Obstructive sleep apnea and atrial arrhythmogenesis

Abstract

Atrial fibrillation (AF) is the most common sustained arrhythmia and is associated with relevant morbidity and mortality. Besides hypertension, valvular disease and cardiomyopathy, mainly ischemic and dilated, also other conditions like obesity, alcohol abusus, genetic factors and obstructive sleep apnea (OSA) are discussed to contribute to the progression from paroxysmal to persistent AF. The prevalence of OSA among patients with AF is 40-50%. OSA is characterized by periodic or complete cessation of effective breathing during sleep due to obstruction of the upper airways. Obstructive respiratory events result in acute intrathoracic pressure swings and profound changes in blood gases together leading to atrial stretch and acute sympatho-vagal dysbalance resulting in acute apnea related to electrophysiological and hemodynamic alterations. Additionally, repetitive obstructive events in patients with OSA may lead to sympathetic and neurohumoral activation and subsequent structural and functional changes in the atrium creating an arrhythmogenic substrate for AF in the long run. This review focuses on the acute and chronic effects of negative thoracic pressure swings, changes in blood pressure and sympatho-vagal dysbalance induced by obstructive respiratory events on atrial electrophysiology and atrial structure in patients with obstructive sleep apnea.

Fig. (1)

Effects of different conditions during acute (see Chapter 3.1) and chronic (see Chapter 3.2) obstructive respiratory events on atrial electrophysiology, atrial substrates and triggers of atrial fibrillation.

Fig. (2)

Changes in atrial electrophysiology during 2 min of tracheal occlusion with (left) or without (right) applied negative tracheal pressure (NTP) at -100 mbar.Individual example of changes in atrial effective refractory period (AERP) (first line) and corresponding original recordings of monophasic action potentials (MAP) at baseline and at 2 minutes of tracheal occlusion (second line). Individual example of corresponding MAP signals during representative AERP-measurements at the end of 2 minutes of tracheal occlusion (bottom). Applied NTP at -100 mbar resulted in a progressive shortening of AERP and MAP and AF was inducible by a premature beat during the S1-S2 AERP measurement procedure. (Heart Rhythm 2011; 8: 1436-43.).

Fig. (3)

Representative atrial multiple action potential (MAP) recordings during AERP-measurements before and after RDN or atenolol in a pig model for OSA. Percent of OSA-maneuvers with inducible atrial fibrillation (AF) and the effect of either atenolol or RDN. (Hypertension 2012; 60: 172-8.).

Fig. (4)

Blood pressure during repetitive OSA-maneuvers: (A) Blood pressure registration in control (Ctr) pigs, (B) pigs with repetitive obstructive respiratory events with applied negative tracheal pressure (NTP) without and (C) with RDN (NTP + RDN). RAAS-signaling components (D and E): Effect of 4 hours of repetitive OSA-maneuvers on (D) plasma renin-activity and (E) plasma aldosterone concentrations. (Hypertension 2013; 62: 767-74.).