Background: Soluble suppression of tumorigenesis-2 (sST2) is a biomarker related to inflammation and fibrosis. Objectives: This study assessed the independent prognostic value of sST2 in chronic heart failure (HF). Methods: Individual patient data from studies that assessed sST2 for risk prediction in chronic HF, together with N-terminal pro−B-type natriuretic peptide (NT-proBNP) and high-sensitivity troponin T (hs-TnT), were retrieved. Results: A total of 4,268 patients were evaluated (median age 68 years, 75% males, 65% with ischemic HF, 87% with left ventricular ejection fraction [LVEF] <40%). NT-proBNP, hs-TnT, and sST2 were 1,360 ng/l (interquartile interval: 513 to 3,222 ng/l), 18 ng/l (interquartile interval: 9 to 33 ng/l), and 27 ng/l (interquartile interval: 20 to 39 ng/l), respectively. During a 2.4-year median follow-up, 1,319 patients (31%) experienced all-cause death (n = 932 [22%] for cardiovascular causes). Among the 4,118 patients (96%) with available data, 1,029 (24%) were hospitalized at least once for worsening HF over 2.2 years. The best sST2 cutoff for the prediction of all-cause and cardiovascular death and HF hospitalization was 28 ng/ml, with good performance at Kaplan-Meier analysis (log-rank: 117.6, 61.0, and 88.6, respectively; all p < 0.001). In a model that included age, sex, body mass index, ischemic etiology, LVEF, New York Heart Association functional class, glomerular filtration rate, HF medical therapy, NT-proBNP, and hs-TnT, the risk of all-cause death, cardiovascular death, and HF hospitalization increased by 26%, 25%, and 30%, respectively, per each doubling of sST2. sST2 retained its independent prognostic value across most population subgroups. Conclusions: sST2 yielded strong, independent predictive value for all-cause and cardiovascular mortality, and HF hospitalization in chronic HF, and deserves consideration to be part of a multimarker panel together with NT-proBNP and hs-TnT.
Bibliographical noteFunding Information:
Dr. Bayes-Genis has received grant support from Roche Diagnostics; has received lecture honoraria from Roche Diagnostics and Critical Diagnostics; and has received consulting income from Roche Diagnostics, Critical Diagnostics, and Novartis. Dr. Lupón has received lecture honoraria from Roche Diagnostics. Dr. Latini has received grant support and travel reimbursements from Roche Diagnostics. Dr. Gravning has received lecture fees from AstraZeneca, Siemens, and Abbott Laboratories. Dr. Brunner-La Rocca has received consulting fees from Roche Diagnostics; and has received unrestricted research grants from Roche Diagnostics, Novartis, and GlaxoSmithKline. Dr. de Boer has received research funding and consultancy fees from AstraZeneca, Bristol-Myers Squibb, Roche, and Trevena; has been a consultant for MandalMed, Inc.; has received speakers fees from Servier and Novartis; and is a minority shareholder of scPharmaceuticals. Dr. Gaggin has received grant support from Janacare, Roche, and Portola; has received consulting income from Roche Diagnostics, Amgen, and Ortho Clinical; and has received research payments for clinical endpoint committees from EchoSense and Radiometer. Dr. Januzzi has received grant support from Siemens, Singulex, and Prevencio; has received consulting income from Roche Diagnostics, Critical Diagnostics, Sphingotec, Phillips, and Novartis; and has participated in clinical endpoint committees for Novartis, Amgen, Janssen, and Boehringer Ingelheim. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
© 2018 American College of Cardiology Foundation
- heart failure
- troponin T