Key result
HCM is linked to more severe sleep-disordered breathing than controls despite similar overall prevalence.
Why the study?
The prevalence and clinical correlations of sleep-disordered breathing in patients with hypertrophic cardiomyopathy were not well characterized.
Is sleep-disordered breathing more prevalent or severe in patients with hypertrophic cardiomyopathy compared to controls?
Case-Control (n=113)
Is sleep-disordered breathing more prevalent or severe in patients with hypertrophic cardiomyopathy compared to controls?
Absolute Event Rate: 82.5% vs 72%
p-value: p=not significant
Sleep-disordered breathing is highly prevalent and more severe in patients with hypertrophic cardiomyopathy compared to controls, and its severity correlates with NYHA class and left ventricular end-diastolic diameter.
SDB screening may merit consideration in HCM; leaves open whether treatment modifies progression or outcomes.
The authors investigated the prevalence of sleep-disordered breathing (SDB) together with its clinical correlations in patients with hypertrophic cardiomyopathy (HCM). A total of 113 consecutive patients including 63 patients with HCM (40 men; mean age, 59.5±13.0 years; New York Heart Association class, 2.0±0.9) underwent cardiorespiratory polygraphy in addition to their clinical work-up including echocardiography. Patients with an apnea-hypopnea-index (AHI) ≥5/h were considered to have SDB. If thoracic and abdominal inspiration efforts were documented, SDB was considered to be obstructive sleep apnea (OSA), otherwise SDB was considered to be central sleep apnea (CSA). The age- and sex-matched control group of 50 patients had exclusion of coronary artery disease by angiography, and normal left ventricular (ejection fraction ≥55%) and valvular function. SDB was diagnosed in 52 patients (82.5% vs 72% in the control group; P =not significant) with a mean AHI of 23.0±17.8/h. Severity of SDB was higher in patients with HCM than in the control group (AHI 12.2±7.6/h; P =.003). OSA was documented in 39 patients (AHI 21.2±16.5/h) and CSA in 13 (AHI 28.4±20.9/h). The severity of SDB correlated with New York Heart Association functional class (η=0.9, η(2) =0.811) and with left ventricular end-diastolic (r=0.6, P <.01) and left atrial (r=0.4, P <.01) diameter. No correlations were found between SDB and other clinical or echocardiographic parameters. SDB is common in patients with hypertrophic cardiomyopathy, with a predominance of OSA and correlations with markers of left ventricular function.
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Prinz et al. (2011) conducted a case-control in Hypertrophic cardiomyopathy (n=113). Hypertrophic cardiomyopathy vs. Age- and sex-matched controls with normal left ventricular and valvular function and no coronary artery disease was evaluated on Diagnosis of sleep-disordered breathing (apnea-hypopnea-index ≥5/h) (p=not significant). Patients with hypertrophic cardiomyopathy had greater severity of sleep-disordered breathing than controls (P=0.003), despite similar overall SDB prevalence (82.5% vs 72%; P=NS).
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