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. 2022 Feb;12(1):123-134.
doi: 10.21037/cdt-21-338.

Coronary computed tomography angiography-based assessment of vascular inflammation in patients with obstructive sleep apnoea and coronary artery disease

Affiliations

Coronary computed tomography angiography-based assessment of vascular inflammation in patients with obstructive sleep apnoea and coronary artery disease

Jeremy Yuvaraj et al. Cardiovasc Diagn Ther. 2022 Feb.

Abstract

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.

Keywords: Obstructive sleep apnoea (OSA); coronary artery disease (CAD); coronary computed tomography angiography (coronary CTA); epicardial adipose tissue (EAT); pericoronary adipose tissue.

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Conflict of interest statement

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cdt.amegroups.com/article/view/10.21037/cdt-21-338/coif). SJN received research support from Amgen, Anthera, AstraZeneca, Cerenis, Eli Lilly, Esperion, InfraReDx, Liposcience, Novartis, The Medicines Company, Resverlogix, Roche, Sanofi-Regeneron, The Medicines Company, and consulting fees from Akcea, Anthera, AstraZeneca, Boehringer Ingelheim, CSL Behring, Eli Lilly, Esperion, Merck, Omthera, Resverlogix, Sanofi-Regeneron and Takeda. GSH received equipment to support research from ResMed, Philips Respironics and Air Liquide Healthcare. DW received honoraria for lectures from Eli-Lilly, Pfizer and Boehringer. DTLW serves as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from February 2021 to January 2023. The other authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Comparison of adipose tissue attenuation in Group 1 (severe OSA and high plaque burden) shown in blue, versus Group 2 (mild-moderate OSA or low plaque burden) shown in yellow. Boxes represent attenuation values in Hounsfield units (HU) for median and IQR; whiskers represent maximum and minimum attenuation values. (A) EAT attenuation in Group 1 [−87.6 HU (IQR, −90.8 to −84.0 HU)] compared to Group 2 [−84.0 HU (IQR, −87.1 to −80.0 HU)]. (B) PCAT attenuation in Group 1 [−90.4 HU (IQR, −94.9 to −86.1 HU)] compared to Group 2 [−83.4 HU (IQR, −90.9 to −79.0 HU)]. EAT, epicardial adipose tissue; PCAT, pericoronary adipose tissue; OSA, obstructive sleep apnoea; IQR, interquartile range.
Figure 2
Figure 2
Comparison of adipose tissue attenuation in patients with severe OSA and high plaque burden shown in blue, versus those with a low plaque burden shown in green. Boxes represent attenuation values in Hounsfield units (HU) for median and IQR; whiskers represent maximum and minimum attenuation values. (A) EAT attenuation in patients with severe OSA and high plaque burden [−87.6 HU (IQR, −90.8 to −84.0 HU)] compared to patients with severe OSA and low plaque burden [−80.3 HU (IQR, −84.0 to −77.0 HU)]. (B) PCAT attenuation in patients with severe OSA and high plaque burden [−90.4 HU (IQR, −94.9 to −86.1 HU)] compared to patients with severe OSA and low plaque burden [−80.9 HU (IQR, −83.1 to −76.5 HU)]. EAT, epicardial adipose tissue; PCAT, pericoronary adipose tissue; OSA, obstructive sleep apnoea; IQR, interquartile range.
Figure 3
Figure 3
Comparison of adipose tissue attenuation in patients with low plaque burden and severe OSA shown in green, versus patients with low plaque burden and mild-moderate OSA shown in purple. Boxes represent attenuation values in Hounsfield units (HU) for median and IQR; whiskers represent maximum and minimum attenuation values. (A) EAT attenuation in patients with low plaque burden and severe OSA [−80.3 HU (IQR, −84.0 to −77.0 HU)] compared to patients with low plaque burden and mild-moderate OSA [−84.0 HU (IQR, −87.1 to −81.0 HU)]. (B) PCAT attenuation in patients with low plaque burden and severe OSA [−80.9 HU (IQR, −83.1 to −76.5 HU)] compared to patients with low plaque burden and mild-moderate OSA [−83.8 HU (IQR, −90.7 to −79.0 HU)]. EAT, epicardial adipose tissue; PCAT, pericoronary adipose tissue; OSA, obstructive sleep apnoea; IQR, interquartile range.

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