## 3 Epicardial Adipose Tissue
### Epicardial Fat Volume and Atherosclerosis Progression  
Recent studies have demonstrated that EAT volume is associated with the development and progression of atherosclerotic plaques. Therefore, previous studies reported greater EAT volumes in patients with angiographic evidence of coronary stenoses than those without [110,111]. Similarly, [PERSON] et al., enrolling patients with intermediate CAD risk undergoing cardiac CT with contextual EAT volume quantification, showed a higher EAT volume in patients with coronary stenosis >50% compared with those with <50%. Moreover, the multivariate regression analysis revealed an independent association between coronary stenosis severity, plaque burden, and EAT volume [112].  
Notably, EAT volume is also associated with atherosclerosis progression and, more specifically, with the development of high-risk plaques. In this regard, [PERSON] et al. demonstrated that EAT was higher in patients with mixed/non-calcified plaques than those with calcified lesions [113]. The same evidence was reported by [PERSON] et al., that quantified epicardial fat volume in 1308 patients with symptomatic CAD and a zero-calcium score. EAT was greater in patients with obstructive atherosclerotic plaques than no plaque and even more in those with vulnerable plaque than no plaque [114]. Similarly, a recent meta-analysis by [PERSON] et al. confirmed the association between EAT volume and high-risk plaques [115]. [PERSON] et al. found that EAT volume in ACS patients was significantly higher than in those suffering from CCS [116]. Finally, [PERSON] et al. demonstrated a significant positive correlation between EAT volume and necrotic plaque detected using intravascular ultrasound imaging (IVUS) and a negative correlation between EAT volume and fibrous plaque [117].  
Several studies also reported a direct relationship between EAT and CAC score. [PERSON] et al. demonstrated increased CAC in patients with EAT volume >100 cm\({}^{3}\) than in those with EAT volume <100 cm\({}^{3}\), with a higher incidence of CAD in the same group [118]. These results were confirmed in the study conducted by [PERSON] et al., where EAT volume was independently associated with CAC \(\geq\) 100 AU (per 10 cm\({}^{3}\) increase: OR 1.11 (1.02-1.20)) [119].  
Another measurable parameter derived from EAT assessment and associated with a worse prognosis is fat radiodensity. [PERSON] et al. demonstrated in 140 patients undergoing CT-scan that one standard deviation lower EAT attenuation (5 HU) was associated with 1.9 and 1.07 higher odds (for men and women respectively) of being in higher CAC class (0, 1 to 100, 101 to 400, and >400) [120]. Similarly, [PERSON] et al. quantified both EAT volume and density in 456 asymptomatic patients; EAT volume resulted lowest in patients without coronary calcium and higher in patients with severe atherosclerosis, while EAT density resulted lower in patients with high coronary calcium and increased occurrence of adverse clinical events [121].  
Finally, all this evidence allows identifying EAT volume as a predictor of MACEs. For example, [PERSON] et al. quantify EAT volume in asymptomatic patients from the EISNER (Early Identification of Subclinical Atherosclerosis by Noninvasive Imaging Research) trial, showing its association with increased risk of MACE after 14 \(\pm\) 3 years of follow-up. It was also demonstrated that MACE risk progressively increased with EAT volume \(\geq\) 113 cm\({}^{3}\) and CAC \(\geq\) 100 AU [122]. Thus, [PERSON] et al. revealed that patients with CAD who died from sudden cardiac death had significantly higher EAT thickness [123]. Moreover, in the Heinz Nixdorf Recall Study, the incidence of coronary events increased directly with EAT quartiles, with a doubling of EAT volume associated with a 1.5-fold risk of coronary events independently from other traditional CV risk factors [124].