PubMed was searched using the search term “sleep apnoea” with relevant phrases including “cardiovascular disease”, “hypertension”, “cardiac hypertrophy”, “heart failure”, “coronary artery disease”, “ischaemic heart disease”, “stroke”, “cardiac arrhythmias”, and “cerebrovascular disease”. Only papers published in English between 1997 and 2008 were used. Publications referred to in the identified articles were also reviewed and were cited if they provided important data not addressed in
SeminarObstructive sleep apnoea and its cardiovascular consequences
Introduction
Obstructive sleep apnoea (OSA) is a disorder in which loss of pharyngeal dilator muscle tone at sleep onset causes recurrent pharyngeal collapse and temporary cessation of breathing (apnoea). An abnormally narrowed or collapsible pharynx puts individuals at greater risk.1 Such apnoeas cause repetitive hypoxia and carbon-dioxide retention, and provoke awakenings (ie, arousals) that restore pharyngeal dilator muscle tone and airflow. However, this respite is brief: pharyngeal obstruction recurs once sleep resumes, and recurrent arousals, although protective, disrupt sleep. An OSA disorder is generally defined as five or more apnoeas–hypopneas per hour of sleep (ie, the apnoea–hypopnoea index [AHI]).2, 3
After the initial description of OSA, a proposition was made that cardiovascular stresses evoked by OSA could contribute to the pathogenesis of cardiovascular diseases.4 However, in 1997, Wright and colleagues5 concluded that there was insufficient evidence to support this concept. Over the subsequent decade, data from epidemiological, observational, and interventional studies have transformed our appreciation of how OSA could contribute to the burden of cardiovascular diseases, and how its treatment might lessen this burden. The purpose of this Seminar is, first, to review our current understanding of mechanisms by which OSA might contribute to the pathogenesis of cardiovascular disease; second, to assess epidemiological evidence concerning a potential link between these two conditions; third, to review cardiovascular effects of treating OSA; and finally, to identify gaps in our knowledge in need of resolution.
Section snippets
Definition and diagnosis of OSA
A diagnosis of OSA requires the presence of repetitive apnoeas and hypopnoeas during sleep. This presence is most reliably shown by attended overnight polysomnography in a sleep laboratory, in which sleep stages, arterial oxyhaemoglobin saturation, and respiratory movements of the rib cage and abdomen or respiratory effort, or both, are recorded.2
Apnoea is an absence of tidal volume for at least 10 s, and hypopnoea is a decrease in tidal volume of at least 50%, but above zero, for at least 10 s
Pathophysiology
During non-rapid-eye movement sleep, metabolic rate, sympathetic nervous activity, blood pressure, and heart rate all decrease, whereas cardiac vagal tone increases from wakefulness.16, 17, 18 OSA interrupts this cardiovascular quiescence by triggering a cascade of acute haemodynamic, autonomic, chemical, inflammatory, and metabolic effects, with chronic after-effects capable of initiating or exacerbating cardiovascular disease (figure).
These cycles of hypoxia and carbon-dioxide retention
Prevalence
In the USA, the prevalence of OSA (AHI≥5) in the adult, mainly white, population aged 30–60 years, has been estimated at 24% in men and 9% in women, and, at an AHI≥15, at 9% in men and 4% in women, with no major differences noted between African-Americans and White people.58 The corresponding prevalence of OSA syndrome has been estimated at 4% in men and 2% in women.3 In European populations, the most comprehensive data come from Spain, where 26% of men and 28% of women aged 30–70 years had an
Cardiovascular effects of treating OSA
In this section we review the findings of randomised controlled trials of OSA treatment on cardiovascular endpoints. Currently, there is no effective drug therapy for OSA. Oral appliances, electrical stimulation of the pharyngeal dilator muscles, or surgery are less effective than CPAP.129, 130, 131 Atrial overdrive pacing, which, in an initial report, caused a modest improvement in OSA in patients with bradyarrhythmias,132 is ineffective in those without bradyarrhythmias.133, 134, 135 CPAP and
Prevention of OSA
The most important modifiable risk factor for OSA is excess body weight. In patients with OSA, weight loss has been shown to decrease the AHI.160 Unfortunately, because obesity is increasing substantially in industrialised countries, the prevalence of OSA is anticipated to also increase. Thus, the most important public-health measure that could be taken to prevent OSA would be to promote avoidance or reversal of weight gain, especially in children.
Summary, controversies, and future challenges
Data from animal models, epidemiological studies, and randomised clinical trials provide strong evidence that OSA can cause hypertension, and that its treatment can lower blood pressure. Indeed, OSA might well be the commonest treatable cause of secondary hypertension. A consistent finding of trials on CPAP therapy in patients with heart failure and OSA is an improvement in left-ventricular systolic function and a decrease in activity of the sympathetic nervous system, two important clinical
Search strategy and selection criteria
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