Epicardial fat with its close proximity to coronary arteries has been suggested to
be a significant predictor of cardiovascular disease. We studied the relations among
acquired obesity, low-grade inflammation, and genetic factors in the accumulation
of epicardial fat. A rare sample (n = 15) of healthy monozygotic (MZ) twin pairs discordant
for obesity (intrapair difference in body mass index ≥3 kg/m2) and 9 concordant MZ pairs 23 to 33 years old were examined for cardiac structure,
function, epicardial fat thickness (echocardiography), abdominal subcutaneous tissue,
and visceral adipose tissue (VAT), liver fat (magnetic resonance imaging/spectroscopy),
and serum high-sensitivity C-reactive protein. In the entire sample, MZ cotwins were
remarkably similar in most echocardiographic measurements including epicardial fat
(intraclass correlation 0.63, p = 0.0004). However, in the discordant pairs, the obese
cotwins (16.5 kg, 23% heavier) had 26% more epicardial fat (p = 0.0029) than nonobese
cotwins. They also had significantly larger atrial and left ventricular dimensions.
Epicardial fat correlated with VAT (r = 0.49, p = 0.02) in individual twins and when
using intrapair differences of measurements within pairs (r = 0.39, p = 0.06). In
multiple regression analyses including abdominal subcutaneous tissue, VAT, and liver
fat, high-sensitivity C-reactive protein was the only factor that remained significantly
associated with epicardial fat in individual twins and within pairs. In conclusion,
subjects who share the same genes seem to have similar cardiac dimensions. However,
acquired obesity increases epicardial fat independent of genetic factors. The close
relation between epicardial fat and low-grade inflammation is likely to contribute
to the development of cardiovascular disease in obesity.
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Article info
Publication history
Published online: February 13, 2012
Accepted:
December 19,
2011
Received in revised form:
December 19,
2011
Received:
October 9,
2011
Footnotes
The work was supported by Helsinki University Hospital Research Funds, Helsinki, Finland (Dr. Rissanen and Dr. Pietiläinen), Special Governmental Subsidy for Health Sciences, Helsinki, Finland (Dr. Lundbom), grants from Novo Nordisk, Helsinki, Finland, Gyllenberg, Helsinki, Finland, Yrjö Jahnsson, Helsinki, Finland, Biomedicum Helsinki, Helsinki, Finland, the Jalmari and Rauha Ahokas Foundation, Helsinki, Finland, the Diabetes Research Foundation, Helsinki, Finland, and the Finnish Foundation for Cardiovascular Research, Helsinki, Finland (Dr. Pietiläinen), and the Academy of Finland Center of Excellence in Complex Disease Genetics, Helsinki, Finland (Dr. Kaprio).
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© 2012 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
