Sleep apnoea and the heart

Abstract

Sleep apnoea is associated with significant daytime functioning impairment and marked cardiovascular morbidities, leading to a significant increase in mortality. Sympathetic activation, oxidative stress and systemic inflammation have been shown to be the main intermediary mechanisms associated with sleep apnoea and intermittent hypoxia. There are now convincing data regarding the association between hypertension, arrhythmias, coronary heart disease, heart failure, increased cardiovascular mortality and sleep apnoea. This has been evidenced in sleep apnoea patients and is supported by experimental data obtained in intermittent hypoxia. Whether treating sleep apnoea enables chronic cardiovascular consequences to be reversed is not fully established as regard coronary heart disease, arrhythmias and heart failure. In this late condition, complex bidirectional relationships occur, with obstructive sleep apnoea being a risk factor for heart failure whilst central sleep apnoea mainly appears as a consequence of heart failure. It remains to be established in adequately designed studies, i.e. large randomised controlled trials, whether treating sleep apnoea can improve heart failure morbidity and mortality.

Figure 1.

Main mechanisms linking obstructive sleep apnoea (OSA), intermittent hypoxia and cardiovascular diseases.

Figure 2.

Kaplan–Meier plot on appropriate cardioverter-defibrillator therapies arranged according to mild or no sleep-disordered breathing (SDB), obstructive sleep apnoea (OSA) and central sleep apnoea (CSA) (cut-off apnoea/hypopnoea index ≥15 events·h⁻¹). Reproduced from [90].

Figure 3.

Severity of obstructive sleep apnoea predicts coronary artery plaque burden. a) Coronary computed tomography angiography showing calculation of the plaque volume. b) Invasive coronary angiogram of the same patient confirming obstructive distal left anterior descending coronary artery stenosis (arrow). c) Mean plaque volume in subjects with low and high apnoea/hypopnoea index (AHI). The two groups are otherwise comparable for demographics, symptoms, comorbidities and cardiovascular risks. ^#: p = 0.017. Reproduced from [119] with permission.