Christian Schlatzer1, Esther I Schwarz1, Noriane A Sievi1, Christian F Clarenbach1, Thomas Gaisl1, Laurent M Haegeli2, Firat Duru3, John R Stradling4, Malcolm Kohler5. 1. Sleep Disorders Centre and Pulmonary Division, University Hospital Zurich, Raemistrasse 100, Zurich 8091, Switzerland. 2. Cardiac Arrhythmia Unit, Cardiovascular Centre, University Hospital Zurich, Zurich, Switzerland. 3. Cardiac Arrhythmia Unit, Cardiovascular Centre, University Hospital Zurich, Zurich, Switzerland Zurich Centre for Integrative Human Physiology, University of Zurich, Zurich, Switzerland. 4. Oxford Centre for Respiratory Medicine and NIHR Oxford Biomedical Research Centre, Churchill Hospital, Oxford, UK. 5. Sleep Disorders Centre and Pulmonary Division, University Hospital Zurich, Raemistrasse 100, Zurich 8091, Switzerland Zurich Centre for Integrative Human Physiology, University of Zurich, Zurich, Switzerland malcolm.kohler@usz.ch.
Abstract
AIMS: There is preliminary evidence for a link between obstructive sleep apnoea (OSA) and arrhythmias such as paroxysmal atrial fibrillation (PAF) and sudden cardiac death but underlying mechanisms remain largely unknown. METHODS AND RESULTS: In this interventional crossover study, we evaluated whether intrathoracic pressure changes, induced by simulated OSA, trigger premature cardiac beats, and alter measures of ventricular repolarization [QTc and Tpeak-to-Tend (TpTec) intervals] in patients with PAF. 12-Lead-electrocardiograms were recorded continuously in 44 patients, while simulating obstructive apnoea (Mueller manoeuvre, MM), obstructive hypopnoea (inspiration through a threshold load, ITH), end-expiratory central apnoea (AP), and during normal breathing (NB) in randomized order. The prevalence of OSA in these 44 patients was assessed by a sleep study. Atrial premature beats (APBs) occurred more frequently during MM (55% of patients) and ITH (32%), but not during AP (14%), compared with NB (9%) (P < 0.001, P = 0.006 and P = 0.688, respectively). Mueller manoeuvre led to a significant prolongation of QTc and TpTec intervals (+17.3 ms, P < 0.001 and +4.3 ms, P = 0.005). Inspiration through a threshold load significantly increased QTc (+9.6 ms, P < 0.001) but not TpTec. End-expiratory central apnoea did not alter QTc and TpTec intervals. According to the sleep study, 56% of patients had OSA (apnoea hypopnoea index ≥5). CONCLUSION: Simulated OSA induces APBs which may be important in patients with PAF, because the majority of episodes of PAF has been shown to be triggered by APBs. Simulated OSA leads to a significant prolongation of ventricular repolarization. Published on behalf of the European Society of Cardiology. All rights reserved.
RCT Entities:
AIMS: There is preliminary evidence for a link between obstructive sleep apnoea (OSA) and arrhythmias such as paroxysmal atrial fibrillation (PAF) and sudden cardiac death but underlying mechanisms remain largely unknown. METHODS AND RESULTS: In this interventional crossover study, we evaluated whether intrathoracic pressure changes, induced by simulated OSA, trigger premature cardiac beats, and alter measures of ventricular repolarization [QTc and Tpeak-to-Tend (TpTec) intervals] in patients with PAF. 12-Lead-electrocardiograms were recorded continuously in 44 patients, while simulating obstructive apnoea (Mueller manoeuvre, MM), obstructive hypopnoea (inspiration through a threshold load, ITH), end-expiratory central apnoea (AP), and during normal breathing (NB) in randomized order. The prevalence of OSA in these 44 patients was assessed by a sleep study. Atrial premature beats (APBs) occurred more frequently during MM (55% of patients) and ITH (32%), but not during AP (14%), compared with NB (9%) (P < 0.001, P = 0.006 and P = 0.688, respectively). Mueller manoeuvre led to a significant prolongation of QTc and TpTec intervals (+17.3 ms, P < 0.001 and +4.3 ms, P = 0.005). Inspiration through a threshold load significantly increased QTc (+9.6 ms, P < 0.001) but not TpTec. End-expiratory central apnoea did not alter QTc and TpTec intervals. According to the sleep study, 56% of patients had OSA (apnoea hypopnoea index ≥5). CONCLUSION: Simulated OSA induces APBs which may be important in patients with PAF, because the majority of episodes of PAF has been shown to be triggered by APBs. Simulated OSA leads to a significant prolongation of ventricular repolarization. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Camila M de Melo; Luigi Taranto-Montemurro; James P Butler; David P White; Stephen H Loring; Ali Azarbarzin; Melania Marques; Philip J Berger; Andrew Wellman; Scott A Sands Journal: Sleep Date: 2017-10-01 Impact factor: 5.849
Authors: Christian Schlatzer; Daniel J Bratton; Esther I Schwarz; Thomas Gaisl; Justin C T Pepperell; John R Stradling; Malcolm Kohler Journal: J Thorac Dis Date: 2018-08 Impact factor: 2.895
Authors: Thomas Gaisl; Annette M Wons; Valentina Rossi; Daniel J Bratton; Christian Schlatzer; Esther I Schwarz; Giovanni Camen; Malcolm Kohler Journal: PLoS One Date: 2016-04-12 Impact factor: 3.240