TY - JOUR
T1 - Composite acute phase glycoproteins with coronary artery calcification depends on metabolic syndrome presence – The Brazilian Longitudinal Study of Adult Health (ELSA-Brasil)
AU - Harada, Paulo H.
AU - Benseñor, Isabela M.
AU - Bittencourt, Márcio S.
AU - Nasir, Khurram
AU - Blaha, Michael J.
AU - Jones, Steven R.
AU - Toth, Peter P.
AU - Lotufo, Paulo A.
N1 - Funding Information:
This research (ELSA-Brasil) was supported by the Brazilian Ministry of Health (Science and Technology Department) and the Brazilian Ministry of Science and Technology (Financiadora de Estudos e Projetos and CNPq National Research Council; grants 01 06 0010.00 RS, 01 06 0212.00 BA, 01 06 0300.00 ES, 01 06 0278.00 MG, 01 06 0115.00 SP, and 01 06 0071.00 RJ). The ancillary ELSA-Brasil CAC study was funded by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP 2011/12256-4). None of these agencies had any role in study design. This research received no grant from any funding agency in the public, commercial, or not-for-profit sectors.
Funding Information:
This research (ELSA-Brasil) was supported by the Brazilian Ministry of Health (Science and Technology Department) and the Brazilian Ministry of Science and Technology ( Financiadora de Estudos e Projetos and CNPq National Research Council; grants 01 06 0010.00 RS , 01 06 0212.00 BA , 01 06 0300.00 ES , 01 06 0278.00 MG , 01 06 0115.00 SP , and 01 06 0071.00 RJ ). The ancillary ELSA-Brasil CAC study was funded by Fundação de Amparo à Pesquisa do Estado de São Paulo ( FAPESP 2011/12256-4 ). None of these agencies had any role in study design. This research received no grant from any funding agency in the public, commercial, or not-for-profit sectors.
Publisher Copyright:
© 2018
PY - 2019/5
Y1 - 2019/5
N2 - 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.
AB - 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.
KW - Coronary artery calcium
KW - GlycA
KW - High sensitivity C-reactive protein
KW - Inflammation
KW - Metabolic syndrome
UR - http://www.scopus.com/inward/record.url?scp=85059146302&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85059146302&partnerID=8YFLogxK
U2 - 10.1016/j.jjcc.2018.09.006
DO - 10.1016/j.jjcc.2018.09.006
M3 - Article
C2 - 30595405
AN - SCOPUS:85059146302
SN - 0914-5087
VL - 73
SP - 408
EP - 415
JO - Journal of Cardiology
JF - Journal of Cardiology
IS - 5
ER -