Central sleep apnea is associated with an increased risk of atrial fibrillation, and treating it with therapies such as transvenous phrenic nerve stimulation may reduce atrial fibrillation burden.
This review highlights the pathophysiological links between central sleep apnea and atrial fibrillation, suggesting that treating CSA, potentially with transvenous phrenic nerve stimulation, may improve AF management.
Precipitating factors and chronic diseases associated with atrial fibrillation (AF) are detailed in the literature. Emerging evidence over the last several decades suggests a potential causal relationship between central sleep apnea (CSA) and AF. Mechanisms including apnea-induced hypoxia with intermittent arousal, fluctuating levels of carbon dioxide, enhanced sympathetic/neurohormonal activation and oxidative stress causing inflammation have been implicated as etiologic causes of AF within this subpopulation. CSA affects the efficacy of pharmacologic and catheter-based antiarrhythmic treatments, which is why treating CSA prior to these interventions may lead to lower rates of AF. Subsequently, a reduction in the AF burden with transvenous phrenic nerve stimulation (TPNS) has become a topic of interest. The present review describes the relationship between these conditions, pathophysiologic mechanisms implicating the role of CSA in development of AF, and emerging therapeutic interventions.
Sanchez et al. (Thu,) conducted a review in Central sleep apnea and atrial fibrillation. Central sleep apnea is associated with an increased risk of atrial fibrillation, and treating it with therapies such as transvenous phrenic nerve stimulation may reduce atrial fibrillation burden.