Why the study?
Obstructive sleep apnoea is associated with increased CAD plaque burden, but the role of vascular inflammation in this relationship is unclear.
Is severe obstructive sleep apnoea with high plaque burden associated with altered vascular inflammation on coronary CTA?
Cross-Sectional (n=91)
Is severe obstructive sleep apnoea with high plaque burden associated with altered vascular inflammation on coronary CTA?
Answers are grounded in this paper and cite their sources.
Severe OSA with high plaque burden is associated with decreased EAT and PCAT attenuation on coronary CTA, though severe OSA with low plaque burden showed increased EAT attenuation, highlighting a complex interplay between OSA and vascular inflammation.
Background: Obstructive sleep apnoea (OSA) is associated with increased coronary artery disease (CAD) plaque burden, but the role of vascular inflammation in this relationship is unclear. Coronary computed tomography angiography (CTA) enables surrogate assessment of systemic inflammation via subcutaneous adipose tissue attenuation (SCAT-a), and of coronary inflammation via epicardial adipose tissue volume and attenuation (EAT-v and EAT-a) and pericoronary adipose tissue attenuation (PCAT-a). We investigated whether patients with severe OSA and high plaque burden have increased vascular inflammation. Methods: Patients with overnight polysomnography within ≤12 months of coronary CTA were included. Severe OSA was classified as apnoea/hypopnoea index (AHI) >30. High plaque burden was defined as a CT-adapted Leaman score (CT-LeSc) ≥8.3. Patients with both severe OSA and high plaque burden were defined as ‘Group 1’, all other patients were classified as ‘Group 2’. ScAT, PCAT and EAT attenuation and volume were assessed on semi-automated software. Results: A total of 91 patients were studied (59.3±11.1 years). Severe OSA was associated with high plaque burden (P=0.02). AHI correlated with CT-LeSc (r=0.24, P=0.023). Group 1 had lower EAT-a and PCAT-a compared to Group 2 (EAT-a: −87.6 vs. −84.0 HU, P=0.011; PCAT-a: −90.4 vs. −83.4 HU, P<0.01). However, among patients with low plaque burden, EAT-a was higher in the presence of severe OSA versus mild-moderate OSA (−80.3 vs. −84.0 HU, P=0.020). On multivariable analysis, severe OSA and high plaque burden associated with EAT-a (P<0.02), and severe OSA and high plaque burden (P<0.01) and hypertension (P<0.01) associated with PCAT-a. Conclusions: EAT and PCAT attenuation are decreased in patients with severe OSA and high plaque burden, but EAT attenuation was increased in patients with severe OSA and low plaque burden. These divergent results suggest vascular inflammation may be increased in OSA independent of CAD, but larger studies are required to validate these findings.
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Yuvaraj et al. (2021) conducted a cross-sectional in Obstructive sleep apnoea and coronary artery disease (n=91). Severe OSA and high plaque burden vs. All other patients was evaluated on Epicardial adipose tissue attenuation (EAT-a) (p=0.011).
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