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Repeated ST2 measurements predict adverse outcome in acute heart failure patients

American College of Cardiology News Nov 03, 2017

Repeated ST2 measurements, in addition to N-terminal pro–B-type natriuretic peptide (NT-proBNP) measurements, may be helpful in identifying patients with heart failure (HF) who are at increased risk of adverse outcomes, according to a study published October 30, in the Journal of the American College of Cardiology.

Using data from the TRIUMPH clinical cohort study, Laura C. van Vark, MD, et al., sought to assess the association of baseline and repeated biomarker ST2 measurements in patients with acute HF. ST2 is an interleukin-1 (IL-1) receptor family member with membrane-bound (ST2L) and soluble (sST2) isoforms.

Patients were enrolled in 14 hospitals in the Netherlands between 2009 and 2014. Blood samples were drawn during a one-year follow-up and ST2 and NT-proBNP levels were measured in a central laboratory. The primary endpoint was the composite of all-cause mortality and HF rehospitalization.

Of the 475 patients in this analysis, 37% were women and the median age was 74 years. The primary endpoint was reached in 188 patients (40%) during a median follow-up of 325 days. The median baseline ST2 level was 71 ng/ml (interquartile range, 46-102).

When adjusted for clinical factors and NT-proBNP, the baseline ST2 measurement was associated with an increased risk for the primary endpoint, with a hazard ratio (HR) of 1.30 per a one standard deviation (SD) increase of the baseline ST2 level. For repeated ST2 measurements, this HR increased to 1.85 for each SD increase in the ST2 level.

Additionally, the average ST2 levels appeared to increase several weeks before the time of the primary endpoint.

The study authors state that repeated ST2 measurements are a strong and independent predictor of adverse outcomes in patients after they are hospitalized for acute HF. They concluded: “Repeated measurements take into account the dynamic and continuous change in ST2 level over time that may better re?ect the true changes that occur in the underlying pathophysiological processes in the individual patient with HF.”
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