Abstract MP47: The Association of Socioeconomic Status with Subclinical Myocardial Damage
Background: The association between socioeconomic status (SES) and clinical cardiovascular events is well established. However, little is known about the relationship between SES and subclinical myocardial damage, as assessed by a novel highly sensitive assay for cardiac troponin T (hs-cTnT).
Methods: We conducted a cross-sectional analysis of 11,411 participants from the ARIC Study with no history of cardiovascular disease who had hs-cTnT measured at visit 2 (1990-1992). SES was defined using either annual household income, categorized as: low (<$16,000), mid-level ($16,000 - $34,999), high (≥ $35,000), or lifetime educational attainment, categorized as: low (<12th grade), mid-level (12th grade/some college) and high (college degree or higher). hs-cTnT was categorized as non-elevated (<14 ng/L) and elevated (≥ 14ng/L). Poisson regression was used to generate prevalence ratios for elevated hs-cTnT, separately by level of income and education after adjusting for demographic, clinical, and behavioral factors.
Results: Persons with low income or low education were more likely to have subclinical myocardial damage as assessed by elevated hs-cTnT (≥14ng/L). Adjusted prevalence ratios for elevated troponin comparing low to high levels of income and education were 1.74 (95% CI: 1.32, 2.29) and 1.54 (95% CI: 1.21, 1.97), respectively (Table, Model 1). These results were slightly attenuated, but remained statistically significant after adjusting for cardiovascular risk factors and health behaviors (Models 2 and 3). Race-stratified results demonstrate a somewhat stronger and only significant association of low education with subclinical myocardial damage in blacks compared to whites (PR 1.83 vs 1.05, p-interaction =0.08). There was no race interaction with income (p-interaction =0.33).
Conclusions: Low SES was associated with elevated hs-cTnT, independent of cardiovascular risk factors, especially in blacks. Further research is needed to explore how low SES contributes to subclinical myocardial damage.
Author Disclosures: A.E. Fretz: None. A.L.C. Schneider: None. J. McEvoy: None. R. Hoogeveen: B. Research Grant; Significant; Received grant support from Roche Diagnostics and co-investigator on a provisional patient filed by Roche for use of biomarkers in heart failure prediction.. C. Other Research Support; Significant; Reagents for the high sensitivity cardiac troponin T assays were donated by Roche Diagnostics. C.M. Ballantyne: B. Research Grant; Significant; Received grant support from Roche Diagnostics and co-investigator on a provisional patient filed by Roche for use of biomarkers in heart failure prediction.. C. Other Research Support; Significant; Reagents for the high sensitivity cardiac troponin T assays were donated by Roche Diagnostics.. J. Coresh: None. E. Selvin: None.
- © 2015 by American Heart Association, Inc.