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JUSTIN L. GRODIN JAVED BUTLER MARCO METRA G. MICHAEL FELKER ADRIAAN A. VOORS JOHN J. MCMURRAY PAUL W ARMSTRONG ADRIAN F. HERNANDEZ CHRISTOPHER O&#x;CONNOR RANDALL C. STARLING W.H. WILSON TANG 《Journal of cardiac failure》2018,24(8):512-519
Background
Circulating cardiac troponin levels (cTn), representative of myocardial injury, are commonly elevated in heart failure (HF) and related to adverse clinical events. However, whether cTn represents a spectrum of risk in HF is unclear.Methods
Baseline, 48–72-hour, and 30-day plasma cTnI was measured with the use of a new highly sensitive assay in 900 subjects with acute decompensated HF (ADHF) in ASCEND-HF. Multivariable models determined the relationship between cTnI and outcomes.Results
The median (interquartile range) cTnI was 16.4 (9.3–31.6) ng/L at baseline, 14.1 (7.8–29.7) ng/L at 48–72 hours, and 11.6 (6.8–22.5) ng/L at 30 days. After additional adjustment for N-terminal pro–B-type natriuretic peptide (NT-proBNP) to established risk predictors, both baseline (odds ratio [OR] 1.25; P?=?.03) and 48–72-hour (OR 1.43; P?=?.001) cTnI were associated with higher risk for death or worsening HF before discharge. However, only cTnI at 30 days was associated with 180-day death (hazard ratio 1.25; P?=?.007). There were no curvilinear associations between changing cTnI and clinical outcomes.Conclusions
Circulating cTnI level was associated with clinical outcomes in ADHF, but these observations diminished with additional adjustment for NT-proBNP. Although they likely represent a spectrum of risk in ADHF, these findings question the implications of changing cTnI levels during treatment. 相似文献15.
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