Why the study?
Increased epicardial adipose tissue is an identified risk factor for coronary artery disease, but its exact role in CAD development remains unclear.
Are epicardial adipose tissue volumes associated with different stages of coronary artery disease when balanced for age, sex, and BMI?
Are epicardial adipose tissue volumes associated with different stages of coronary artery disease when balanced for age, sex, and BMI?
Epicardial adipose tissue volume does not significantly differ between patients with CAD, prior MI, and healthy controls when balanced for age, sex, and BMI, highlighting the importance of correcting for confounding CVD risk factors.
Cross-sectional EAT-CAD associations remain hypothesis-generating; prospective studies needed before any clinical role.
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. 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. Results: -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). 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.
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Meijeren et al. (2022) studied this question.
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