Multi-Marker Strategy in Heart Failure: Combination of ST2 and CRP Predicts Poor Outcome.

Anne Marie Dupuy,François Roubille,Corentin Curinier,Florence Leclercq,Jean Paul Cristol,Fabien Huet,Jean Marc Davy,Nils Kuster,Markus M Bachschmid

doi:10.1371/journal.pone.0157159

Abstract

Natriuretic peptides (BNP and NT-proBNP) are recognized as gold-standard predictive markers in Heart Failure (HF). However, currently ST2 (member of the interleukin 1 receptor family) has emerged as marker of inflammation, fibrosis and cardiac stress. We evaluated ST2 and CRP as prognostic markers in 178 patients with chronic heart failure in comparison with other classical markers such as clinical established parameters but also biological markers: NT-proBNP, hs-cTnT alone or in combination. In multivariate analysis, subsequent addition of ST2 led to age, CRP and ST2 as the only remaining predictors of all-cause mortality (HR 1.03, HR 1.61 and HR 2.75, respectively) as well as of cardiovascular mortality (HR 1.00, HR 2.27 and HR 3.78, respectively). The combined increase of ST2 and CRP was significant for predicting worsened outcomes leading to identify a high risk subgroup that individual assessment of either marker. The same analysis was performed with ST2 in combination with Barcelona score. Overall, our findings extend previous data demonstrating that ST2 in combination with CRP as a valuable tool for identifying patients at risk of death.

Highlights

Heart failure (HF) results from multiple conditions leading to structural and functional changes
Mortality clearly increased across quartiles of ST2, NT-proBNP, Creactive protein (CRP) and high-sensitivity cardiac troponin T (hs-cTnT) (Fig 1, p
We evaluated the prognostic ability of four biomarkers (ST2, NT-proBNP, CRP and hs-cTnT) known to be involved in various pathophysiological pathways closely intertwined, in a population with stable chronic HF

Summary

Introduction

Heart failure (HF) results from multiple conditions leading to structural and functional changes. HF is not a mechanical failure of the heart pump. In addition to the classical sympathetic overstimulation, various pathophysiological ways are involved. One of the main pathophysiological ways leading to HF is myocardial stress resulting in neurohormonal activation by natriuretic peptides, including B-type natriuretic peptide (BNP) and its amino-terminal cleavage fragment, NT-proBNP. Their interest is well established in both diagnosis and prognosis [1].

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