Despite the development of preventive medicine, heart disease remains a major cause of death. Epicardial adipose tissue (EAT) is part of the visceral adipose tissue that surrounds the heart, and it has unique properties that distinguish it from other depots of visceral fat. EAT has a unique anatomical intimacy with the underlying heart muscle, sharing an unobstructed microcirculation with adjacent myocardial tissue, thus allowing the facilitated transit of both hormonal factors and pluripotent cells. EAT is a source of inflammatory bioactive substances that can substantially modulate cardiovascular morphology and function. Many pathological processes have been proposed as possible underlying mechanisms. In metabolic disorders, the release of adiponectin from EAT declines, and the synthesis of proinflammatory adipokines increases (leptin, tumor necrosis factor-α, interleukin 1-β and interleukin-6, and resistin). This promotes the infiltration of macrophages, destruction of microvascular systems, and activation of profibrotic pathways.

Mesenchymal stem cells from the epicardium can migrate to ventricular muscle and be transformed into fibroblasts. The coronary artery could be directly influenced by inflammatory cytokines. Together with increased reactive oxygen species generation, this may contribute to cardiac disease progression. Both mechanistic and epidemiological studies have demonstrated that EAT is associated with increased cardiovascular risk. EAT measurement by echocardiography, computed tomography, or cardiac magnetic resonance imaging has served as a potential marker in assessing cardiovascular risk, but a uniform standardized method has not yet been determined. On the other hand, EAT may be an important target for therapeutic interventions since drugs that modify the quantity and biology of EAT exert parallel effects to influence the risk of cardiovascular disorders. Despite this, there are several aspects to be clarified before we understand whether EAT is a marker that could improve risk stratification and guide future clinical decision-making.

In this Special Issue, we are looking for papers that will bring an innovative and integrated vision on the following subjects and provide state-of-the-art knowledge on those topics. Original research as well as review articles are welcome.

Potential topics include but are not limited to the following:

• In vitro/in vivo aspects of cardiovascular inflammation and tissue injury
• New technology for the diagnosis of pathological EAT
• The role of EAT in coronary atherosclerosis
• Association between EAT and serum biochemical indicators
• EAT and cardiovascular risk assessment
• The prognostic role of EAT assessment
• The value of echocardiography, cardiac magnetic resonance, and/or cardiac computed tomography for the assessment of EAT
• Associations between EAT and cardiovascular diseases, diet, and exercise
• Potential EAT targets and drug treatments of cardiovascular disease