Erschienen in:
25.01.2016 | Original Paper
Impact of obstructive and central apneas on ventricular repolarisation: lessons learned from studies in man and pigs
verfasst von:
Dominik Linz, Alisa Denner, Susanne Illing, Mathias Hohl, Christian Ukena, Felix Mahfoud, Sebastian Ewen, Jan C. Reil, Klaus Wirth, Michael Böhm
Erschienen in:
Clinical Research in Cardiology
|
Ausgabe 8/2016
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Abstract
Background
Sleep apnea (SA) is associated with sudden cardiac death. Compared to central apneas, obstructive apneas are associated with negative intrathoracic pressure swings inducing autonomic imbalance, which may disturb ventricular repolarisation resulting in arrhythmias.
Objectives
To identify the influence of obstructive apneas versus central apneas on ventricular repolarisation.
Methods
In 14 patients with SA, duration (RT-intervals) and dispersion of ventricular repolarisation [Tpeak-to-Tend-interval (TpTe)] were determined during central apneas compared to obstructive apneas. To identify mechanisms, hypoxia alone or hypoxia with applied negative thoracic pressure was applied in a pig model for SA before and after atropine (n = 7), atenolol (n = 5) and sympathetic renal denervation (RDN, n = 7).
Results
In patients with SA, obstructive apneas during sleep were always associated with a prolongation of RT- as well as TpTe intervals. By contrast central apneas did not affect ventricular repolarisation significantly in the same patients. In the pig model for SA, 2 min of acute tracheal occlusion with applied negative thoracic pressure resulted in a prolongation in RT- and TpTe-interval. These changes in ventricular repolarisation could be inhibited by atenolol as well as by RDN and were not influenced by parasympathetic blockade by atropine. By contrast hypoxia alone did not affect ventricular repolarisation.
Conclusions
Intrathoracic pressure swings during obstructive apneas contribute to changes in ventricular repolarisation, which are not observed with central apneas. These changes are mainly driven by sympathetic activation and may represent mechanisms for increased occurrence of sudden cardiac death in obstructive SA.