Longitudinal changes of cardiac troponin and inflammation reflect progressive myocyte stretch and likelihood for hypertension in a Black male cohort: the SABPA study

Abstract

Inflammation was cross-sectionally associated with subclinical wall remodeling and hypertension. Whether longitudinal changes (∆) in inflammation, myocyte injury (troponin T), and stretch (N-terminal-pro-B-type natriuretic peptide) are associated with hypertension and ECG left ventricular hypertrophy (ECG-LVH) is unclear. The first prospective analysis in Africa assessing these associations included a cohort of Black and White teachers (N = 338; aged 20–63 years). Fasting blood samples were obtained to measure tumor necrosis factor-alpha (TNF-α), cardiac troponin T (cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP). Ambulatory blood pressure, 2-lead ECG and resting 10-lead ECG values were obtained. A higher mean hypertensive status (62%) was evident in Blacks compared to Whites (44%, p < 0.001). Over 3-years, NT-proBNP increased in both ethnic groups. No associations were evident in women or in White men. In Black men, ECG-LVH at follow-up was positively associated with baseline cTnT (Adj R2 0.43; β = 0.48; 95% CI 0.28–0.68, p < 0.001) and baseline SBP (Adj R2 0.43; β = 0.29; 95% CI 0.09–0.49, p = 0.006). In Black men, baseline TNF-α (OR = 1.49, 95% CI 1.05–2.14, p = 0.03) and decreased ΔTNF-α (OR = 2.07, 95% CI 1.26–3.40, p = 0.004) increased the likelihood for cTnT levels ≥ 4.2 ng/L. Here, baseline NT-proBNP (OR = 1.12, 95% CI 1.01–1.23, p = 0.03) and ΔNT-proBNP progression (OR = 1.09, 95% CI 1.00–1.81, p = 0.04) increased the likelihood for 24-h hypertension. In conclusion, chronically increased levels of markers of myocyte injury accompanied by progressive myocardial stretch, reflective of cardiac metabolic overdemand, may ultimately increase hypertension and ischemic heart disease risk in a cohort of Black males