We searched PubMed for articles published through July, 2012, with the terms “sleep apnoea”, “sleep apnea”, “OSA”, “hypertension”, “myocardial ischaemia”, “myocardial infarction”, “arrhythmias”, “heart failure”, “stroke”, “sudden death”, “oxidative stress”, “sympathetic activation”, “inflammation”, “hypercoagulability”, “diabetes”, “dyslipidemia”, “metabolic dysregulation”, “metabolic syndrome”, and “endothelial dysfunction”. We mainly selected publications from the past 5 years, but did not
ReviewObstructive sleep apnoea and cardiovascular disease
Introduction
Obstructive sleep apnoea (OSA) is a common disease that affects 3–7% of the middle-aged population (30–70 years) and becomes more prevalent with age.1 It is caused by intermittent collapse of the upper airway during sleep, which leads to transient asphyxia. Although OSA can be asymptomatic, clinically it is characterised by intermittent snoring, unrefreshing sleep, and daytime sleepiness. OSA is an important public health issue, because it is associated with development of cardiovascular events, negative effect on quality of life, and has a causative role in traffic accidents. Only around 10% of individuals with OSA are diagnosed and treated. This shortfall has direct consequences on public health because of the high financial costs of untreated OSA. The events associated with collapse of the upper airway lead to brain arousal, changes in intrathoracic pressure, and intermittent episodes of hypoxaemia and reoxygenation. These events take place in repetitive cycles during sleep and induce the activation of various pathways (intermediate mechanisms) that predispose to atherosclerosis. Basic research and epidemiological and clinical data support the notion that OSA has a role in the initiation or progression of several cardiovascular diseases. In this Review, we describe mechanisms by which OSA might contribute to pathogenesis of cardiovascular disease, and assess clinical and epidemiological evidence of such an association.
Section snippets
Intermediate mechanisms linking OSA with cardiovascular disease
The mechanisms for initiation and aggravation of cardiovascular disease have not been fully elucidated. Several pathogenic factors are proposed as intermediate mechanisms linking OSA with cardiovascular disease, mainly oxidative stress, sympathetic activation, inflammation, hypercoagulability, endothelial dysfunction, and metabolic dysregulation (figure). Although described here separately, these mechanisms are closely interrelated and manifest simultaneously in patients with OSA.
Hypertension
Hypertension is a common feature of patients with OSA. It is estimated that a third of hypertensive patients have OSA, and about half of patients with OSA are hypertensive.45 OSA is present in about 80% of patients with resistant hypertension, and is the leading recognisable cause of hypertension in about two-thirds of these patients.46 The sympathetic activation associated with obstructive events during sleep might blunt nocturnal lowering of blood pressure and result in a higher occurrence of
Conclusions: clinical practice and research agenda
Obstructive sleep apnoea should be suspected in hypertensive individuals, particularly in patients with resistant hypertension. CPAP treatment reduces blood pressure, with effectiveness related to initial blood pressure and treatment compliance. OSA is probably a risk factor for cardiovascular disease or cardiovascular death. Available data suggest that stroke and heart failure are the most relevant events related to OSA. Risk of coronary heart disease might be limited to middle-aged men with
Search strategy and selection criteria
References (114)
Obstructive sleep apnoea syndrome—an oxidative stress disorder
Sleep Med Rev
(2003)- et al.
8-Isoprostane, a marker of oxidative stress, is increased in exhaled breath condensate of patients with obstructive sleep apnea after night and is reduced by continuous positive airway pressure therapy
Chest
(2003) - et al.
Age and gender differences in behavioral and morphological outcome after 6-hydroxydopamine-induced lesion of the substantia nigra in rats
Behav Brain Res
(2005) - et al.
Continuous positive airway pressure normalizes cardiac autonomic and hemodynamic responses to a laboratory stressor in apneic patients
Chest
(2001) - et al.
Hemostatic alterations in patients with obstructive sleep apnea and the implications for cardiovascular disease
Chest
(2003) - et al.
CPAP reduces hypercoagulability, as assessed by thromboelastography, in severe obstructive sleep apnoea
Respir Physiol Neurobiol
(2012) - et al.
Nasal continuous positive airway pressure improves myocardial perfusion reserve and endothelial-dependent vasodilation in patients with obstructive sleep apnea
J Cardiovasc Magn Reson
(2010) - et al.
Plasma aldosterone is related to severity of obstructive sleep apnea in subjects with resistant hypertension
Chest
(2007) - et al.
Cardiac function after CPAP therapy in patients with chronic heart failure and sleep apnea: a multicenter study
Sleep Med
(2008) - et al.
Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study
Lancet
(2005)