Pál Maurovich-Horvat1,2, Kimberly Kallianos1, Leif-Christopher Engel1, Jackie Szymonifka3, Christopher L Schlett1,4, Wolfgang Koenig5, Udo Hoffmann1, Quynh A Truong6. 1. Cardiac MR PET CT Program, Division of Cardiology and Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA. 2. MTA-SE Lendulet Cardiovascular Imaging Research Group, Heart and Vascular Center, Semmelweis University, Budapest, Hungary. 3. Department of Biostatistics, Massachusetts General Hospital, Boston, Massachusetts, USA. 4. Department of Diagnostic and Interventional Radiology, University Hospital Heidelberg, Heidelberg, Germany. 5. Department of Internal Medicine II - Cardiology, University of Ulm Medical Center, Ulm, Germany. 6. Department of Radiology, New York-Presbyterian Hospital and Weill Cornell Medical College, Dalio Institute of Cardiovascular Imaging, New York City, New York, USA.
Abstract
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.
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.
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