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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Prognostic value of high-sensitivity cardiac troponin T in acute ischemic stroke.
Journal of Stroke and Cerebrovascular Diseases : the Official Journal of National Stroke Association 2014 Februrary
BACKGROUND: Cardiac troponins have been investigated as prognostic markers in the setting of ischemic stroke with diverging results. A new generation of highly sensitive troponin assays have recently been developed that allow for the detection of concentrations 5 to 10 times lower than those measureable with conventional assays. The aim of this study was to determine the association between high-sensitivity cardiac troponin T (hs-cTnT) elevation on admission and mortality after acute ischemic stroke.
METHODS: Serum concentrations of hs-cTnT were measured at the time of admission in 347 patients with acute ischemic stroke. Clinical data and background information were obtained. Total follow-up time was 1.5 ± 0.7 years, and all-cause mortality was used as the outcome measure.
RESULTS: Median hs-cTnT on admission in the whole group was 15.2 ng/L (interquartile range [IQR] 7.5-27.8), and was higher in nonsurvivors than survivors (28.2 ng/L [IQR 15.6-39.5] vs 11.4 ng/L [IQR 6.0-21.2]; P < .001). In multivariate analysis, high hs-cTnT (the fourth quartile) was independently associated with all-cause mortality during the follow-up period, with a hazard ratio of 1.65 (95% confidence interval [CI] 1.04-2.63; P = .035). The addition of hs-cTnT as a continuous variable to the multivariate model resulted in both incremental discrimination and reclassification of patients (C-index increase from 0.819 to 0.834 [P = .007]; integrated discrimination index 0.011 [95% CI 0.001-0.021; P = .028]).
CONCLUSIONS: Circulating hs-cTnT levels are closely associated with the risk of death in patients with acute ischemic stroke, and even levels below the upper reference limit appear to have prognostic value.
METHODS: Serum concentrations of hs-cTnT were measured at the time of admission in 347 patients with acute ischemic stroke. Clinical data and background information were obtained. Total follow-up time was 1.5 ± 0.7 years, and all-cause mortality was used as the outcome measure.
RESULTS: Median hs-cTnT on admission in the whole group was 15.2 ng/L (interquartile range [IQR] 7.5-27.8), and was higher in nonsurvivors than survivors (28.2 ng/L [IQR 15.6-39.5] vs 11.4 ng/L [IQR 6.0-21.2]; P < .001). In multivariate analysis, high hs-cTnT (the fourth quartile) was independently associated with all-cause mortality during the follow-up period, with a hazard ratio of 1.65 (95% confidence interval [CI] 1.04-2.63; P = .035). The addition of hs-cTnT as a continuous variable to the multivariate model resulted in both incremental discrimination and reclassification of patients (C-index increase from 0.819 to 0.834 [P = .007]; integrated discrimination index 0.011 [95% CI 0.001-0.021; P = .028]).
CONCLUSIONS: Circulating hs-cTnT levels are closely associated with the risk of death in patients with acute ischemic stroke, and even levels below the upper reference limit appear to have prognostic value.
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