Serial high sensitivity cardiac troponin T measurement in acute heart failure: insights from the RELAX-AHF study.
OBJECTIVE
Troponin elevation is common in acute heart failure (AHF) and may be useful for prognostication; however, available data are mixed and many previous studies used older, less sensitive assays. We examined the association between serial measurements of high-sensitivity cardiac troponin T (hs-cTnT) and outcomes in RELAX-AHF.


RESULTS
Hs-cTnT was measured at baseline and days 2, 5, and 14. We assessed the relationship between baseline, peak and peak change hs-cTnT with dyspnoea relief by visual analogue scale, cardiovascular death, or HF/renal hospitalization to 60 days and cardiovascular mortality to 180 days. Models were adjusted for clinical variables and treatment assignment. Whether baseline troponin status affected the treatment effect of serelaxin was assessed using interactions terms. In 1074 patients, the median baseline troponin was 0.033 µg/L, and 90% of patients were above the 99th upper reference limit (URL). Patients with hs-cTnT >median were more likely to be men with ischaemic heart disease, worse renal function, and higher N-terminal pro-brain natriuretic peptide. Higher baseline or peak hs-cTnT and greater peak change were associated with worse outcomes independent of adjustment for covariates, but relationships were generally strongest for 180-day cardiovascular mortality (hazard ratio per doubling of baseline hs-cTnT = 1.36, 95% confidence interval 1.15-1.60). Troponin was most strongly associated with death from heart failure or from other cardiovascular causes. The treatment effect of serelaxin did not differ by baseline troponin levels.


CONCLUSIONS
Hs-cTnT was elevated above the 99% URL in the majority of AHF patients. Baseline, peak, and peak change hs-cTnT were associated with worse outcomes, with the strongest relationship with 180-day cardiovascular mortality.
Duke Clinical Research Institute, DUMC Box 3850, Durham, NC, 27710, USA.
G Michael
GM
Felker
Duke Clinical Research Institute, DUMC Box 3850, Durham, NC, 27710, USA.
Robert J
RJ
Mentz
University of California-San Francisco and San Francisco Veterans Affairs Medical Center, San Francisco, CA, USA.
John R
JR
Teerlink
University of Groningen, Groningen, the Netherlands.
Adriaan A
AA
Voors
Indiana University School of Medicine, Indianapolis, IN, USA.
Peter S
PS
Pang
Medical University, Clinical Military Hospital, Wroclaw, Poland.
Piotr
P
Ponikowski
University of California San Diego, La Jolla, CA, USA.
Barry H
BH
Greenberg
Athens University Hospital, Attikon, Athens, Greece.
Gerasimos
G
Filippatos
Momentum Research Inc., Durham, NC, USA.
Beth A
BA
Davison
Momentum Research Inc., Durham, NC, USA.
Gad
G
Cotter
Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA.
Margaret F
MF
Prescott
Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA.
Tsushung A
TA
Hua
Columbia University, New York, NY, USA.
Sara
S
Lopez-Pintado
Novartis Pharma AG, Basel, Switzerland.
Thomas
T
Severin
University of Brescia, Brescia, Italy.
Marco
M
Metra
D000208:Acute Disease; D000368:Aged; D004311:Double-Blind Method; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000188:drug therapy / Q000401:mortality; D006801:Humans; D008297:Male; D011994:Recombinant Proteins; D012065:Relaxin / Q000627:therapeutic use; D016896:Treatment Outcome; D020107:Troponin T / Q000097:blood*
D011994:Recombinant Proteins; D020107:Troponin T; C577649:serelaxin protein, human; D012065:Relaxin
Acute heart failure; Dyspnoea; High-sensitivity cardiac troponin T; Outcomes; mortality