Autonomic Dysfunction Increases Cardiovascular Risk in the Presence of Sleep Apnea

Javier Milagro,Eduardo Gil,Bertien Buyse,Pascal Borzée,Carolina Varon,Margot Deviaene,Dries Testelmans,Raquel Bailón,Sabine Van Huffel,Jesús Lázaro,Rik Willems

doi:10.3389/fphys.2019.00620

Abstract

The high prevalence of sleep apnea syndrome (SAS) and its direct relationship with an augmented risk of cardiovascular disease (CVD) have raised SAS as a primary public health problem. For this reason, extensive research aiming to understand the interaction between both conditions has been conducted. The advances in non-invasive autonomic nervous system (ANS) monitoring through heart rate variability (HRV) analysis have revealed an increased sympathetic dominance in subjects suffering from SAS when compared with controls. Similarly, HRV analysis of subjects with CVD suggests altered autonomic activity. In this work, we investigated the altered autonomic control in subjects suffering from SAS and CVD simultaneously when compared with SAS patients, as well as the possibility that ANS assessment may be useful for the early stage identification of cardiovascular risk in subjects with SAS. The analysis was performed over 199 subjects from two independent datasets during night-time, and the effects of the physiological response following an apneic episode, sleep stages, and respiration on HRV were taken into account. Results, as measured by HRV, suggest a decreased sympathetic dominance in those subjects suffering from both conditions, as well as in subjects with SAS that will develop CVDs, which was reflected in a significantly reduced sympathovagal balance (p < 0.05). In this way, ANS monitoring could contribute to improve screening and diagnosis, and eventually aid in the phenotyping of patients, as an altered response might have direct implications on cardiovascular health.

Highlights

Sleep apnea syndrome (SAS) is a complex sleep-related breathing disorder characterized by a repetitive total or partial upper-airway collapse, an absence of respiratory drive, or a combination of both
A tendency toward lower values of ReLF/HF and PeLFn in the cardiac comorbidity group than in the control group was assessed when excluding apneic episodes from the analysis. These differences were statistically significant during Non-Rapid Eye Movement (NREM) sleep
In order to study the relationship between autonomic nervous system (ANS), SAS, and cardiovascular diseases (CVD), we considered the UZ Leuven database described in section 2.1, since it is composed by SAS patients with and without cardiac comorbidities that were matched based on age, gender, Body Mass Index (BMI), and smoking habits

Summary

Introduction

Sleep apnea syndrome (SAS) is a complex sleep-related breathing disorder characterized by a repetitive total (apnea) or partial (hypopnea) upper-airway collapse (obstructive sleep apnea, OSA), an absence of respiratory drive (central sleep apnea, CSA), or a combination of both (mixed sleep apnea). The apneic episode is often stopped by the arousal of the subject, resulting in a fragmented sleep Combination of all these effects has been closely related with excessive daytime sleepiness, chronic hypertension, and increased mortality (Somers et al, 2008). SAS has been related with a 5-fold increase in the risk for developing cardiovascular diseases (CVD), which could rise to 11-fold if not conveniently treated (Peker et al, 2002) In this way, SAS represents a well-known cause of secondary systemic and pulmonary hypertension, and a significant risk factor for coronary artery disease, cardiac arrhythmias, and heart failure (Yacoub et al, 2017; Tietjens et al, 2019). Some CVD such as heart failure, atrial fibrillation, or stroke may exert a negative effect in SAS, as a deficient blood conduction could lead to a dysregulation of PaCO2 and trigger CSA episodes (Kasai et al, 2012)

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