The epicardial adipose inflammatory triad: coronary atherosclerosis, atrial fibrillation, and heart failure with a preserved ejection fraction.

Milton Packer M.D.
Packer, M. (2018). “The epicardial adipose inflammatory triad: coronary atherosclerosis, atrial fibrillation, and heart failure with a preserved ejection fraction.” Eur J Heart Fail Sep 17. [Epub ahead of print].
Effect of epicardial adipose inflammation on coronary arteries: Classically, coronary atherosclerosis has been viewed as an inflammatory response to the transit of lipoproteins from the bloodstream across the endothelium and into the vessel wall. However, accelerated coronary atherosclerosis is also a prominent feature of many systemic inflammatory disorders, in a manner that is independent of circulating lipoproteins. How can systemic inflammation promote the development of obstructive coronary artery disease? Systemic inflammation leads to the accumulation and deranged biology of epicardial adipocytes. The resulting transmission of pro‐inflammatory cytokines and mesenchymal cells from the perivascular adipose tissue across the vascular adventitia can lead to plaque formation within the coronary vessels. In chronic inflammatory states, the accumulation of epicardial adipose tissue is closely associated with the presence, severity and progression of coronary artery disease, in a manner that is independent of circulating lipids or adiposity. Focal obstructive lesions reside in the coronary arterial segments that are immediately adjacent to areas of epicardial fat with the greatest thickness, and experimental resection of the epicardium ameliorates coronary atherosclerosis. These observations support the hypothesis that the accumulation of epicardial adipose tissue (and inflammation of perivascular fat) can act in a paracrine manner to adversely influence the structure and function of the coronary arteries. (Excerpt from text, p. 2; no abstract available.)