Background: Unhealthy lifestyles and inflammation contribute to cardiovascular disease (CVD). GlycA is a novel biomarker of systemic inflammation representing post-translational glycosylation of acute phase reactants and associated with increased clinical CVD risk. Hypothesis: We hypothesized that ideal cardiovascular health (CVH), as assessed by (higher) Life's Simple 7 (LS7) scores, would be associated with lower GlycA levels among individuals free of CVD in a multiethnic community-based population. Methods: This was a cross-sectional study of 6479 Multi-Ethnic Study of Atherosclerosis participants [53% women; mean age 62 ± 10 years] with GlycA levels measured at baseline by nuclear magnetic resonance spectroscopy. The LS7 metrics (smoking, physical activity, diet, body mass index, blood pressure, cholesterol, and glucose) were each scored as ideal (2), moderate (1), or poor (0). Total scores were summed and categorized as optimal (12-14), average (8-11), and inadequate (0-7). Linear regression assessed percent difference in GlycA by LS7 scores, after adjusting for age, sex, ethnicity, education, income, family history of CVD, and other inflammatory biomarkers. Results: GlycA levels were 403.4 ± 63.1, 374.4 ± 59.2, and 350.3 ± 56.2 micromoles per liter (μmol/L) for inadequate, average, and optimal CVH, respectively (P-trend <0.001). After multivariable adjustment, GlycA remained independently and inversely associated with CVH categories, with a lower mean GlycA level of 5 μmol/L (95% confidence interval 4.5-5.8) for each one unit increment in LS7 score. Conclusions: Among this group of ethnically diverse individuals without CVD, suboptimal CVH is associated with higher GlycA levels, independent of traditional inflammatory biomarkers. Strategies aimed at improving CVH might reduce GlycA, which could be a marker of reduced risk of future CVD events.
Bibliographical noteFunding Information:
The authors thank the investigators, staff, and participants of the MESA study for their valuable contributions. E.D.M. and D.Z. were supported by the Blumenthal Scholars Fund for Preventive Cardiology at Johns Hopkins University. MESA 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 National Heart, Lung, and Blood Institute, and by grants UL1-TR-000040, UL1-TR-001079, and UL1-TR-001420 from NCATS. S.M. is supported by the NIH/NHLBI (R01HL134811 and K24 HL136852) and the NIH/NIDDK (DK112940).
© 2018 Wiley Periodicals, Inc.
- cardiovascular health