JACC. Clinical electrophysiology · 2019
The Effect of Left Cardiac Sympathetic Denervation on Exercise in Patients With Long QT Syndrome.
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Anderson Heather N, Bos J Martijn, Rohatgi Ram K, Ackerman Michael J
Аннотация
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.
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.