BACKGROUND: Aim of this study was to evaluate the predictors of hs-cTnT in a non-ACS patient cohort admitted to the emergency department. HYPOTHESIS: Atrial fibrillation and hypertension may not always be sufficient for elevation for hs-cTnT. METHODS: We performed a retrospective, single center study encompassing in total 1003 patients. Individuals were retrospectively divided in ACS- and non-ACS patients by two independent investigators reviewing the medical records. In order to identify predictors of hs-cTnT elevation hazard ratios were calculated for age, gender, vital signs, cardiovascular risk factors, LVEF, serum levels of CRP, hemoglobin, and creatinine. Elevation of hs-cTnT was defined by exceeding 14 ng/L (upper reference limit [URL]). RESULTS: About 987 patients were included while 25 patients were excluded because of missing data. 307 patients (31.4%) met the current guideline requirements of diagnosing an ACS, whereas 671 patients (68.6%) were hospitalized with excluded ACS. In the multivariate analysis age, anemia, CRP, creatinine, and reduced systolic left ventricular ejection fraction were independent predictors of elevated troponin T levels in the non-ACS group. However, hypertensive systolic blood pressure, atrial fibrillation and tachycardia were not predictive for Troponin T elevation in non-ACS patients in this multivariate analysis. CONCLUSIONS: In an unselected, non-ACS patient cohort age, chronic renal failure, inflammatory state, and reduced left ventricular systolic function were associated with hs-cTnT levels above the upper reference limit. Rather, often supposed predictors as atrial fibrillation, hypertension, and tachycardia cannot sufficiently explain increased hs-cTnT in our study. Hence, further studies are needed to assess whether isolated hypertension, tachycardia, or atrial fibrillation sufficiently explain elevated hs-cTnT.
BACKGROUND: Aim of this study was to evaluate the predictors of hs-cTnT in a non-ACSpatient cohort admitted to the emergency department. HYPOTHESIS: Atrial fibrillation and hypertension may not always be sufficient for elevation for hs-cTnT. METHODS: We performed a retrospective, single center study encompassing in total 1003 patients. Individuals were retrospectively divided in ACS- and non-ACSpatients by two independent investigators reviewing the medical records. In order to identify predictors of hs-cTnT elevation hazard ratios were calculated for age, gender, vital signs, cardiovascular risk factors, LVEF, serum levels of CRP, hemoglobin, and creatinine. Elevation of hs-cTnT was defined by exceeding 14 ng/L (upper reference limit [URL]). RESULTS: About 987 patients were included while 25 patients were excluded because of missing data. 307 patients (31.4%) met the current guideline requirements of diagnosing an ACS, whereas 671 patients (68.6%) were hospitalized with excluded ACS. In the multivariate analysis age, anemia, CRP, creatinine, and reduced systolic left ventricular ejection fraction were independent predictors of elevated troponin T levels in the non-ACS group. However, hypertensive systolic blood pressure, atrial fibrillation and tachycardia were not predictive for Troponin T elevation in non-ACSpatients in this multivariate analysis. CONCLUSIONS: In an unselected, non-ACSpatient cohort age, chronic renal failure, inflammatory state, and reduced left ventricular systolic function were associated with hs-cTnT levels above the upper reference limit. Rather, often supposed predictors as atrial fibrillation, hypertension, and tachycardia cannot sufficiently explain increased hs-cTnT in our study. Hence, further studies are needed to assess whether isolated hypertension, tachycardia, or atrial fibrillation sufficiently explain elevated hs-cTnT.
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