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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Composite acute phase glycoproteins with coronary artery calcification depends on metabolic syndrome presence - The Brazilian Longitudinal Study of Adult Health (ELSA-Brasil)

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Harada, Paulo H. [1] ; Bensenor, Isabela M. [1, 2] ; Bittencourt, Marcio S. [1] ; Nasir, Khurram [3, 4] ; Blaha, Michael J. [3] ; Jones, Steven R. [3] ; Toth, Peter R. [3, 5] ; Lotufo, Paulo A. [1, 2]
Total Authors: 8
[1] Univ Sao Paulo, Univ Hosp, Ctr Clin & Epidemiol Res, Ave Lineu Prestes, 2565, BR-05508000 Sao Paulo - Brazil
[2] Univ Sao Paulo, Dept Med, Sch Med, Sao Paulo - Brazil
[3] Johns Hopkins Univ, Ciccarone Ctr Prevent Heart Dis, Baltimore, MD - USA
[4] Yale Univ, YNHH, Populat Hlth & Hlth Syst Res, Ctr Outcomes Res & Evaluat, New Haven, CT - USA
[5] Univ Illinois, Coll Med Peoria, Illinois CGH Med Ctr, Sterling, IL - USA
Total Affiliations: 5
Document type: Journal article
Source: JOURNAL OF CARDIOLOGY; v. 73, n. 5, p. 408-415, MAY 2019.
Web of Science Citations: 1

Background: Inflammation has been weakly associated with coronary artery calcium (CAC) in the overall population. However, it is currently unknown whether this varies according to the cardio-metabolic profile. We evaluated the association between GlycA, a unique composite biomarker of pro-inflammatory acute phase glycoproteins, high sensitivity C-reactive protein (hsCRP), uric acid, and their composite values (composite inflammation) in the overall population and strata according to cardiovascular risk. Methods: This is a cross-sectional study of 3753 Sao Paulo site participants of the ELSA-Brasil cohort that were free of cardiovascular/chronic inflammatory disease and not taking statins or allopurinol. We measured GlycA by nuclear magnetic resonance spectroscopy. For each biomarker quartile (Qs), we ran adjusted logistic and linear regression for CAC > 0 and CAC score. Results: In the overall analysis, the 4th vs. 1st GlycA Q odds ratio (OR) for CAC > 0 was 1.53 (95% CI: 1.18, 1.98, p trend < 0.001) adjusted for demographics and lifestyle, but null after adding metabolic syndrome (MS) components, OR 1.14 (95% CI: 0.86,1.51, p trend = 0.140). Likewise, for continuous CAC values there was no difference across GlycA Qs in the fully adjusted analysis. Similarly, hsCRP, uric acid, and composite inflammation were not associated with CAC > 0 or CAC score. In stratified analysis, GlycA was associated with CAC > 0 in No-MS individuals, standardized (SD) OR 1.23 (95% CI: 1.08, 1.40); but not in MS individuals, SD OR 1.01 (95% CI: 0.89,1.15)(p interaction 0.037). We found similar interaction in stratified analysis for continuous CAC on composite inflammation. Conclusions: GlycA and composite inflammation are associated with CAC among low cardiovascular risk individuals (No-MS), but not otherwise. GlycA and composite biomarkers may better represent sources of inflammation apart from visceral obesity and traditional cardiovascular risk factors, which may have relevant effect on CAC accumulation in low cardiovascular risk individuals. (C) 2018 Published by Elsevier Ltd on behalf of Japanese College of Cardiology. (AU)

FAPESP's process: 11/12256-4 - Calcium score and coronary atherosclerosis in an adult cohort
Grantee:Paulo Andrade Lotufo
Support type: Regular Research Grants