Cardiovascular manifestations in obstructive sleep apnea: current evidence and potential mechanisms

Abstract

as nonrestorative sleep and excessive daytime sleepiness (EDS). 7,8In addition to EDS, OSA is associated with reduced quality of life, poor cognitive function, and road traffic accidents, independent of age or sex. 9 -11 The principal morbidity and mortality of the condition, however, are due to the increased risk of the development and progression of numerous CVDs. 4 A large body of evidence has accumulated to date strengthening the association between OSA and CVD, with increased risk persisting after correction for common cardiovascular risk factors. 12 Obstructive sleep apnea is associated with increased incidence of systemic arterial hypertension, coronary artery disease, congestive cardiac failure, and stroke, 4,13,14 and although Introduction Obstructive sleep apnea (OSA) is a growing public health problem. 1 The prevalence of the disorder has been increasing rapidly over the last 2 decades in line with the obesity epidemic in the developed world. 2-4 It is estimated that OSA affects nearly 1 billion people worldwide. However, a significant proportion of patients remain undiagnosed, 5 with one estimate suggesting that more than 30 million people are undiagnosed in Europe alone. 1 There is a male to female predominance of 2 to 1, and OSA is more common in the middle -aged and elderly population. 6 Obstructive sleep apnea is characterized by recurrent partial or complete upper airway collapse during sleep leading to intermittent hypoxia (IH) and recurrent arousals culminating in disrupted sleep quality that typically manifests

Novel Insights into the Predictors of Obstructive Sleep Apnea Syndrome in Patients with Chronic Coronary Syndrome: Development of a Predicting Model

“…In addition, severe and moderate OSAS has been related to poor CAD prognosis, deteriorated sleep-related symptoms, and impaired sleep-related quality of life [ 30 , 31 ]. In accordance with previous studies, our findings also showed that CCS patients with moderate to severe OSAS were more vulnerable to diabetes mellitus, obesity, hyperlipidemia, and more severe inflammatory response [ 30 – 34 ]. Although OSAS is a well-documented risk for adverse cardiovascular outcomes [ 6 , 13 , 30 – 34 ], few studies have evaluated the polysomnographic feature of hospitalized CCS patients in previous studies.…”

Silencing MR-1 Protects against Myocardial Injury Induced by Chronic Intermittent Hypoxia by Targeting Nrf2 through Antioxidant Stress and Anti-Inflammation Pathways

“…Along with recurrent episodes of complete or partial nocturnal breathing interruption, pathophysiologic alterations are known to occur in OSA patients, including hypertension, congestive heart failure, coronary artery disease, episodic hypoxemia, insulin resistance, and neurocognitive dysfunction [ 2 ]. OSA has been identified as an independent risk element for cardiovascular diseases [ 3 ]. Chronic intermittent hypoxia (CIH) is a key factor in OSAHS causing cardiovascular disease.…”

“…Furthermore, anomalies in the oxidative stress system have been linked to endoplasmic reticulum stress. High-level oxidative stress in the endoplasmic reticulum harasses the healthy functioning of cells, causing various heart diseases such as cardiac hypertrophy, myocardial infarction, cardiac insufficiency, and heart failure [ 3 , 6 ]. The extensive clinical and animal experiments have expounded that OSA induces an increase in the ratio of heart weight : body weight (HW : BW) and enhances the levels of plasma atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and angiotensin II (An g II) [ 7 – 11 ].…”

Hypoxic Regulation of the Large-Conductance, Calcium and Voltage-Activated Potassium Channel, BK

“…OSA adversely alters the cardiovascular structure, inducing changes such as endothelial dysfunction. Additionally, OSA is reported as an independent risk factor for initiation or progression of cardiovascular diseases like hypertension, heart failure, ischemic heart disease, and stroke ( Marin et al, 2005 ; Bradley and Floras, 2009 ; Wang et al, 2013 ; Orrù et al, 2020 ; Chen et al, 2021 ; O’Donnell et al, 2021 ). The treatment of OSA includes continuous positive airway pressure (CPAP) and mandibular advancement devices (MAD), but there is no effective drug therapy for OSA.…”

“…CPAP and MAD keep the upper airway open during sleep. It has been suggested that CPAP and MAD therapies attenuate some cardiovascular diseases including atherosclerosis, hypertension, heart failure, and cardiac arrhythmias ( Barnes et al, 2004 ; Gotsopoulos et al, 2004 ; Bradley and Floras, 2009 ; Marklund et al, 2019 ; Yamamoto et al, 2019 ; Chen et al, 2021 ; O’Donnell et al, 2021 ).…”