| Title: | Association of epicardial adipose tissue with different stages of coronary artery disease: A cross-sectional UK Biobank cardiovascular magnetic resonance imaging substudy |
| Journal: | IJC Heart & Vasculature |
| Published: | 29 Mar 2022 |
| Pubmed: | https://pubmed.ncbi.nlm.nih.gov/35372662/ |
| DOI: | https://doi.org/10.1016/j.ijcha.2022.101006 |
Publication 13894
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Abstract
Objective: Increased epicardial adipose tissue (EAT) has been identified as a risk factor for the development of coronary artery disease (CAD). However, the exact role of EAT in the development of CAD is unclear. This study aims to compare EAT volumes between healthy controls and individuals with stable CAD and a history of myocardial infarction (MI). Furthermore, associations between clinical and biochemical parameters with EAT volumes are examined.</p>
Methods: This retrospective cross-sectional study included 171 participants from the United Kingdom Biobank (56 healthy controls; 60 stable CAD; 55 post MI), whom were balanced for age, sex and body mass index (BMI). EAT volumes were quantified on end-diastolic cardiac magnetic resonance (CMR) imaging short-axis slices along the left and right ventricle and indexed for body surface area (iEAT) and iEAT volumes were compared between groups.</p>
Results: iEAT volumes were comparable between control, CAD and MI cases (median [IQR]: 66.1[54.4-77.0] vs. 70.9[55.8-85.5] vs. 67.6[58.6-82.3] mL/m2, respectively (p > 0.005 for all). Increased HDL-cholesterol was associated with decreased iEAT volume (β = -14.8, CI = -24.6 to -4.97, p = 0.003) and suggestive associations (P-value < 0.05 and ≥ 0.005) were observed between iEAT and triglycerides (β = 3.26, CI = 0.42 to 6.09, p = 0.02), Apo-lipoprotein A (β = -16.3, CI = -30.3 to -2.24, p = 0.02) and LDL-cholesterol (β = 3.99, CI = -7.15 to -0.84, p = 0.01).</p>
Conclusions: No significant differences in iEAT volumes were observed between patients with CAD, MI and healthy controls. Our results indicate the importance of correcting for confounding by CVD risk factors, including circulating lipid levels, when studying the relationship between EAT volume and CAD. Further mechanistic studies on causal pathways and the role of EAT composition are warranted.</p>
11 Authors
- Anne Ruth van Meijeren
- Daan Ties
- Marie-Sophie L.Y. de Koning
- Randy van Dijk
- Irene V. van Blokland
- Pablo Lizana Veloz
- Gijs van Woerden
- Rozemarijn Vliegenthart
- Gabija Pundziute
- Daan B. Westenbrink
- Pim van der Harst
1 Application
| Application ID | Title |
|---|---|
| 12010 | Determinants of human cardiac structure and function and relation with outcome |
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