Key result
In patients with chest discomfort, reduced renal function independently increased hs-cTn concentrations and amplified the risk of adverse events per 1 ng/L rise in hs-cTnT (HR 1.07) compared to normal renal function (HR 1.02).
Why the study?
High-sensitivity cardiac troponins are elevated in myocardial injury and other conditions like renal dysfunction, complicating interpretation in patients with chest discomfort.
Does renal function independently influence high-sensitivity cardiac troponin concentrations and their prognostic value in patients with chest discomfort?
Cross-Sectional (n=1,864)
No
Does renal function independently influence high-sensitivity cardiac troponin concentrations and their prognostic value in patients with chest discomfort?
Answers are grounded in this paper and cite their sources.
Renal function independently influences high-sensitivity cardiac troponin concentrations in patients with chest discomfort, highlighting the need to account for eGFR when interpreting baseline hs-cTn levels for risk stratification.
BACKGROUND: High-sensitivity cardiac troponins (hs-cTn) are the preferred biomarkers to detect myocardial injury, making them promising risk-stratifying tools for patients with symptoms of chest pain. However, circulating hs-cTn are also elevated in other conditions like renal dysfunction, complicating appropriate interpretation of low-level hs-cTn concentrations. METHODS: A cross-sectional analysis was performed in 1864 patients with symptoms of chest discomfort from the cardiology outpatient department who underwent cardiac computed tomographic angiography (CCTA). Serum samples were analyzed using hs-cTnT and hs-cTnI assays. Renal function was measured by the estimated glomerular filtration rate (eGFR), established from serum creatinine and cystatin C. On follow-up, the incidence of adverse events was assessed. RESULTS: Median hs-cTnT and hs-cTnI concentrations were 7.2(5.8-9.2) ng/L and 2.6(1.8-4.1) ng/L, respectively. Multivariable regression analysis revealed that both assay results were more strongly associated with eGFR (hs-cTnT:stβ:-0.290;hs-cTnI:stβ:-0.222) than with cardiac imaging parameters, such as coronary calcium score, CCTA plaque severity score and left ventricular mass (all p<0.01). Furthermore, survival analysis indicated lower relative risks in patients with normal compared to reduced renal function for hs-cTnT [HR(95%CI), 1.02(1.00-1.03) compared to 1.07(1.05-1.09)] and hs-cTnI [1.01(1.00-1.01) compared to 1.02(1.01-1.02)] (all p<0.001). CONCLUSION: In patients with chest discomfort, we identified an independent influence of renal function on hs-cTn concentrations besides CAD, that affected the association of hs-cTn concentrations with adverse events. Estimating renal function is therefore warranted when interpreting baseline hs-cTn concentrations.
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Cardinaels et al. (2016) conducted a cross-sectional in Chest discomfort (n=1,864). Reduced renal function (eGFR <90 mL/min/1.73m²) vs. Normal renal function (eGFR ≥90 mL/min/1.73m²) was evaluated on Adverse events (mortality and major adverse cardiovascular events) per 1 ng/L rise in hs-cTnT (HR 1.07, 95% CI 1.05-1.09, p=<0.001). In patients with chest discomfort, reduced renal function independently increased hs-cTn concentrations and amplified the risk of adverse events per 1 ng/L rise in hs-cTnT (HR 1.07) compared to normal renal function (HR 1.02).
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