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Relationship of thoracic fat depots with coronary atherosclerosis and circulating inflammatory biomarkers
Author(s) -
MaurovichHorvat Pál,
Kallianos Kimberly,
Engel LeifChristopher,
Szymonifka Jackie,
Schlett Christopher L.,
Koenig Wolfgang,
Hoffmann Udo,
Truong Quynh A.
Publication year - 2015
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21080
Subject(s) - medicine , adiponectin , coronary artery disease , cardiology , adipose tissue , inflammation , pathogenesis , myocardial infarction , obesity , insulin resistance
Objective The aim of the study was to determine the relationship of various thoracic fat depots with the presence and extent of coronary artery plaque and circulating biomarkers. Methods In 342 patients (52 ± 11 years, 61% male, BMI 29.1 ± 5.9 kg/m 2 ) with coronary computed tomography (CT), angiography, we measured the fat volume in four thoracic depots (pericoronary, epicardial, periaortic, extracardiac), assessed coronary plaque, and determined the circulating levels of C‐reactive protein, tumor necrosis factor alpha, plasminogen activator inhibitor‐1, monocyte chemoattractant protein‐1, and adiponectin. The extent of coronary plaque was classified into three groups: 0, 1−3, and >3 segments. Results Patients with plaque ( n =169, 49%) had higher volumes of all four fat depots as compared to patients without plaque (all P < 0.01), despite similar BMI ( P = 0.18). Extracardiac fat was most strongly correlated with BMI ( r = 0.45, P < 0.001), while pericoronary fat was least ( r = 0.21, P < 0.001). Only pericoronary fat remained associated with coronary plaque in adjusted analyses. Inflammatory biomarkers showed a positive correlation with pericoronary fat (all P < 0.0001), whereas adiponectin was not associated with this fat compartment ( P = 0.60) and showed a negative correlation with all other fat depots (all P < 0.001). Conclusions Pericoronary fat is independently associated with coronary artery disease (CAD). Its correlation with inflammatory biomarkers suggests that while systemic inflammation plays a role in the pathogenesis of CAD, there are additional local effects that may exist.