학술논문

Abstract 14434: Left Cardiac Sympathetic Efferent Denervation is Protective Against Premature Ventricular Contraction-Induced Cardiomyopathy.
Document Type
Article
Source
Circulation. 2018 Supplement, Vol. 138, pA14434-A14434. 1p.
Subject
*CARDIOMYOPATHIES
*ATRIAL arrhythmias
*AUTONOMIC nervous system
*VENTRICULAR arrhythmia
*DENERVATION
*ARRHYTHMIA
Language
ISSN
0009-7322
Abstract
Introduction: Frequent premature ventricular contractions (PVCs) are known to perturb the autonomic nervous system and cause PVC-induced cardiomyopathy (PVC-CM) and pro-arrhythmia. Hypothesis: We hypothesized that post-ganglionic left cardiac sympathetic efferent denervation (LCSD) reduces sympathetic outflow to the heart and protects against PVC-CM. Methods: Twelve canines were implanted with pacemakers to the RV apex to deliver PVCs and radiotelemetry unit to record nerve activity (NA) from left stellate ganglion (SNA) and left cardiac vagus (VNA). Among them, we performed LCSD (caudal half of left stellate and T2-4 sympathetic ganglia) using cryo-ablation (-40oC) in 5 canines and compared them with 7 animals without LCSD. We then administered bigeminal PVCs (200ms coupling) for 12 weeks to induce PVC-CM, and then disabled PVCs for 4-weeks to allow LV systolic function to recover. Results: After 12 weeks of PVCs, the non-LCSD group demonstrated a significant decrease in LVEF (p=0.006, Table) with an increase in SNA (p=0.002), VNA (p=0.04), mean HR (p=0.004) and incidence of spontaneous atrial (p=0.02) and non-sustained ventricular arrhythmias (p=0.08) vs baseline. SNA (p=0.004), HR (p=0.03) and pro-arrhythmia (p=0.03) remained elevated despite elimination of PVCs and complete LVEF recovery. In contrast, the LCSD group did not have a significant decline in LVEF (p=0.08) with only an increase in LVEDV (p=0.005) after 12-weeks of PVCs. Furthermore, there was a trend towards increased VNA (p=0.1) and decrease in mean HR (p=0.006) from baseline to PVC-CM and recovery. Incidence of atrial arrhythmias decreased from baseline to PVC-CM (p=0.006) and recovery (p=0.009) and no animals had ventricular arrhythmias. Compared with non-LCSD, the LCSD group had less arrhythmias (p=0.004), and did not have a significant decline in LVEF (p=0.03). Conclusions: In a canine model, LCSD is antiarrhythmic and protective against PVC-CM. These findings imply that abnormal sympathetic nerve activity is involved in the pathogenesis of PVC-CM. [ABSTRACT FROM AUTHOR]