Review Articles

Epicardial Fat

Pathophysiology and Clinical Significance

Douglass, Elijah MD^*; Greif, Shana MD^†; Frishman, William H. MD^‡

From the ^*Department of Medicine, Weill-Cornell Medical Center, New York, NY; ^†Department of Internal Medicine, Kaiser Permanente Los Angeles Medical Center, Los Angeles, CA; and ^‡Department of Medicine, Westchester Medical Center, New York Medical College, Valhalla, NY.

Disclosure: The authors have no conflict of interest to report.

Correspondence: William H. Frishman, MD, Department of Medicine, New York Medical College, Valhalla, NY 10595. E-mail: [email protected].

Cardiology in Review 25(5):p 230-235, September/October 2017. | DOI: 10.1097/CRD.0000000000000153

Abstract

Over the last decade and a half there has been much interest in understanding the role of epicardial adipose tissue (EAT) in cardiac pathology. EAT is a visceral adipose deposit with putative paracrine function. In the nondiseased state, EAT releases cardioprotective cytokines and chemokines to the coronary vasculature. In pathological states, EAT releases an inflammatory cytokine profile that is believed to contribute to the development and progression of coronary artery disease (CAD). EAT imaging with echocardiography, computed tomography, and magnetic resonance imaging has demonstrated a correlation between EAT size and CAD. Small interventional studies have found evidence that the pathological state of EAT is at least somewhat reversible. The relationship between EAT size and the development and/or progression of CAD may present future clinicians with a new tool for risk assessment and intervention response monitoring. In this article we review current basic science and clinical research, comment on the role of EAT imaging in the management of patients at risk for CAD, and suggest areas for future investigation.