Abstract
BackgroundThere is still insufficient knowledge on the potential effect of mild to moderate sleep-disordered breathing (SDB) that is widely prevalent, often asymptomatic, and largely undiagnosed in patients with stable coronary artery disease (CAD). SDB affects 34% of men and 17% of women aged between 30 and 70. The objective of this study was to evaluate the association between SDB and left ventricular (LV) hypertrophy as well as structural remodeling in stable CAD patients.MethodsThe study was based on a cross-sectional design. Echocardiography and polysomnography was performed in 772 patients with CAD and with untreated sleep apnea. All study participants underwent testing by Epworth Sleepiness Scale questionnaire. Their mean age, NYHA and left ventricular ejection fraction were, respectively: 57 ± 9 years, 2.1 ± 0.5 and 51 ± 8%, and 76% were men. Sleep apnea (SA) was defined as an apnea-hypopnea-index (AHI) ≥5 events/h, and, non-SA, as an AHI <5.ResultsSleep apnea was present in 39% of patients, and a large fraction of those patients had no complaints on excessive daytime sleepiness. The patients with SA were older, with higher body mass and higher prevalence of hypertension. LV hypertrophy (LVH), defined by allometrically corrected (LV mass/height2.7) gender-independent criteria, was more common among the patients with SA than those without (86% vs. 74%, p < 0.001). The frequency of LVH by wall thickness criteria (interventricular septal thickness or posterior wall thickness ≥ 12 mm: 49% vs. 33%, p < 0.001) and concentric LVH (61% vs. 47%, p = 0.001) was higher in CAD patients with SA. The patients with SA had significantly higher values of both interventricular septal thickness and posterior wall thickness. Multiple logistic regression analysis showed that even mild sleep apnea was an independent predictor for LVH by wall thickness criteria and concentric LVH (OR = 1.5; 95% CI 1.04–2.2 and OR = 1.9; 1.3–2.9 respectively).ConclusionsWe concluded that unrecognized sleep apnea was highly prevalent among patients with stable CAD, and the majority of those patients did not report daytime sleepiness. Mild to moderate sleep apnea was associated with increased LV wall thickness, LV mass, and with higher prevalence of concentric LV hypertrophy independently of coexisting obesity, hypertension, diabetes mellitus or advancing age.
Highlights
There is still insufficient knowledge on the potential effect of mild to moderate sleep-disordered breathing (SDB) that is widely prevalent, often asymptomatic, and largely undiagnosed in patients with stable coronary artery disease (CAD)
The candidate explanatory variables for entering in the multiple regression model were hypoxemia during sleep SaO2 and age, AHI (4 categories), body mass index (BMI) (4 categories), age over 60, sex, hypertension, diabetes mellitus, New York Heart Association (NYHA) class, current smoking, history of Myocardial infarction (MI) as well as LV ejection fraction (LVEF) lower than 45%, excessive daytime sleepiness (ESS ≥ 10)
General characteristics comparison according to sleep apnea (SA) status Compared to non-SA patients, individuals with SA were on average older (SA: 59 ± 9 years vs. non-SA: 56 ± 9 years, p < 0.001), more frequently male (83% vs. 72%; p = 0.004), and had a higher prevalence of traditional CV risk factors such as obesity and hypertension (53% vs. 43% and 91% vs. 78%, respectively; both p < 0.01)
Summary
There is still insufficient knowledge on the potential effect of mild to moderate sleep-disordered breathing (SDB) that is widely prevalent, often asymptomatic, and largely undiagnosed in patients with stable coronary artery disease (CAD). According to data from the Framingham Heart Study, a population-based longitudinal study, nearly one-half of males and one-third of females over 40 years of age will develop some manifestation of CAD [1]. Sleep-disordered breathing (SDB) and the related clinical syndrome, sleep apnea (SA), are highly prevalent in patients with ischemic heart disease and often remain undiagnosed, even after admission for myocardial infarction treatment [2, 3]. SDB and nocturnal hypoxaemia are highly prevalent in stable heart failure with reduced left ventricular function and were identified as independent predictor of all-cause mortality in these patients [8]. Evidence linking SA and the severity of SDB to increased mortality and CV morbidity has been conflicting and inconclusive in both stable and unstable patients with established CAD [6, 12,13,14,15,16,17]
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