The heart (epicardial adipose tissue and coronary TC)

Epicardial adipose tissue (EAT) is a unique and multifunctional adipose compartment of the heart, located between the myocardium and the epicardium. EAT is a white adipose tissue, albeit it also has brown or beige fat-like features. No muscle fascia divides EAT and myocardium; this allows a direct interaction and crosstalk between the epicardial fat and the myocardium. Due to its distinctive transcriptome and functional proximity to the heart, pericoronary adipose tissue (PCAT) and left atrial EAT can play a key role in the development and progression of coronary artery disease, atrial fibrillation, and heart failure. EAT can be clinically measured with cardiac imaging techniques such as echocardiography, computed tomography (CT), and magnetic resonance imaging, that can help to predict and stratify cardiovascular risk. Clinically, EAT, given its rapid metabolism and simple measurability, can be considered a novel therapeutic target, owing to its responsiveness to drugs with pleiotropic and clear beneficial cardiovascular effects such as the glucagon-like peptide-1 receptor (GLP-1R) agonists. Routine coronary CT angiography (CCTA) also allows the evaluation of EAT and PCAT attenuation, which is a measure of density expressed in Hounsfield units (HU), which ranges between −30 HU and −190 HU, where a lower negative means higher density. Radiographic fat density is determined by adipocyte hypertrophy, hyperplasia, and fibrosis which oppositely influence fat CT attenuation. Hypertrophic and hyperplastic fat depots usually have low density. Increased EAT and PCAT attenuation, reported in patients with CAD or severe COVID-19, could be caused by inflammation and fibrosis, mitigating the expected effects of hypertrophic or hyperplastic fat cells on fat CT attenuation. EAT and PCAT attenuation, could be considered a biosensor of vascular inflammation and may be used to track response to drugs with pleiotropic and clear beneficial cardiometabolic effects.