Echocardiographic measurements of epicardial adipose tissue and comparative ability to predict adverse cardiovascular outcomes in patients with coronary artery disease

Abstract

The present study aimed to compare echocardiography measurements of epicardial adipose tissue (EAT) thickness and other risk factors regarding their ability to predict adverse cardiovascular outcomes in patients with coronary artery disease (CAD). Outcomes of 107 patients (86 males, 21 females, mean age 63.6 years old) submitted to diagnostic echocardiography and coronary angiography were prospectively analyzed. EAT (measures over the right ventricle, interventricular groove and complete bulk of EAT) and left ventricle ejection fraction (LVEF) were performed by echocardiography. Coronary complexity was evaluated by Syntax score. Primary endpoints were major adverse cardiovascular events (MACE’s), composite of cardiovascular death, myocardial infarction, unstable angina, intra-stent re-stenosis and episodes of decompensate heart failure requiring hospital attention during a mean follow up of 15.94 ± 3.6 months. Mean EAT thickness was 4.6 ± 1.9 mm; and correlated with Syntax score and body mass index; negatively correlated with LVEF. Twenty-three cases of MACE's were recorded during follow up, who showed higher EAT. Diagnostic ability of EAT to discriminate MACE's was comparable to LVEF (AUROC > 0.5); but higher than Syntax score. Quartile comparison of EAT revealed that measurement of the complete bulk of EAT provided a better discrimination range for MACE's, and higher, more significant adjusted risk (cutoff 4.6 mm, RR = 3.91; 95% CI 1.01–15.08; p = 0.04) than the other risk factors. We concluded that echocardiographic measurement of EAT showed higher predicting ability for MACE’s than the other markers tested, in patients with CAD. Whether location for echocardiographic measurement of EAT impacts the diagnostic performance of this method deserves further study.

Epicardial adipose tissue is a robust measure of increased risk of myocardial infarction – a meta-analysis on over 6600 patients and rationale for the EPIC-ACS study

“…Overall, 6641 patients (mean aged 58.9 years, 53% male) from 7 studies were included (Table 1 ). [ 11 12 13 14 15 16 17 ] Of those, 296 patients had either a myocardial infarction at inclusion for cross-sectional studies (n = 128 events) or developed a myocardial infarction during follow-up for longitudinal studies (n = 168 events). Patients with myocardial infarction had 37% higher measures of EAT compared to patients without myocardial infarction (95% confidence interval: 21% to 54%, Fig.…”

“…2 ). Studies on CT added 5980 participants from 4 studies[ 12 13 14 16 ] to the analysis (215 myocardial infarctions), whereas only 251 patients from 2 studies using echocardiography[ 15 17 ] were included (56 myocardial infarctions). This imbalance between CT and echocardiography based studies was predominantly caused by the study by Mahabadi et al, [14] including 4093 subjects.…”

Epicardial adipose tissue predicts incident cardiovascular disease and mortality in patients with type 2 diabetes

“…Cheng et al [5] confirmed these findings in patients with asymptomatic CHD, and furthermore found a trend that EAT could improve MACE prediction when added to the Framingham Risk Score and coronary calcium scoring (CCS). Following these findings, more longitudinal studies unanimously concluded that high levels of EAT were associated with increased risk of CVD in patients with known or suspected CHD [8–10, 14]. A recent study showed that EAT volume is higher and density lower in subjects with coronary calcium compared to subjects without, and that EAT was more significantly associated with MACE than the calcium score [33].…”

The correlation of retinol-binding protein-4 and lipoprotein combine index with the prevalence and diagnosis of acute coronary syndrome

“…Studies have also confirmed that adipose tissues such as epicardial adipose tissue, pericardial adipose tissue, and thoracic adipose tissue secrete adipocytokines such as adiponectin, tumor necrosis factor-α (TNF-α), and omentin-1. Moreover, the clinical risk factors such as diabetes, hypertension, dyslipidemia are strongly linked with the pathophysiological mechanisms of CAD [ 14 , 34 – 38 ]. Although these efforts have improved the screening, diagnosis, treatment, and prognosis of CAD, the prevalence of CAD remains high and it is still one of the major health issues in the world.…”