Epicardial Fat and Coronary Vulnerability

Abstract

Coronary artery disease (CAD) represents the major cause of mortality and long-term disability worldwide. Despite new improvements in primary and secondary prevention methods, CAD-related mortality and morbidity demonstrate an increasing trend in the last decades. [1][2][3] CAD represents the most common and severe consequence of atherosclerosis. 4 Atherosclerotic plaque rupture, leading to acute coronary syndromes as the most severe outcome, consists in a complex biomechanical process resulting from the interaction between traditional risk factors, structural features, hemodynamical stresses, and biological processes. 5,6 In the last years, an increased attention has been given to the role of epicardial adipose tissue (EAT) as a marker of cardiovascular risk, as well as to the assessment of atheromatous plaque instability. 7,8 Recent reports suggest that an increased volume of EAT is directly associated with the presence of high-risk features in the coronary plaques, as subjects with unstable coronary lesions have significantly larger EAT volumes than those without high-risk plaques. 8 EAT represents an adipose depot rich in proinflammatory and proatherogenic molecules. Based on the anatomic proximity of EAT to the arterial adventitia of coronary arteries, the "outside in" hypothesis of atherosclerosis has been recently launched, according to which EAT components may trigger vascular inflammation and plaque destabilization through paracrine and vasocrine mechanisms. [9][10][11][12][13] It has been demonstrated that the amount of EAT is directly correlated with both the length and the severity of coronary lesions, at the same time being associated with the transformation of atherosclerotic plaques into a vulnerable phenotype, considered to be "high risk" for major cardiovascular events. 11 In a large study conducted by Nerlekar et al., a strong correlation was found between several CT features of vulnerable atherosclerotic plaques, such as low-attenuation lesions and positive remodeling at the lesion site. 9 In the largest study to date, Motoyama et al. identified plaque features strongly correlated with future acute coronary syndrome (ACS) development in 3,158 subjects. 14 Moreover, in a trial of non-obese subjects who underwent repeated coronary CT follow-up in a 4-year period, increased EAT volume proved to be associated with high-risk plaques as well as with future ACS despite optimal treatment of CV risk factors. 15 However, the major weakness of these trials remains CORRESPONDENCE Roxana Hodas Str. Gheorghe Marinescu nr. 38