TY - JOUR
T1 - Circulating Cardiac Troponin I Levels Measured by a Novel Highly Sensitive Assay in Acute Decompensated Heart Failure
T2 - Insights From the ASCEND-HF Trial
AU - GRODIN, JUSTIN L.
AU - BUTLER, JAVED
AU - METRA, MARCO
AU - FELKER, G. MICHAEL
AU - VOORS, ADRIAAN A.
AU - MCMURRAY, JOHN J.
AU - ARMSTRONG, PAUL W.
AU - HERNANDEZ, ADRIAN F.
AU - O'CONNOR, CHRISTOPHER
AU - STARLING, RANDALL C.
AU - TANG, W. H.WILSON
N1 - Publisher Copyright:
© 2018
PY - 2018/8
Y1 - 2018/8
N2 - 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.
AB - 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.
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U2 - 10.1016/j.cardfail.2018.06.008
DO - 10.1016/j.cardfail.2018.06.008
M3 - Article
C2 - 30012361
AN - SCOPUS:85053200950
SN - 1071-9164
VL - 24
SP - 512
EP - 519
JO - Journal of Cardiac Failure
JF - Journal of Cardiac Failure
IS - 8
ER -