Key result
In stable patients on chronic hemodialysis, increased cardiac troponin T correlated with increased BNP (r=0.531, p<0.001) and was associated with mortality and hospitalized heart failure.
Why the study?
Increased cTnT identifies high-risk end-stage renal disease patients, but its mechanism of elevation remains unclear in those without ACS.
Do elevated levels of cardiac troponin T, BNP, and ANP predict adverse clinical outcomes in stable patients on chronic hemodialysis?
Cohort (n=174)
Do elevated levels of cardiac troponin T, BNP, and ANP predict adverse clinical outcomes in stable patients on chronic hemodialysis?
In stable hemodialysis patients without acute coronary syndrome, elevated cTnT reflects increased left ventricular end-diastolic pressure and predicts heart failure-related events and mortality, but not arteriosclerotic events.
May aid risk stratification in stable hemodialysis; leaves open whether biomarker monitoring improves outcomes.
BACKGROUND: An increased cardiac troponin T (cTnT) level identifies a high-risk group in patients with end-stage renal disease; however, the mechanism of cTnT elevation remains unclear in such patients without acute coronary syndrome (ACS). Therefore, we explored the relationship between cTnT levels and the hemodynamic parameters and the prognostic potential of cTnT in stable patients with chronic hemodialysis (HD). METHODS: We included consecutive 174 patients with HD who were referred for coronary angiography due to stable coronary artery disease (CAD), peripheral artery disease (PAD), or heart failure (HF). Hemodynamic measurement was performed, and plasma cTnT, B-type natriuretic peptide (BNP), and A-type natriuretic peptide (ANP) were measured at the same time. The potential of 3 biomarkers to predict all-cause mortality, cardiac death or hospitalized HF, and vascular event was assessed. RESULTS: Increased log cTnT levels were correlated with increased log BNP and log ANP levels (r = 0.531, p < 0.001 and r = 0.411, p < 0.001, respectively). Not increased log cTnT, but increased log BNP and log ANP were associated with the presence of CAD and the extent of CAD. In contrast, they were all associated with the New York Heart Association functional classification and the presence of PAD and significantly correlated with left ventricular end-diastolic pressure (LVEDP) in an independent manner. Increased cTnT and BNP levels were associated with the mortality and hospitalized HF. However, increased cTnT was not associated with vascular events, unlike increased BNP. CONCLUSIONS: In patients with chronic HD without ACS, increased cTnT reflected increased LVEDP and the presence of HF or PAD independently, and it did not reflect the presence of CAD in contrast to increased BNP. cTnT and BNP were significant prognostic predictors; however, increased cTnT was associated with HF-related events, not with arteriosclerotic events.
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Niizuma et al. (2019) conducted a cohort in Chronic hemodialysis and cardiovascular disease (n=174). Cardiac troponin T (cTnT) vs. B-type natriuretic peptide (BNP) and A-type natriuretic peptide (ANP) was evaluated on All-cause mortality, cardiac death or hospitalized HF, and vascular event. In stable patients on chronic hemodialysis, increased cardiac troponin T correlated with increased BNP (r=0.531, p<0.001) and was associated with mortality and hospitalized heart failure.
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