Pacemaker therapy in sleep apnea syndrome

Abstract

Sleep apnea syndrome (SAS) is a serious health problem that particularly afflicts patients with cardiovascular disease. Pathophysiologically, an obstructive form of SAS with loss of air flow despite thorax movements and a central form of SAS with simultaneous cessation of air flow and respiratory movements are distinguished. Central SAS is present in almost 50% of patients with severe heart failure (HF). It induces alternating bradycardia and tachycardia related to fluctuations of the vago-sympathetic tone. Suppression or reduction of heart rate fluctuations by pacing may mitigate sleep apnea. In HF with marked nocturnal bradycardia, increasing the heart rate may improve cardiac output, shorten circulation time and decrease pulmonary congestion, thus diminishing the apneic threshold. Potentially, stimulation of vagal and sympathetic nerve fibers behind the superior vena cava/right atrial junction by pacing may directly influence cardiac vagal or sympathetic afferent neurons reducing central sleep apnea episodes. In obstructive SAS, polysomnography characterizes a specific pattern of sleep apnea where bradycardia precedes the onset of apnea. This could result from hypervagotonia first inducing bradycardia and then apnea. Atrial overdrive pacing may counteract hypervagotonia by maintaining sympathetic activity. Pacing might not benefit obstructive SAS due to excessive adiposity, anatomical obstacles or unrelated to bradycardia. In the future, cardiac pacing might be considered as an ancillary therapy for SAS in patients with bradycardia and/or hypervagotonia during sleep. Larger studies need to confirm this hypothesis in patients without a conventional indication for pacing. Device recording of sleep apnea could become a powerful tool to guide SAS therapy.