Obstructive sleep apnoea – a marker of increased cardiovascular risk

Obstructive sleep apnoea (OSA) is the temporary cessation of breathing due to continuous respiratory effort against a closed glottis (1). The apnoea causes repeated episodes of hypoxia and carbon dioxide retention. The arousal provoked then causes awakening which restores integrity of pharyngeal dilator muscle tone and airflow ensues, but as sleep returns so does the OSA cycle. OSA is measured using the apnoea–hypopnoea index (AHI) and the definition includes five or more AHI episodes per hour (mild 5–15, moderate 15–30 and severe over 30). It is not surprising that daytime sleepiness follows which can be pronounced and involuntary, and when severe affects communication (falling asleep at meetings) or even driving. Obstructive sleep apnoea is believed to affect 24% of men and 9% of women which strongly suggests under-diagnosis. This is important because OSA has significant cardio and cerebrovascular consequences. Studies have identified significant and independent associations between OSA and obesity, hypertension, coronary artery disease, arrhythmias, cardiac failure, stroke, the metabolic syndrome, erectile dysfunction and testosterone deficiency (2,3). The mechanisms include hypoxia-related autonomic imbalance on endothelial dysfunction. During non-rapid eye movement (NREM) sleep, parasympathetic nervous system tone is increased and the heart rate, blood pressure, cardiac output and systemic vascular resistance decreased (4,5). We could say the cardiovascular system is ‘relaxed’. In contrast, in rapid eye movement (REM) sleep, sympathetic activity is increased with increases in heart rate, blood pressure and irregular breathing. Normally 75–85% of sleep is NREM but OSA shifts the pattern to increasing REM sleep with adverse cardiovascular consequences. Obstructive sleep apnoea generates negative intrathoracic pressure, increasing right heart venous return and distension of the right ventricle, whilst increased sympathetic activity causes vasoconstriction and an increase in afterload (6). The right ventricular septum impinges on the left ventricle (LV) in diastole, reducing LV filling and stroke volume as well as delaying LV relaxation (7). Left atrial volume is increased and atrial fibrillation may develop which in the OSA-induced hypercoaguable state combines cerebral hypoxia with the risk of emboli (8). The presence of a patent foramen ovale which is seen in 10–25% of individuals undergoing transoesophageal echocardiography will then be a further risk for stroke (9). Obstructive sleep apnoea certainly increases and is a marker of increased risk for stroke (10). In addition, in randomised clinical trials, OSA causes hypertension and importantly its treatment lowers blood pressure [continuous positive airways pressure (CPAP)] (2). CPAP also improves systolic function, decreasing the adverse effects of the sympathetic nervous system, and improves myocardial oxygen supply (less nocturnal ischaemia) and a reduction in cardiovascular events (2,11). The OSA-related adverse increase in aldosterone raises the question of angiotensin receptor antagonists as a means of therapy. Reducing obesity is the obvious preventative measure and an ear, nose and throat specialist opinion should rule out a mechanical cause (12). Obstructive sleep apnoea is often associated with a history of regular snoring due to increased pharyngeal airways resistance. Snoring is often a joked about family issue, but it could well be a reflection of OSA and an explanation for ‘he died in his sleep’.