Key result
Epicardial adipose tissue volume was not an independent predictor for the presence (OR 1.00; P=0.88) or extent of coronary artery disease after adjusting for traditional cardiovascular risk factors.
Why the study?
Does epicardial adipose tissue volume independently predict the presence and extent of coronary artery disease in patients presenting with stable chest pain?
Cross-Sectional (n=410)
Does epicardial adipose tissue volume independently predict the presence and extent of coronary artery disease in patients presenting with stable chest pain?
Odds Ratio: 1
p-value: p=0.88
Although epicardial adipose tissue volume is higher in patients with diabetes and impaired fasting glucose, it does not independently predict the presence or extent of coronary artery disease after adjusting for traditional cardiovascular risk factors.
EAT volume should not guide CAD assessment in stable chest pain; leaves open its incremental value in prospective cohorts.
AIMS: Epicardial adipose tissue (EAT) volume has been associated with coronary artery disease (CAD). As diabetes mellitus type 2 (DM2) patients have higher EAT volumes, it has been suggested that EAT may play a role in promoting CAD in these patients. The aim of this study was to examine the association between EAT and CAD in DM2, impaired fasting glucose (IFG) and control patients presenting with stable chest pain. METHODS AND RESULTS: A total of 410 stable chest pain patients underwent multidetector cardiac computed tomography angiography (CCTA) to assess the presence of CAD. The extent of CAD was expressed as the number of affected segments. The EAT volume was measured using three-dimensional volumetric quantification. The EAT was compared using ANOVA, logistic and linear regression models were used to assess its predictive value. Multivariable regression analysis corrected for traditional risk factors was performed. Eighty-three patients had DM2, 118 IFG and there were 209 controls. DM2 as well as IFG patients had higher EAT volumes compared with controls (98 ± 41, 92 ± 39, and 75 ± 34 cm(3), respectively; P < 0.001). EAT predicted the presence (OR: 1.01; P < 0.001) and the extent of CAD (B: 0.01; P < 0.001). The associations were equal in all subgroups. However, in a multivariable regression model corrected for traditional cardiovascular risk factors, EAT was not an independent predictor for the presence or extent of CAD (OR: 1.00; P = 0.88 and B: -0.11; P = 0.68, respectively). CONCLUSION: The EAT volume is associated with CAD in DM2, IFG, and control patients. However, EAT is not an independent predictor for CAD in patients presenting with stable chest pain.
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Versteylen et al. (2012) conducted a cross-sectional in stable chest pain (n=410). Epicardial adipose tissue volume was evaluated on presence of CAD (OR 1.00, p=0.88). Epicardial adipose tissue volume was not an independent predictor for the presence (OR 1.00; P=0.88) or extent of coronary artery disease after adjusting for traditional cardiovascular risk factors.
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