Increased intrathoracic and hepatic visceral adipose tissue independently correlates with coronary artery calcification in asymptomatic patients |
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Authors: | Harshal R. Patil MD Nirav T. Patil MD Samantha I. King MD Evan O’Keefe Rajiv Chhabra MD Shaya Ansari MD Kevin F. Kennedy MS Damini Dey PhD James H. O’Keefe MD FASNC John H. Helzberg MD Randall C. Thompson MD FASNC |
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Affiliation: | 1. Saint Luke’s Mid America Heart Institute, 4330 Wornall Road Suite 2000, Kansas City, MO, 64111, USA 4. University of Missouri-Kansas City School of Medicine, Kansas City, MO, USA 2. Saint Luke’s Department of Gastroenterology, Kansas City, MO, USA 3. Saint Luke’s Hospital, Kansas City, MO, USA 5. Saint Luke’s Department of Radiology, Kansas City, MO, USA 6. Cedars Sinai Medical Center CA, Los Angeles, CA, USA
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Abstract: | Background Visceral adipose tissue (VAT) is associated with cardiac events, but it is not clear which, if any of the various measures of VAT independently correlate with coronary artery disease (CAD). Methods We studied 400 patients undergoing computed tomography to determine coronary artery calcium (CAC) score. VAT was measured in the form of epicardial adipose tissue (EAT) volume and thickness, intrathoracic adipose tissue volume (ITAV), and hepatic steatosis. Results Of the 400 subjects, the average CAC score was 112.2 ± 389.3. When each measure of VAT (EAT volume and thickness, ITAV, hepatic steatosis) was added to the traditional model (they were independently associated with greater risk of CAC score ≥100 AU as measured by IDI/NRI (P < .05). On univariable logistic regression analysis, each of the 4 measures of VAT showed association with greater risk of a CAC score of ≥100 AU (OR > 1). Conclusions Each measure of VAT is a strong correlate of CAC score ≥100 AU in asymptomatic subjects—these VAT assessments correlate more significantly than do traditional CAD risk factors. This incremental power in the predictive models is likely the result of measurement of a fundamental expression of the metabolic syndrome and consequent proatherogenic derangements. |
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