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Sleep Breath. 2016 May;20(2):483-93. doi: 10.1007/s11325-015-1236-5. Epub 2015 Jul 30.

CPAP therapy induces favorable short-term changes in epicardial fat thickness and vascular and metabolic markers in apparently healthy subjects with obstructive sleep apnea-hypopnea syndrome (OSAHS).

Author information

1
Therapeutic Clinic Alexandra, Hospital University of Athens, Athens, Greece.
2
Pulmonary Department-Oncology Unit, "G. Papanikolaou" General Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece. pzarog@hotmail.com.
3
Department of Interventional Pneumology, Ruhrlandklinik, University Hospital Essen, University of Essen-Duisburg, Tueschener Weg 40, 45239, Essen, Germany. pzarog@hotmail.com.

Abstract

BACKGROUND:

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is an independent risk factor for hypertension, coronary artery disease, and diabetes mellitus. Epicardial fat has been recently recognized as a new risk factor and active participant on cardiometabolic risk. The aim of this study was to assess an independent relationship between sleep apnea severity, metabolic and vascular markers, and epicardial fat, at baseline and after 3 months of continuous positive airway pressure (CPAP) therapy.

MATERIALS AND METHOD:

Our study group consisted of 48 patients with suspected OSAHS and no prior history of cardiovascular disease or diabetes mellitus. All patients underwent full overnight polysomnography. Thickness of epicardial and visceral adipose tissue, brachial artery flow-mediated dilation (FMD), carotid intima media thickness (cIMT), pulse wave velocity (PWV), plasma C-reactive protein (CRP) levels, fasting glucose levels, HbA1c, homeostatic model assessment of insulin resistance index (HOMA), and lipid profile were measured at baseline and after 3 months of CPAP use in patients with moderate to severe OSAHS.

RESULTS:

In OSAHS patients (Apnea-hypopnea index (AHI) ≥15/h, N = 28), epicardial fat correlated with fasting glucose (rho = 0.406, p = 0.04) and HOMA (rho = 0.525, p = 0.049) but was not associated with visceral fat (rho = 0.126, p = 0.595). Epicardial adipose tissue (EAT) (p = 0.022) increased across AHI severity along with PWV (p = 0.045) and carotid intima media thickness (IMT) (p = 0.034) while FMD (p = 0.017) decreased. Therapy with CPAP reduced both epicardial (p < 0.001) and visceral fat (p = 0.001). Alterations in epicardial fat across the follow-up were associated with changes in PWV (p = 0.026) and HOMA (p = 0.037) independently of major confounders.

CONCLUSIONS:

Epicardial fat thickness was associated with OSA severity and may be an additional marker of cardiovascular risk as well as of future diabetes in these patients. CPAP therapy reduced epicardial fat, suggesting its potentially beneficial role in reducing cardiometabolic risk in OSA patients.

KEYWORDS:

Cardiometabolic risk; Continuous positive airways pressure (CPAP); Epicardial adipose tissue (EAT); Insulin resistance (HOMA); Obstructive sleep apnea syndrome (OSAHS); Pulse wave velocity (PWV)

PMID:
26223484
DOI:
10.1007/s11325-015-1236-5
[Indexed for MEDLINE]

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