We discuss the anatomy, physiology, and pathophysiology of epicardial adipose tissue
and its relationship to coronary atherosclerosis. Epicardial fat stores triglyceride
to supply free fatty acids for myocardial energy production and produces adipokines.
It shares a common embryological origin with mesenteric and omental fat. Like visceral
abdominal fat, epicardial fat thickness, measured by echocardiography, is increased
in obesity. Epicardial fat could influence coronary atherogenesis and myocardial function
because there is no fibrous fascial layer to impede diffusion of free fatty acids
and adipokines between it and the underlying vessel wall as well as the myocardium.
Segments of coronary arteries lacking epicardial fat or separated from it by a bridge
of myocardial tissue are protected against the development of atherosclerosis in those
segments. However, when epicardial fat is totally absent in congenital generalized
lipodystrophy, coronary atherosclerosis can still occur. Macrophages are more numerous
and densely packed in the periadventitial fat of human atherosclerotic coronary arteries
with lipid cores than in that of fibrocalcific or nonatherosclerotic coronary arteries.
In obese patients with multiple cardiovascular risk factors, epicardial fat around
atheromatous coronaries secretes several proinflammatory cytokines and is infiltrated
by macrophages, lymphocytes, and basophils. Epicardial adipokine expression in obesity
without coronary atherosclerosis has not been determined. In nonobese patients, epicardial
fat around atheromatous coronary arteries expresses proinflammatory cytokines but
produces either less adiponectin, a vasoprotective adipokine, than fat around nonatheromatous
coronaries or a similar amount compared with thoracic subcutaneous fat. Further studies
should be done to test the hypothesis that adipokines produced by and released from
human epicardial adipose tissue might contribute locally to the pathogenesis of coronary