TY - JOUR
T1 - Prognostic value of high-sensitivity troponin T in chronic heart failure an individual patient data meta-analysis
AU - Aimo, Alberto
AU - Januzzi, James L.
AU - Vergaro, Giuseppe G.V.
AU - Ripoli, Andrea
AU - Latini, Roberto
AU - Masson, Serge
AU - Magnoli, Michela
AU - Anand, Inder S.
AU - Cohn, Jay N.
AU - Tavazzi, Luigi
AU - Tognoni, Gianni
AU - Gravning, Jørgen
AU - Ueland, Thor
AU - Nymo, Ståle H.
AU - Brunner-La Rocca, Hans Peter
AU - Genis, Antoni Bayes
AU - Lupón, Josep
AU - De Boer, Rudolf A.
AU - Yoshihisa, Akiomi
AU - Takeishi, Yasuchika
AU - Egstrup, Michael
AU - Gustafsson, Ida
AU - Gaggin, Hanna K.
AU - Eggers, Kai M.
AU - Huber, Kurt
AU - Tentzeris, Ioannis
AU - Tang, Wai H.W.
AU - Grodin, Justin
AU - Passino, Claudio
AU - Emdin, Michele
N1 - Funding Information:
Dr Januzzi has received grant support from Siemens, Singu-lex, and Prevencio; consulting income from Roche Diagnostics,
Publisher Copyright:
© 2017 American Heart Association, Inc.
PY - 2018
Y1 - 2018
N2 - Background: Most patients with chronic heart failure have detectable troponin concentrations when evaluated by high-sensitivity assays. The prognostic relevance of this fnding has not been clearly established so far. We aimed to assess high-sensitivity troponin assay for risk stratifcation in chronic heart failure through a meta-analysis approach. METHODS: Medline, EMBASE, Cochrane Library, and Scopus were searched in April 2017 by 2 independent authors. The terms were "troponin" AND "heart failure" OR "cardiac failure" OR "cardiac dysfunction" OR "cardiac insuffciency" OR "left ventricular dysfunction." Inclusion criteria were English language, clinical stability, use of a high-sensitivity troponin assay, follow-up studies, and availability of individual patient data after request to authors. Data retrieved from articles and provided by authors were used in agreement with the PRISMA statement. The end points were all-cause death, cardiovascular death, and hospitalization for cardiovascular cause. RESULTS: Ten studies were included, reporting data on 11 cohorts and 9289 patients (age 66±12 years, 77% men, 60% ischemic heart failure, 85% with left ventricular ejection fraction <40%). High-sensitivity troponin T data were available for all patients, whereas only 209 patients also had high-sensitivity troponin I assayed. When added to a prognostic model including established risk markers (sex, age, ischemic versus nonischemic etiology, left ventricular ejection fraction, estimated glomerular fltration rate, and N-terminal fraction of pro-B-type natriuretic peptide), high-sensitivity troponin T remained independently associated with all-cause mortality (hazard ratio, 1.48; 95% confdence interval, 1.41-1.55), cardiovascular mortality (hazard ratio, 1.40 95% confdence interval, 1.33-1.48), and cardiovascular hospitalization (hazard ratio, 1.42 95% confdence interval, 1.36-1.49), over a median 2.4-year follow-up (all P<0.001). High-sensitivity troponin T signifcantly improved risk prediction when added to a prognostic model including the variables above. It also displayed an independent prognostic value for all outcomes in almost all population subgroups. The area under the curve-derived 18 ng/L cutoff yielded independent prognostic value for the 3 end points in both men and women, patients with either ischemic or nonischemic etiology, and across categories of renal dysfunction. CONCLUSIONS: In chronic heart failure, high-sensitivity troponin T is a strong and independent predictor of all-cause and cardiovascular mortality, and of hospitalization for cardiovascular causes, as well. This biomarker then represents an additional tool for prognostic stratifcation.
AB - Background: Most patients with chronic heart failure have detectable troponin concentrations when evaluated by high-sensitivity assays. The prognostic relevance of this fnding has not been clearly established so far. We aimed to assess high-sensitivity troponin assay for risk stratifcation in chronic heart failure through a meta-analysis approach. METHODS: Medline, EMBASE, Cochrane Library, and Scopus were searched in April 2017 by 2 independent authors. The terms were "troponin" AND "heart failure" OR "cardiac failure" OR "cardiac dysfunction" OR "cardiac insuffciency" OR "left ventricular dysfunction." Inclusion criteria were English language, clinical stability, use of a high-sensitivity troponin assay, follow-up studies, and availability of individual patient data after request to authors. Data retrieved from articles and provided by authors were used in agreement with the PRISMA statement. The end points were all-cause death, cardiovascular death, and hospitalization for cardiovascular cause. RESULTS: Ten studies were included, reporting data on 11 cohorts and 9289 patients (age 66±12 years, 77% men, 60% ischemic heart failure, 85% with left ventricular ejection fraction <40%). High-sensitivity troponin T data were available for all patients, whereas only 209 patients also had high-sensitivity troponin I assayed. When added to a prognostic model including established risk markers (sex, age, ischemic versus nonischemic etiology, left ventricular ejection fraction, estimated glomerular fltration rate, and N-terminal fraction of pro-B-type natriuretic peptide), high-sensitivity troponin T remained independently associated with all-cause mortality (hazard ratio, 1.48; 95% confdence interval, 1.41-1.55), cardiovascular mortality (hazard ratio, 1.40 95% confdence interval, 1.33-1.48), and cardiovascular hospitalization (hazard ratio, 1.42 95% confdence interval, 1.36-1.49), over a median 2.4-year follow-up (all P<0.001). High-sensitivity troponin T signifcantly improved risk prediction when added to a prognostic model including the variables above. It also displayed an independent prognostic value for all outcomes in almost all population subgroups. The area under the curve-derived 18 ng/L cutoff yielded independent prognostic value for the 3 end points in both men and women, patients with either ischemic or nonischemic etiology, and across categories of renal dysfunction. CONCLUSIONS: In chronic heart failure, high-sensitivity troponin T is a strong and independent predictor of all-cause and cardiovascular mortality, and of hospitalization for cardiovascular causes, as well. This biomarker then represents an additional tool for prognostic stratifcation.
KW - Heart failure
KW - Metaanalysis
KW - Prognosis
KW - Troponin T
KW - Ventricular dysfunction, left
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U2 - 10.1161/CIRCULATIONAHA.117.031560
DO - 10.1161/CIRCULATIONAHA.117.031560
M3 - Review article
C2 - 29335288
AN - SCOPUS:85045767511
SN - 0009-7322
VL - 137
SP - 286
EP - 297
JO - Circulation
JF - Circulation
IS - 3
ER -