الفهرس 
Epicardial adipose tissue: General overviewOnly 14 pages are availabe for public view
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Abstract
INTRODUCTION
isceral adiposity has been increasingly recognized as a
marker for cardiovascular risk and metabolic syndrome,
including glucose intolerance, hypertension, dyslipidemia,
hyperinsulinemia, and atherosclerosis. The pathophysiology
may be explained by its action as an endocrine and paracrine
organ with various biological and metabolic functions,
including a reservoir for several atherogenic inflammatory
cytokines (Das, 2001).
Visceral adipose tissue expresses numerous genes for
secretory proteins, and several biologically active molecules
secreted from adipose tissue (adipocytokines) may have
important roles in the development of atherosclerotic diseases
(Funahashi et al., 1999).
Epicardial adipose tissue (EAT) is a particular form of
visceral adipose tissue deposited around the heart and found in
considerable quantities around subepicardial coronary arteries.
EAT shares a common embryological origin with
abdominal adipose tissue. additionally, EAT of patients with
significant coronary artery disease (CAD) has been shown to be
a source of several inflammatory mediators and exhibited
significant inflammatory responses, independant of body mass
index (BMI) or diabetes (Mazurek et al., 2003).
Earlier studies in cadavers showed that the weight of
dissected epicardial fat is correlated with the heart weight, and
that coronary atherosclerotic plaque tend to be more prominent
on the arterial side in contact with EAT deposits.
Other studies have shown that EAT supplies free fatty
acids for myocardial energy production and synthesis
cytokines. Data from animal studies suggested that the rate of
fatty acid synthesis is significantly greater in EAT than in any
other depots of the body (Marchington et al., 1989;
Marchington et al., 1990).
EAT measured either on the right ventricle or the amount
surrounding the whole heart is significantly related to waist
circumference, diastolic blood pressure, left ventricular mass, high
level of insulin, and the severity of CAD assessed by coronary
angiography (Iacobellis et al., 2003; Iacobellis et al., 2005).
All these findings suggest that EAT plays a role in the
development of coronary atherosclerosis via the association with
conventional risk factors and also direct endocrine and paracrine
effects. This hypothesis was suspected many years ago based on
studies demonstrating the absence of atherosclerosis in human
intramyocardial, but not epicardial, coronary arteries (Geiringer
et al., 1951; Robicsek et al., 1994).
Segments of coronary arteries lacking EAT or separated
from it by a bridge of myocardial tissue appear to be protected
against the development of atherosclerosis. This may be due to
the absence of adipose tissue in the myocardium as compared
with epicardial coronary arteries (Chaldakov et al., 2001).
de Vos et al. evaluated the relationship between pericoronary
EAT and cardiovascular risk factors and coronary
artery calcification in 573 healthy post-menopausal women
selected from participants in the PROSPECT study (de Vos et
al., 2008).
The wide range of using the Multi-slice computed
tomography (MSCT) in diagnosis of atherosclerotic
cardiovascular diseases raise the need for another simple
techniques that add diagnostic tool to other risk factors without
additional coast and during the same CT examination.