Relationship between obstructive sleep apnea and distribution of epicardial adipose tissue
摘要
This study aimed to investigate the distribution of epicardial adipose tissue (EAT) and adipose metabolism in patients with obstructive sleep apnea (OSA) without comorbidities, such as cardiovascular disease and diabetes—an approach to eliminate confounding factors and explore the role of EAT in OSA-related visceral adipose disorders.
MethodsThe clinical data of 180 patients were retrospectively collected from July 2017 to December 2023 at the Department of Otolaryngology-Head and Neck Surgery, Second Affiliated Hospital of Xi'an Jiaotong University. Patients were categorized into mild–moderate (apnea–hypopnea index, AHI < 30 events/hour) and severe OSA groups (AHI ≥ 30 events/hour) based on their polysomnography (PSG) results. Epicardial adipose tissue volume (EATV) and attenuation (EATA) were quantified using coronary computed tomography angiography and 3D-Slicer software, with adipose tissue defined by a Hounsfield unit threshold of -190 to -30 HU. The Chinese visceral adiposity index (CVAI) is a composite metric specific to the Chinese population that integrates age, body mass index, waist circumference, triglyceride, and high-density lipoprotein levels.
ResultsSignificant differences were observed in EATV, EATA, and CVAI between the mild–moderate and severe OSA groups (all p < 0.05). Elastic net regression, restricted cubic spline curves, and subgroup analysis using forest plots demonstrated that CVAI had the strongest correlation with the apnea–hypopnea index (AHI) and OSA severity among the visceral adipose parameters (all p < 0.05). After controlling for the effects of baseline data and visceral adipose tissue, multiple linear regression analysis revealed that OSA severity still affected the EATV and EATA (all p < 0.05).
ConclusionsOSA progression without cardiovascular disease and diabetes may promote an increase in EATV, especially in the atrial region. In addition, the change in epicardial adipose tissue appears to be independent of visceral adipose tissue. This underscores EAT as a distinct fat depot and highlights its potential role in early cardiovascular risk assessment for OSA patients, offering perspectives for future research into mechanistic pathways and clinical interventions.