Sleep Apnea

Abstract

Sleep apnea is highly prevalent in patients with cardiovascular disease. These disordered breathing events are associated with a profile of perturbations that include intermittent hypoxia, oxidative stress, sympathetic activation, and endothelial dysfunction, all of which are critical mediators of cardiovascular disease. Evidence supports a causal association of sleep apnea with the incidence and morbidity of hypertension, coronary heart disease, arrhythmia, heart failure, and stroke. Several discoveries in the pathogenesis, along with developments in the treatment of sleep apnea, have accumulated in recent years. In this review, we discuss the mechanisms of sleep apnea, the evidence that addresses the links between sleep apnea and cardiovascular disease, and research that has addressed the effect of sleep apnea treatment on cardiovascular disease and clinical endpoints. Finally, we review the recent development in sleep apnea treatment options, with special consideration of treating patients with heart disease. Future directions for selective areas are suggested.

Practical Recommendations of the Obesity Management Task Force of the European Association for the Study of Obesity for the Post-Bariatric Surgery Medical Management

“…The major risk factors for OSA are obesity, older age and male gender. Individuals suffering from OSA have increased risk of several adverse health outcomes, including all-cause mortality, traffic accidents, hypertension, type 2 diabetes, coronary heart disease, arrhythmia, heart failure and stroke [50,51,52,53]. The apnoea-hypopnea index (AHI) is the number of complete cessations (apnoea ≥ 10 s) and partial obstructions (hypopneas) of breathing occurring per hour of sleep.…”

Autonomic regulation during sleep and wakefulness: a review with implications for defining the pathophysiology of neurological disorders

“…Patients experience frequent arousals from sleep, resulting from increased respiratory effort in response to hypoxia or hypercapnia [53]. Respiratory events can be apneas (defined as the absence of inspiratory flow for ≥ 10 s) or hypoapneas (shallow, slow respiration lasting ≥ 10 s), leading to EEG arousals and varying degrees of arterial oxygen desaturation [52]. The etiology of these respiratory events may be obstructive or central.…”

Nonmuscle Myosin Light Chain Kinase: A Key Player in Intermittent Hypoxia‐Induced Vascular Alterations

“…OSA is recognized as an important and independent risk factor for hypertension, coronary heart diseases, and stroke. The deleterious effects of OSA on cardiovascular outcomes are mainly triggered by intermittent hypoxia (IH) severity and the subsequent oxidative stress, leading to activation of the autonomic nervous system 1, 2, 3. Vascular endothelial dysfunction is a major intermediate mechanism of cardiovascular complications in patients with OSA,4, 5, 6 preceding and predicting late cardiovascular events, such as hypertension, atherosclerosis, and coronary diseases 1.…”