Abstract

PurposeVisceral adipose tissue (VAT) is proinflammatory and is associated with cardiovascular (CV) disease. We investigated the relationship between obstructive sleep apnea (OSA) and visceral adipose tissue (VAT) metabolic activity in a pilot group of patients using positron-emission tomography/magnetic resonance imaging (PET/MRI) with 18F-fluorodeoxyglucose (FDG) tracer as a novel marker of adipose tissue inflammation.Patients and MethodsWe analyzed patients from an ongoing study, recruiting those with newly diagnosed, untreated OSA (Respiratory Disturbance Index [RDI] ≥ 5), using home sleep apnea testing (WatchPAT-200 Central-Plus). PET/MRI scans were acquired before continuous positive airway pressure (CPAP)-initiation, and after 3 months of CPAP therapy. Adipose tissue metabolic activity (18F-FDG-uptake) was measured using standardized uptake values (SUV) within the adipose tissue depots. The primary outcome was VAT SUVmean, and secondary outcomes included VAT volume, and subcutaneous adipose tissue (SAT) volume/SUVmean. Reproducibility and reliability of outcome measures were analyzed using intraclass correlation coefficients (ICC). Multivariable linear regression was used to evaluate the association between OSA and primary/secondary outcomes.ResultsOur analytical sample (n = 16) was 81% male (mean age 47 ± 15 years, mean BMI of 29.9 ± 4.8kg/m2). About 56% had moderate to severe OSA (mean RDI 23 ± 6 events/hour), and 50% were adherent to CPAP. We demonstrated excellent inter/intra-rater reliability and reproducibility for the primary and secondary outcomes. Patients with moderate-to-severe OSA had a higher VAT SUV mean compared to those with mild OSA (0.795 ± 0.154 vs 0.602 ± 0.19, p = 0.04). OSA severity was positively associated with VAT SUVmean (primary outcome), adjusted for age and BMI (B [SE] = 0.013 ± 0.005, p = 0.03). Change in VAT volume was inversely correlated with CPAP adherence in unadjusted analysis (B [SE] = −48.4 ± 18.7, p = 0.02).ConclusionDerangements in VAT metabolic activity are implicated in adverse cardiometabolic outcomes and may be one of the key drivers of CV risk in OSA. Our results are hypothesis-generating, and suggest that VAT should be investigated in future studies using multi-modal imaging to understand its role as a potential mediator of adverse cardiometabolic risk in OSA.

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