A US study showed that intensive systolic blood pressure (SBP) lowering increased hs-cTnT (high-sensitivity cardiac troponin T), mediated by reduced kidney filtration; and decreased NT-proBNP (N-terminal pro-B-type natriuretic peptide), mediated by the drop in SBP. The observed changes in hs-cTnT and NT-proBNP levels with intensive SBP lowering were associated with clinical outcomes. hs-cTnT and NT-proBNP were measured at baseline and 1 year from stored specimens in Systolic Blood Pressure Intervention Trial. Intensive SBP lowering (versus standard SBP management) resulted in a 3% increase in hs-cTnT levels over 1-year follow-up (geometric mean ratio, 1.03) and a higher proportion of participants with ≥50% increase (odds ratio, 1.47). In contrast, intensive SBP lowering led to a 10% decrease in NT-proBNP (geometric mean ratio, 0.90) and a lower probability of ≥50% increase in NT-proBNP (odds ratio, 0.57). The association of intensive treatment on change in hs-cTnT was completely attenuated after accounting for changes in estimated glomerular filtration rate over follow-up, whereas the association of intensive treatment with NT-proBNP was completely attenuated after adjusting for change in SBP. Increases in hs-cTnT and NT-proBNP from baseline to 1 year were associated with higher risk for heart failure and death, with no significant interactions by treatment assignment. The findings highlight the role of noncardiac factors influencing biomarker changes and the complexity of using cardiac-specific biomarkers as disease surrogates. Source: https://www.ahajournals.org/
