## 4 Discussion  
The peculiarity of EAT lies both in its specific anatomic site and, especially, in its histological, biochemical and functional properties [3; 4; 5; 6]. According to the literature, there is a close correlation between EAT amount and increased cardiovascular risk [5; 7; 8; 17]. Cytokines, such as IL-6 and TNF-\(\alpha\), promote a series of negative cascade effects including the onset of insulin resistance, inhibiting the functions performed by insulin and increasing lipolysis and lipogenesis. Epicardial fat is a metabolically active organ, being a count not only of pro-inflammatory adipokines but also of anti-inflammatory mediators such as adiponectin [18]. Echocardiography, cardiac magnetic resonance and CCT can be used to quantify EAT distribution and volume [7; 18]. Due to its high spatial resolution, dedicated software and post-processing techniques, CCT is the method of choice [19]. In the literature, the attenuation thresholds for post-contrast CCT epicardial fat identification are variable and usually range from \(-\)250/\(-\)190 HU, as regards the lower limit, to \(-\)50/\(-\)5 HU for the upper threshold, with intermediate values between the limit values [20; 21; 22]. A modified range between \(-\)175 and \(-\)15 HU for CCT images was proposed, due to the relative contrast enhancement of EAT [12]. We already tested the segmentation accuracy of our software by calculating the Dice Similarity Coefficient (DSC) (92.48%) and the Mean Absolute Distance (MAD) (2.87) in the CCT datasets; we also calculated the correlation between the ground-truth epicardial fat volume and the corresponding automated measurement with the Pearson and Spearman coefficients, obtaining 0.9591 and 0.9490 for the calcium score and 0.9513 and 0.9319 for the CCT datasets, respectively [13]. Statins represent the targeted treatment for both the primary and the secondary prevention of cardiovascular diseases. Statins are not just hypocholesterolem drugs, thanks to their pleiotropic effect, they also act at a systemic level, reducing the risk of morbidity and mortality of cardiac and cerebrovascular diseases, by decreasing endothelial dysfunction [23]. So, in addition to their use for the treatment of hyperlipidemia and dyslipidemia, statins have a broad spectrum of clinical indications and are administered, for example, for the primary and secondary prevention of atherosclerotic cardiovascular disease and atherosclerosis [24]. The analysis of epicardial fat through a computer application could allow a more detailed global analysis of cardiovascular risk in selected patients. Several epidemiological studies showed that cardiovascular risk factors are linked to endothelial dysfunction [23; 25]. Clinically, the improvement of the endothelial function may explain the reduction of ischemic episodes in patients treated with statins. Statins promote a reduction in the inflammatory status, decreasing the TNF-\(\alpha\) and IL-6 levels and inhibiting the NF-kB protein pathway [26]. Recently, EAT has become a pharmacological target of statin therapy. [PERSON] et al. [27] demonstrated that the thickness of EAT decreased more in patients treated with atorvastatin than in the controls treated with the simvastatin-ezetimibe combination. [PERSON] et al. [28] demonstrated an EAT volume reduction at CCT in post-menopausal women with dyslipidemia treated with atorvastatin. At the end of the follow-up, there was a significant reduction in the volume of EAT in the atorvastatin group compared to the pravastatin group. The effect of atorvastatin on EAT was independent of the blood cholesterol levels and the progression of coronary artery disease. [PERSON] et al. [29], in a population of patients with aortic stenosis, demonstrated that patients treated with statins had lower epicardial fat thickness. Our study showed that statin administration caused significant quantitative (i.e., volume and thickness reduction) and qualitative (i.e., overall density and quartiles attenuation distribution) EAT changes.