regional dispersion of repolarization and T-peak to T-end interval by the right and left stellate ganglia

Author:

Vaseghi Marmar1,Yamakawa Kentaro2,Sinha Arjun1,So Eileen L.1,Zhou Wei2,Ajijola Olujimi A.1,Lux Robert L.3,Laks Michael1,Shivkumar Kalyanam1,Mahajan Aman12

Affiliation:

1. Cardiac Arrhythmia Center, University of California, Los Angeles, California;

2. Division of Cardiac Anesthesiology, David Geffen School of Medicine at University of California, Los Angeles, California; and

3. Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah

Abstract

Left stellate or right stellate ganglion stimulation (LGSG or RSGS, respectively) is associated with ventricular tachyarrhythmias; however, the electrophysiological mechanisms remain unclear. We assessed 1) regional dispersion of myocardial repolarization during RSGS and LSGS and 2) regional electrophysiological mechanisms underlying T-wave changes, including T-peak to T-end (Tp-e) interval, which are associated with ventricular tachyarrhythmia/ventricular fibrillation. In 10 pigs, a 56-electrode sock was placed around the heart, and both stellate ganglia were exposed. Unipolar electrograms, to asses activation recovery interval (ARI) and repolarization time (RT), and 12-lead ECG were recorded before and during RSGS and LSGS. Both LSGS and RSGS increased dispersion of repolarization; with LSGS, the greatest regional dispersion occurred on the left ventricular (LV) anterior wall and LV apex, whereas with RSGS, the greatest regional dispersion occurred on the right ventricular posterior wall. Baseline, LSGS, and RSGS dispersion correlated with Tp-e. The increase in RT dispersion, which was due to an increase in ARI dispersion, correlated with the increase in Tp-e intervals ( R2 = 0.92 LSGS; and R2 = 0.96 RSGS). During LSGS, the ARIs and RTs on the lateral and posterior walls were shorter than the anterior LV wall ( P < 0.01) and on the apex versus base ( P < 0.05), explaining the T-wave vector shift posteriorly/inferiorly. RSGS caused greater ARI and RT shortening on anterior versus lateral or posterior walls ( P < 0.01) and on base versus apex ( P < 0.05), explaining the T-wave vector shift anteriorly/superiorly. LSGS and RSGS cause differential effects on regional myocardial repolarization, explaining the ECG T-wave morphology. Sympathetic stimulation, in line with its proarrhythmic effects, increases Tp-e interval, which correlates with increases in myocardial dispersion of repolarization.

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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