Left Cardiac Sympathetic Denervation in Young Patients—Influence on the Sympathetic Nervous System

Objectives: Left cardiac sympathetic denervation (LCSD) is an additional therapeutic approach in patients with medically uncontrolled ventricular arrhythmias. Data related to effects of LCSD on the sympathetic nervous system are limited. We analyzed changes of blood pressure and Holter ECG as surrogate parameters of the sympathetic nervous system before and immediately after LCSD in young patients.

Patients and Methods: Data from all 29 young patients who underwent LCSD at our institution between May 2003 and August 2015 were collected. Biometrics, Holter ECG, and 24-hour blood pressure monitoring before and 4 to 14 days after the procedure as well as potential side effects were analyzed.

Results: Twenty-nine patients had undergone LCSD (17 females, 59%). Tachyarrhythmias uncontrolled by antiarrhythmic therapy were indication for LCSD in 26 out of 29 (90%) individuals. Of the 26 individuals 15 had long QT syndrome and 11 had catecholaminergic polymorphic ventricular tachycardia, respectively. Out of 29, 2 (7%) subjects had LCSD because of hyperhidrosis and 1 out of 29 (3%) because of truncus coeliacus compression syndrome. Median age at LCSD was 15.1 (range: 1.7–43) years, median body weight was 50.4 (range: 9.7–90.5) kg, and median follow-up after LCSD was 28 (range: 1–140) months. Out of 29, 24 (83%) individuals had an ICD. After LCSD, arrhythmia burden under antiarrhythmic therapy was reduced to three patients. Complete Horner’s syndrome was present in 13 out of 29 (45%) and incomplete Horner’s syndrome in 9 out of 29 (31%) individuals. Median of mean and maximum heart rates (HRs) on Holter monitor before and after LCSD were not significantly different. Minimum HRs were significantly higher (p = 0.016) after the procedure, while HR variability (SDNN; Kleiger) was significantly reduced (p = 0.003). Twenty-four-hour blood pressure monitoring (n = 7) exhibited a significant increase in average systolic (p = 0.028), mean (p = 0.0042), and diastolic (p = 0.027) blood pressure.

Conclusion: After LCSD, arrhythmia symptoms were strongly reduced. Evaluation of sympathetic nervous system revealed a significant rise in blood pressure and minimum HR as well as reduced HR variability after LCSD. This may be explained by an early reflex sympathetic surge after LCSD. Long-term data are pending.