Author + information
- Received April 3, 2019
- Revision received June 7, 2019
- Accepted June 10, 2019
- Published online September 16, 2019.
- Heather N. Anderson, MDa,
- J. Martijn Bos, MD, PhDa,b,
- Ram K. Rohatgi, MDa and
- Michael J. Ackerman, MD, PhDa,b,c,∗ ()
- aDivision of Pediatric Cardiology, Department of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, Minnesota
- bDepartment of Molecular Pharmacology and Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory, Mayo Clinic College of Biomedical Sciences, Mayo Clinic, Rochester, Minnesota
- cDivision of Heart Rhythm Services, Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota
- ↵∗Address for correspondence:
Dr. Michael J. Ackerman, Mayo Clinic Windland Smith Rice Sudden Death Genomics Laboratory, Guggenheim 501, Mayo Clinic, 200 First Street Southwest, Rochester, Minnesota 55905.
Objectives This study evaluated the effect of left cardiac sympathetic denervation (LCSD) on heart rate, cardiac contractility, and cardiopulmonary fitness in human subjects.
Background The primary treatment for long QT syndrome (LQTS) is beta-blocker (BB) therapy, but some patients experience breakthrough cardiac events or intolerable side effects. LCSD provides a significant antifibrillatory, protective effect in LQTS. However, the effect of LCSD on cardiopulmonary fitness in humans has not been previously described.
Methods A retrospective analysis of patients with LQTS and LCSD (2006 to 2017) who had both pre- and post-LCSD exercise stress tests (N = 55; 39 females; mean age at LCSD 22 ± 12 years; mean follow-up 5.1 ± 2.5 years; 36 patients with LQT1; 15 patients with LQT2). Forty patients (73%) were receiving BBs pre-LCSD.
Results Mean peak heart rate before LCSD was 143 ± 23 beats/min, mean peak oxygen consumption (VO2) was 32 ± 10 ml/kg/min, and mean peak respiratory exchange ratio was 1.14 ± 0.12. There was no difference in peak heart rate, peak VO2, peak QTc, or respiratory exchange ratio pre- and post-LCSD. To evaluate the isolated effect of LCSD, the study performed a subset analysis of patients with LCSD monotherapy (n = 10) or no change in BB dose (n = 12). Patient-matched pre- and post-LCSD exercise testing showed no difference in heart rate, VO2, or left ventricular function following LCSD.
Conclusions LCSD provides increased protection from an LQTS-triggered event without negatively affecting peak heart rate, cardiopulmonary fitness, or cardiac contractility, as assessed by both treadmill exercise stress testing and echocardiography.
- cardiac contractility
- cardiopulmonary fitness
- exercise testing
- left cardiac sympathetic denervation
- long QT syndrome
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Received April 3, 2019.
- Revision received June 7, 2019.
- Accepted June 10, 2019.
- 2019 American College of Cardiology Foundation
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