Undiagnosed Sleep Apnoea Linked to Adverse Myocardial Remodelling in Hypertrophic Cardiomyopathy
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Sleep-disordered breathing (SDB), a condition mediated by intermittent hypoxaemia and autonomic dysregulation, is a well-established contributor to cardiovascular morbidity. A new prospective cohort study suggests that patients with hypertrophic cardiomyopathy (HCM) are particularly at risk, revealing a high prevalence of previously undiagnosed SDB in this population. The research links the presence of SDB with adverse myocardial remodelling, greater diastolic dysfunction, and evidence of subclinical myocardial injury.¹

 

This single-centre, prospective cohort study was conducted between 2018 and 2024 at a tertiary referral centre specialising in HCM care. Researchers enrolled 154 adults with HCM, defined as having a left ventricular wall thickness of 15 mm or greater or carrying pathogenic variants. Key exclusion criteria included a prior diagnosis of SDB or current pregnancy. All participants underwent criterion-standard polysomnography to diagnose and classify SDB, with observers blinded to the results. The primary outcomes were the associations between SDB and various echocardiographic indices, cardiac biomarker expression (troponin-T), and functional status.¹

 

Of the 154 participants (median age 60 years; 66.2% male), 91 (59.1%) received a new diagnosis of SDB. The presence of SDB was associated with several adverse cardiac markers when compared to those without the condition. Patients with SDB had a significantly higher left ventricular mass index (median 128 g/m² vs 109 g/m²; p=0.03) and a higher E/e′ ratio, indicating worse diastolic function (median 12.5 vs 10.0; p=0.04). Furthermore, those with SDB exhibited higher baseline troponin-T levels (median 0.013 ng/mL vs 0.011 ng/mL; p=0.04) and a greater overnight increase in troponin-T (p=0.02), suggesting ongoing subclinical myocardial injury. Symptom burden was also significantly higher in the SDB group, with 52.7% reporting New York Heart Association (NYHA) class II or III symptoms, compared to 27.0% of those without SDB (p=0.005).¹

 

These findings underscore that SDB is a highly prevalent and underdiagnosed comorbidity in the HCM population. The strong associations with increased left ventricular mass, diastolic dysfunction, and markers of myocardial injury suggest that SDB is not merely a bystander but could be a modifiable risk factor that actively contributes to and exacerbates the clinical course of HCM. Screening for SDB in patients with HCM may therefore be warranted to identify those who could benefit from treatment.

 

The study authors concluded that "SDB may contribute to HCM pathophysiology and symptom burden, supporting the rationale for randomized clinical trials to determine the impact of treating SDB on symptoms and clinical outcomes in patients with HCM."¹

References

1. Karim S, Chahal A, Venkataraman S, et al. Prevalence and Clinical Implications of Sleep Apnea in Hypertrophic Cardiomyopathy. JAMA Cardiol. 2025. https://doi.org/10.1001/jamacardio.2025.2877

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