Soluble ST2 in Heart Failure - 22/11/17

Doi : 10.1016/j.hfc.2017.08.005

Cian P. McCarthy, MB, BCh, BAO ^a, James L. Januzzi, MD ^b,^c,^⁎
^a Department of Medicine, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114, USA
^b Division of Cardiology, Department of Medicine, Massachusetts General Hospital, 32 Fruit Street, Yawkey 5984, Boston, MA 02114, USA
^c Baim Institute for Clinical Research, Cardiometabolic Trials, 930 Commonwealth Avenue, Boston, MA 02115, USA

^∗Corresponding author. Massachusetts General Hospital, 32 Fruit Street, Yawkey 5984, Boston, MA 02114.Massachusetts General Hospital32 Fruit StreetYawkey 5984BostonMA02114

Résumé

Suppression of tumorigenicity 2 (ST2) is a member of the interleukin (IL)-1 receptor family, whose role was originally established in the context of inflammatory and autoimmune diseases. More recently, testing for ST2 has been used in the setting of cardiovascular disease. The soluble form of ST2 is a decoy receptor that inhibits beneficial cardioprotective effects of IL-33; such inhibition results in cardiac hypertrophy, myocardial fibrosis, and ventricular dysfunction. Measurement of soluble ST2 has utility for assessing heart failure severity and prognosis. In this review, we examine the role of soluble ST2 in both acute and chronic heart failure.

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Keywords : ST2, Novel cardiac biomarkers, Heart failure, Prognosis, Risk stratification

Plan

Key points

Introduction

The biology of suppression of tumorigenicity 2

Suppression of tumorigenicity 2 analytical considerations

Suppression of tumorigenicity 2 and acute heart failure

Diagnostic Capabilities

Suppression of Tumorigenicity 2 and Cardiac Function and Structure

Suppression of Tumorigenicity 2 and Prognosis in Acute Heart Failure

Serial Measurement of Suppression of Tumorigenicity 2 in Acute Heart Failure

Combination with Other Biomarkers

Chronic heart failure

Suppression of Tumorigenicity 2 and Prognosis in Chronic Heart Failure

Response to Therapy

Summary

Disclosures: Dr J.L. Januzzi has received grant support from Siemens, Singulex, and Prevencio, consulting income from Roche Diagnostics, Critical Diagnostics, Sphingotec, Phillips, and Novartis, and participates in clinical endpoint committees/data safety monitoring boards for Pfizer, Novartis, Amgen, Janssen, and Boehringer Ingelheim. Dr J.L. Januzzi is supported in part by the Hutter Family Professorship in Cardiology. Dr C.P. McCarthy has nothing to disclose.