Epicardial Adipose Tissue Thickness Is an Independent Predictor of Critical and Complex Coronary Artery Disease by Gensini and Syntax Scores

Abstract

Epicardial adipose tissue thickness is associated with the severity and extent of atherosclerotic coronary artery disease. We prospectively investigated whether epicardial adipose tissue thickness is related to coronary artery disease extent and complexity as denoted by Gensini and Syntax scores, and whether the thickness predicts critical disease. After performing coronary angiography in 183 patients who had angina or acute myocardial infarction, we divided them into 3 groups: normal coronary arteries, noncritical disease (≥1 coronary lesion with<70% stenosis), and critical disease (≥1 coronary lesion with <70% stenosis). We used transthoracic echocardiography to measure epicardial adipose tissue thickness, then calculated Gensini and Syntax scores by reviewing the angiograms. Mean thicknesses were 4.3 ± 0.9, 5.2 ± 1.5, and 7.5 ± 1.9 mm in patients with normal coronary arteries, noncritical disease, and critical disease, respectively (P <0.001). At progressive thicknesses (<5, 5-7, and >7 mm), mean Gensini scores were 4.1 ± 5.5, 19.8 ± 15.6, and 64.9 ± 32.4, and mean Syntax scores were 4.7 ± 5.9, 16.6 ± 8.5, and 31.7 ± 8.7, respectively (both P <0.001). Thickness had strong and positive correlations with both scores (Gensini, r =0.82, P <0.001; and Syntax, r =0.825, P <0.001). The cutoff thickness value to predict critical disease was 5.75 mm (area under the curve, 0.875; 95% confidence interval, 0.825-0.926; P <0.001). Epicardial adipose tissue thickness is independently related to coronary artery disease extent and complexity as denoted by Gensini and Syntax scores, and it predicts critical coronary artery disease.

Study of correlation between epicardial fat thickness and severity of coronary artery disease

“…EFT had no association with dyslipidemia and BMI corroborating the findings in other studies that visceral adiposity is more important than total adiposity for cardiovascular risk. 9 , 12 …”

Adipokines and Inflammation: Focus on Cardiovascular Diseases

“…Moreover, it has been proposed that the adipokines released by EAT in pathological conditions have paracrine effects on cardiac electrical activity, affecting conductivity and promoting atrial fibrillation [ 20 ], and in coronary arteries, they cause atherosclerosis through the promotion of inflammation and immune cell infiltration [ 21 , 22 ]. Lately, EAT thickness has been considered a clinical biomarker that correlates to features of heart failure and metabolic syndrome [ 23 , 24 , 25 , 26 , 27 ]. Another fat depot that surrounds the coronary arteries is the perivascular adipose tissue (PVAT).…”

Epicardial Adipose Tissue Removal Potentiates Outward Remodeling and Arrests Coronary Atherogenesis

“…The contiguity of cEAT with coronary arterial adventitia without an intervening fibrous layer (2, 8, 17, 28) might also restrict outward dilation of the proximal conduit coronary artery during diastole. Alternatively, cEAT from obese Ossabaw pigs expresses and secretes vasoconstrictors (29–31) which when removed might result in tonic vasodilation.…”

“…Many human studies conducted on the link between cEAT and CAD development have been observational, showing a positive correlation between cEAT volume and CAD severity (2–7). There remains a need for experimental animal studies to determine a causal role of cEAT in CAD progression (16).…”