TY - JOUR
T1 - The novel inflammatory marker GlycA and the prevalence and progression of valvular and thoracic aortic calcification
T2 - The Multi-Ethnic Study of Atherosclerosis
AU - Ezeigwe, Angelica
AU - Fashanu, Oluwaseun E.
AU - Zhao, Di
AU - Budoff, Matthew J.
AU - Otvos, James D.
AU - Thomas, Isac C.
AU - Mora, Samia
AU - Tibuakuu, Martin
AU - Michos, Erin D.
N1 - Funding Information:
Drs. Michos and Zhao were supported by the Blumenthal Scholars Fund for Preventive Cardiology at Johns Hopkins University . This research was supported by grant R01 HL071739 from the National Heart, Lung, and Blood Institute to Dr. Budoff. This MESA study was funded by contracts HHSN268201500003I , N01-HC-95159 , N01-HC-95160 , N01-HC-95161 , N01-HC-95162 , N01-HC-95163 , N01-HC-95164 , N01-HC-95165 , N01-HC-95166 , N01-HC-95167 , N01-HC-95168 and N01-HC-95169 from the NHLBI , and by grants UL1-TR-000040 , UL1-TR-001079 , and UL1-TR-001420 from NCATS . Dr. Mora was supported by grants K24 HL136852 and R01HL134811 from the NHLBI .
Funding Information:
Dr. Otvos is employed by LabCorp (formerly LipoScience). Dr. Mora received an institutional research grant from Atherotech for work unrelated to this study, and is listed as co-inventor on a patent on the use of GlycA for predicting risk of colorectal cancer. Dr. Budoff receives grant support from NIH and General Electric . The other authors do not report any disclosures.
Funding Information:
Dr. Otvos is employed by LabCorp (formerly LipoScience). Dr. Mora received an institutional research grant from Atherotech for work unrelated to this study, and is listed as co-inventor on a patent on the use of GlycA for predicting risk of colorectal cancer. Dr. Budoff receives grant support from NIH and General Electric. The other authors do not report any disclosures.Drs. Michos and Zhao were supported by the Blumenthal Scholars Fund for Preventive Cardiology at Johns Hopkins University. This research was supported by grant R01 HL071739 from the National Heart, Lung, and Blood Institute to Dr. Budoff. This MESA study was funded by contracts HHSN268201500003I, N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168 and N01-HC-95169 from the NHLBI, and by grants UL1-TR-000040, UL1-TR-001079, and UL1-TR-001420 from NCATS. Dr. Mora was supported by grants K24 HL136852 and R01HL134811 from the NHLBI.
Publisher Copyright:
© 2019 Elsevier B.V.
PY - 2019/3
Y1 - 2019/3
N2 - Background and aims: GlycA is a novel composite biomarker of systemic inflammation reflecting posttranslational glycosylation of acute phase reactants. GlycA has been associated with coronary artery calcium, cardiovascular disease (CVD) events and mortality. Vascular calcifications outside of the coronary arteries are risk markers of CVD and mortality. Whether GlycA is linked to extra-coronary calcifications (ECC) is not well established. Methods: We studied 6462 MESA participants free of clinical CVD who had plasma GlycA measured at baseline. ECCs [calcification in aortic valve (AVC), mitral annulus (MAC), ascending and descending thoracic aorta (ATAC, DTAC)] were ascertained at baseline and follow-up visit (median 2.3-yrs later) by cardiac CT. Poisson regression models with robust variance estimation assessed associations of GlycA with prevalent and incident ECC. Linear mixed models assessed the cross-sectional and 2-year change in ECC. Models were adjusted for demographic and lifestyle factors. Results: In cross-sectional analysis, GlycA (per SD increment) was positively associated with prevalent AVC, ATAC and DTAC with adjusted prevalence ratios (95% CI) of 1.08 (1.01–1.14), 1.18 (1.03–1.34) and 1.10 (1.06–1.14), respectively. There was also a significant association between GlycA and baseline extent of both ATAC and DTAC. Longitudinally, GlycA was positively associated with incident MAC and DTAC, with adjusted incidence ratios of 1.18 (1.03–1.37) and 1.17 (1.07–1.28), respectively. GlycA was also associated with 2-year change in MAC and DTAC extent. Conclusions: In this diverse cohort free from clinical CVD, we found GlycA was positively associated with prevalent and incident ECC measures, in particular for progression of MAC and DTAC.
AB - Background and aims: GlycA is a novel composite biomarker of systemic inflammation reflecting posttranslational glycosylation of acute phase reactants. GlycA has been associated with coronary artery calcium, cardiovascular disease (CVD) events and mortality. Vascular calcifications outside of the coronary arteries are risk markers of CVD and mortality. Whether GlycA is linked to extra-coronary calcifications (ECC) is not well established. Methods: We studied 6462 MESA participants free of clinical CVD who had plasma GlycA measured at baseline. ECCs [calcification in aortic valve (AVC), mitral annulus (MAC), ascending and descending thoracic aorta (ATAC, DTAC)] were ascertained at baseline and follow-up visit (median 2.3-yrs later) by cardiac CT. Poisson regression models with robust variance estimation assessed associations of GlycA with prevalent and incident ECC. Linear mixed models assessed the cross-sectional and 2-year change in ECC. Models were adjusted for demographic and lifestyle factors. Results: In cross-sectional analysis, GlycA (per SD increment) was positively associated with prevalent AVC, ATAC and DTAC with adjusted prevalence ratios (95% CI) of 1.08 (1.01–1.14), 1.18 (1.03–1.34) and 1.10 (1.06–1.14), respectively. There was also a significant association between GlycA and baseline extent of both ATAC and DTAC. Longitudinally, GlycA was positively associated with incident MAC and DTAC, with adjusted incidence ratios of 1.18 (1.03–1.37) and 1.17 (1.07–1.28), respectively. GlycA was also associated with 2-year change in MAC and DTAC extent. Conclusions: In this diverse cohort free from clinical CVD, we found GlycA was positively associated with prevalent and incident ECC measures, in particular for progression of MAC and DTAC.
KW - Aortic valve calcification
KW - GlycA
KW - Inflammation
KW - Mitral annular calcification
KW - Thoracic aortic calcification
UR - http://www.scopus.com/inward/record.url?scp=85060896461&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85060896461&partnerID=8YFLogxK
U2 - 10.1016/j.atherosclerosis.2019.01.011
DO - 10.1016/j.atherosclerosis.2019.01.011
M3 - Article
C2 - 30716566
AN - SCOPUS:85060896461
VL - 282
SP - 91
EP - 99
JO - Atherosclerosis
JF - Atherosclerosis
SN - 0021-9150
ER -