TY - JOUR
T1 - High-Sensitivity Cardiac Troponin Concentrations in Patients with Chest Discomfort: Is It the Heart or the Kidneys As Well?
AU - Cardinaels, Eline P. M.
AU - Altintas, Sibel
AU - Versteylen, Mathijs O.
AU - Joosen, Ivo A.
AU - Jellema, Laurens-Jan C.
AU - Wildberger, Joachim E.
AU - Das, Marco
AU - Crijns, Harry J.
AU - Bekers, Otto
AU - van Dieijen-Visser, Marja P.
AU - Kietselaer, Bastiaan L.
AU - Mingels, Alma M. A.
PY - 2016/4/20
Y1 - 2016/4/20
N2 - 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: st beta:-0.290; hs-cTnI: st beta:-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.
AB - 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: st beta:-0.290; hs-cTnI: st beta:-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.
U2 - 10.1371/journal.pone.0153300
DO - 10.1371/journal.pone.0153300
M3 - Article
C2 - 27096420
SN - 1932-6203
VL - 11
JO - PLOS ONE
JF - PLOS ONE
IS - 4
M1 - e0153300
ER -