Dr Phyllis Murphie, Adrian Zacher 21/04/26
Sleep apnoea is increasingly recognised as a major cardiovascular comorbidity rather than a benign sleep disorder. Both Obstructive and Central sleep apnoea (OSA and CSA) are highly prevalent in patients with hypertension, heart failure, atrial fibrillation and stroke, yet remain substantially under‑diagnosed in routine cardiology practice(1, 2). The relationship between sleep apnoea and cardiovascular disease (CVD) is bidirectional, mechanistically complex and heterogeneous across patient phenotypes, with important implications for screening and management strategies(3, 4).
Pathophysiological Mechanisms Relevant to Cardiology
From a cardiovascular perspective, sleep apnoea exerts adverse effects through several converging mechanisms:
- Intermittent hypoxia and reoxygenation, leading to oxidative stress and endothelial dysfunction
- Sustained sympathetic activation with impaired nocturnal blood pressure dipping
- Large negative intrathoracic pressure swings, increasing left ventricular afterload and myocardial wall stress
- Systemic inflammation and metabolic dysregulation(5-7).
Importantly, contemporary data suggest that hypoxic burden, the cumulative depth and duration of oxygen desaturations correlates more strongly with cardiovascular morbidity and mortality than the apnoea–hypopnoea index (AHI) alone(7, 8).
Heart Failure: Obstructive and Central Sleep Apnoea
Sleep apnoea is present in 40–80% of patients with heart failure, frequently as a mixed or evolving phenotype. Sleep Apnoea contributes to adverse myocardial remodelling via afterload stress and sympathetic activation, while heart failure itself predisposes to central sleep apnoea and Cheyne–Stokes respiration through pulmonary congestion, prolonged circulation time and altered chemoreflex sensitivity(2, 7, 9-11).
Central Sleep Apnoea (CSA)
CSA is present in approximately 10–20% of patients within cardiovascular populations, with higher prevalence observed in those with heart failure, prior stroke and advanced atrial fibrillation (12, 13). CSA is characterised by ventilatory instability and impaired central respiratory drive, rather than upper airway obstruction, and is frequently under‑recognised due to overlapping clinical features with OSA and the absence of excessive daytime sleepiness. Recognition of CSA is therefore critical, as its presence has distinct prognostic implications, including associations with arrhythmia burden, disease progression and increased mortality in selected cardiac cohorts. Importantly, diagnostic pathways and therapeutic strategies for CSA differ substantially from those used in OSA, and inappropriate treatment selection may result in limited efficacy or harm in certain patient groups. Accurate phenotyping of sleep apnoea subtype is therefore essential to inform risk stratification and guide personalised cardiovascular management(14).
Hypertension and Resistant Hypertension
Approximately 50% of patients with hypertension have co‑existing OSA, with a clear dose–response relationship between sleep apnoea severity and blood pressure levels(15). Sleep apnoea is particularly prevalent in resistant hypertension, where nocturnal hypoxia, sympathetic overactivity and impaired baroreflex sensitivity contribute to poor blood pressure control. Although CPAP is generally considered beneficial for blood pressure control, published data indicate only modest reductions in blood pressure (16, 17).
Coronary Artery Disease
OSA is associated with increased prevalence and severity of coronary artery disease (CAD), unstable plaque features and adverse cardiovascular events including myocardial infarction. Proposed mechanistic pathways include endothelial dysfunction, pro‑atherogenic inflammation and coronary vasoreactivity impairment(18).
Although large RCT’s have not shown a clear reduction in major cardiovascular events with CPAP in patients with obstructive sleep apnoea and coronary artery disease, its use remains appropriate. CPAP is recommended for relieving daytime sleepiness and improving quality of life. Patients with good adherence (≥4 hours per night) may gain cardiovascular benefit, particularly those at higher risk or with established disease. CPAP should therefore be individualised and used alongside guideline-directed CAD management rather than viewed as a standalone cardioprotective intervention(19).
Cardiac Arrhythmias: Focus on Atrial Fibrillation
Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia and is associated with significant morbidity and mortality and is strongly associated with both atrial and ventricular arrhythmias(20). The Sleep Heart Health Study demonstrated a four‑fold increase in atrial fibrillation (AF) prevalence among patients with OSA. Mechanisms include atrial stretch, autonomic instability, inflammation and structural remodelling(21).
Observational data suggest that treatment of sleep apnoea may:
- Reduce AF recurrence after cardioversion or ablation
- Improve rhythm control strategies
However, randomised evidence remains mixed, reinforcing the need for integrated cardiology–sleep medicine pathways rather than isolated intervention.
Stroke and Cerebrovascular Disease
Sleep apnoea is an independent risk factor for incident stroke, with risk increasing alongside disease severity and hypoxic burden. Equally important, sleep apnoea both obstructive and central is highly prevalent following stroke, adversely affecting rehabilitation outcomes, recurrent vascular risk and mortality. Routine screening for sleep apnoea in stroke services remains inconsistent despite clear prognostic relevance. Sleep‑disordered breathing and stroke have a two‑way relationship: obstructive sleep apnoea (OSA) increases the risk of stroke and stroke itself can cause or worsen sleep‑disordered breathing depending on stroke location and physiology. OSA diagnosed after stroke (“poststroke OSA”) may reflect either a true consequence of stroke or previously undiagnosed OSA, making the term potentially misleading. The key message is that stroke patients should be actively screened for sleep‑disordered breathing, even without a prior OSA history(22).
Comorbid Insomnia and Sleep Apnoea (COMISA) and CVD
COMISA (comorbid insomnia and obstructive sleep apnoea) is increasingly viewed as a distinct, high‑risk cardiovascular phenotype rather than a simple overlap of two disorders. The combination appears to amplify adverse mechanisms such as persistent sympathetic activation, reduced parasympathetic tone, inflammation, and impaired nocturnal cardiovascular recovery, with physiological studies showing greater autonomic dysregulation in COMISA than in either condition alone. Observational and cohort studies consistently demonstrate higher risks of hypertension, major adverse cardiovascular events, and cerebrovascular disease in COMISA compared with isolated insomnia or OSA, suggesting a negative synergistic effect on cardiovascular outcomes. Importantly, insomnia symptoms are associated with poorer CPAP adherence and persistence, potentially blunting the cardiovascular benefits of OSA treatment when insomnia is unrecognised or untreated. Together, these findings highlight that failure to identify and manage insomnia in patients with OSA may undermine cardiovascular risk reduction, supporting integrated assessment and treatment of both conditions(23-25).
Sex Differences and Under‑Diagnosis
Women with cardiovascular disease often exhibit non‑sleepy or atypical obstructive sleep apnoea (OSA) phenotypes, leading to under‑recognition when screening relies on excessive daytime sleepiness. Compared with men, women are less likely to report sleepiness and more likely to present with fatigue, insomnia, poor sleep quality, or mood symptoms, which are not well captured by standard tools such as the Epworth Sleepiness Scale. Emerging evidence also suggests that cardiovascular harm in women may occur at lower AHI thresholds, with nocturnal hypoxaemia and autonomic stress being stronger predictors of cardiovascular events than AHI alone. Women appear more susceptible to the cardiovascular effects of intermittent hypoxia and sympathetic activation, resulting in higher risks of hypertension, heart failure, and stroke despite milder OSA severity. These findings highlight the need for more nuanced screening approaches in women, particularly those with cardiovascular disease, incorporating atypical symptoms and physiological markers beyond daytime sleepiness(26, 27).
Implications for Cardiology Practice
Sleep apnoea should be considered a modifiable cardiovascular risk marker and disease modifier, particularly in:
- Heart failure
- Atrial fibrillation and cardiac arrythmias
- Resistant hypertension
- Stroke and TIA populations
Moving beyond AHI to incorporate hypoxic burden, sleep apnoea subtype and comorbid insomnia enables more precise cardiovascular risk stratification and personalised management strategies.
Conclusion
For cardiology practitioners sleep apnoea is no longer a peripheral sleep disorder but a core contributor to cardiovascular pathophysiology and prognosis. Improved recognition of clinically relevant sleep apnoea phenotypes, combined with collaborative cardiology and sleep medicine models of care, is essential to optimise cardiovascular outcomes in this high‑risk population.
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