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The effects of simulated obstructive apnea and hypopnea on arrhythmic potential in healthy subjects

Camen, Giovanni ; Clarenbach, Christian ; Stöwhas, Anne-Christin ; Rossi, Valentina ; Sievi, Noriane ; Stradling, John ; Kohler, Malcolm

In: European Journal of Applied Physiology, 2013, vol. 113, no. 2, p. 489-496

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    Title
    • The effects of simulated obstructive apnea and hypopnea on arrhythmic potential in healthy subjects
    Author
    • Camen, Giovanni. Sleep Disorders Center and Pulmonary Division, University Hospital Zurich, Raemistrasse 100, 8091, Zurich, Switzerland
    • Clarenbach, Christian. Sleep Disorders Center and Pulmonary Division, University Hospital Zurich, Raemistrasse 100, 8091, Zurich, Switzerland
    • Stöwhas, Anne-Christin. Sleep Disorders Center and Pulmonary Division, University Hospital Zurich, Raemistrasse 100, 8091, Zurich, Switzerland
    • Rossi, Valentina. Sleep Disorders Center and Pulmonary Division, University Hospital Zurich, Raemistrasse 100, 8091, Zurich, Switzerland
    • Sievi, Noriane. Sleep Disorders Center and Pulmonary Division, University Hospital Zurich, Raemistrasse 100, 8091, Zurich, Switzerland
    • Stradling, John. Oxford Center for Respiratory Medicine, Churchill Hospital, Oxford, UK
    • Kohler, Malcolm. Sleep Disorders Center and Pulmonary Division, University Hospital Zurich, Raemistrasse 100, 8091, Zurich, Switzerland
    Document Type
    • Postprint
    Language
    • English
    Published in
    • European Journal of Applied Physiology, 2013, vol. 113, no. 2, p. 489-496. Springer-Verlag
    Other Version
    OAI-PMH Identifier
    • oai:doc.rero.ch:319400
    Summary
    Preliminary evidence supports an association between OSA and cardiac dysrhythmias. Negative intrathoracic pressure, as occurring during OSA, may provoke cardiac dysrhythmias. Thus, we aimed to study the acute effects of simulated apnea and hypopnea on arrhythmic potential and measures of cardiac repolarization [QTC and T peak to T end intervals ( $$ T_{\text{p}} T_{{{\text{e}}_{\text{c}} }} $$ )] in humans. In 41 healthy volunteers, ECG was continuously recorded prior, during and after simulated obstructive hypopnea (inspiration through a threshold load), simulated apnea (Mueller maneuver), end-expiratory central apnea and normal breathing in randomized order. The number of subjects with premature beats was significantly higher during inspiration through a threshold load (n=7), and the Mueller maneuver (n=7) compared to normal breathing (n=0) (p=0.008 for all comparisons), but not during end-expiratory central apnea (n=3, p=0.125). Inspiration through a threshold load was associated with a non-significant mean (SD) increase of the QTC interval [+5.4 (22.4)ms, 95%CI −1.7 to +12.4ms, p=0.168] and a significant increase of the $$ T_{\text{p}} T_{{{\text{e}}_{\text{c}} }} $$ interval [+3.7 (8.9)ms, 95%CI +0.9 to +6.6ms, p=0.010]. The Mueller maneuver induced a significant increase of the QTC interval [+8.3 (23.4)ms, 95%CI 0.9 to +15.6ms, p=0.035] and the $$ T_{\text{p}} T_{{{\text{e}}_{\text{c}} }} $$ interval (+4.2 (8.2)ms, 95%CI +1.6 to +6.8ms, p=0.002). There were no significant changes of the QTC and $$ T_{\text{p}} T_{{{\text{e}}_{\text{c}} }} $$ intervals during central end-expiratory apnea. These data indicate that simulated obstructive apnea and hypopnea are associated with an increase of premature beats and prolongation of QTC and $$ T_{\text{p}} T_{{{\text{e}}_{\text{c}} }} $$ intervals. Therefore, negative intrathoracic pressure changes may be a contributory mechanism for the association between OSA and cardiac dysrhythmias