Epicardial and perivascular adipose tissues and their influence on cardiovascular disease: Basic mechanisms and clinical associations

Abstract

Increased EAT thickness measured by using echocardiography or EAT/PAT volume by using CT/MRI correlates well with visceral adiposity and hence is associated with multiple components of the metabolic syndrome. Although increased EAT volume is associated with prevalent CAD, this association is most likely due to the systemic inflammation caused by hypertrophied visceral fat depots. There is no strong evidence to date that EAT or PVAT in humans is independently associated with incident CVD. However, EAT may have local paracrine effects on the heart and circulation, as shown by the independent association of EAT volume with coronary calcification, LA volume, AF presence, and burden. This possibility seems increasingly likely in light of evidence that EAT from patients with CAD has increased inflammatory cytokine expression at the tissue level, without evidence of increased proinflammatory cytokines in serum.49 The observation that patients with systolic HF have reduced EAT volume suggests that there may be a beneficial effect of EAT that is lost in systolic dysfunction. Whether this correlates with reduced tissue or plasma levels of cardioprotective adipokines such as ADIPOQ has yet to be demonstrated, and it may also be a manifestation of cardiac cachexia. Certainly, there is ample evidence to suggest that EAT and PAT are potential therapeutic targets that could be modified to affect health or disease. For example, diet, exercise, and gastric bypass have all been shown to reduce visceral and epicardial fat mass and lower cardiometabolic risk.81,109,110 Additional experimental therapeutic strategies may include drugs that inhibit EAT/PAT inflammation, epicardial/pericardial fat removal or transplantation, and stem cell-based protocols in chronic systolic HF. © 2014 The Authors.