Abstract 12124: GlycA is Associated With Both Coronary Artery Calcium Incidence and Progression: ELSA-Brasil Cohort Analysis

Abstract

Introduction: GlycA is an emerging systemic inflammatory marker and quantifies N-acetyl glucosamine within the glycan region of acute phase proteins. Elevated levels of GlycA, are associated with a higher risk for coronary artery disease (CAD). There is conflicting evidence on whether GlycA levels can predict subclinical CAD progression in healthy adults. Hypothesis: High GlycA levels can predict subclinical CAD progression in healthy patients. Methods: We included 2,690 participants from the ELSA-Brasil cohort without cardiovascular/chronic inflammatory disease not receiving statin therapy who had GlycA level measured and two interval coronary artery calcium score (CAC) assessments between 2010 through 2018. Multivariable regression models adjusted for demographics, lifestyle, comorbidities, and laboratory parameters were used to assess the consistency of GlycA levels and CAC incidence and progression (Berry definition). CAC incidence required that the first CAC = 0. CAC progression required that the first CAC > 0. Therefore, the presence of CAC incidence and progression were mutually exclusive. Results: The mean age of participants was 48.6 ± 7.7 years, 56.7% were female, 54.6% and 16.1% (429/2690) were White and Black, respectively. The mean CAC interscan period was 5.1 ± 0.9 years, the mean GlycA level was 414.7 ± 65 μmol/L, and the incidence of CAC was 13.1%. GlycA level odds ratio (OR) for CAC incidence was 1.002 (95% CI 1.0005-1.005, p = .016) adjusted for demographics, lifestyle, early (≤60 years) CAD family history, lipid panel, and comorbidities. The GlycA (≤p25 vs >p75) OR for CAC progression (Berry definition) was 1.77 (95% CI 1.07-2.96, p = .03) in a similar multivariable adjustment model. Conclusions: Higher GlycA levels were associated with CAC incidence and progression even after adjusting for multivariable risk factors in a healthy Brazilian cohort. GlycA may have potential to further stratify CAD risk in healthy patients.