Michele Emdin1, Alberto Aimo2, Giuseppe Vergaro3, Antoni Bayes-Genis4, Josep Lupón4, Roberto Latini5, Jennifer Meessen6, Inder S Anand7, Jay N Cohn6, Jørgen Gravning8, Lars Gullestad9, Kaspar Broch9, Thor Ueland10, Ståle H Nymo9, Hans-Peter Brunner-La Rocca11, Rudolf A de Boer12, Hanna K Gaggin13, Andrea Ripoli14, Claudio Passino3, James L Januzzi13. 1. Institute of Life Sciences, Scuola Superiore Sant'Anna, Pisa, Italy; Fondazione Toscana G. Monasterio, Pisa, Italy. Electronic address: m.emdin@santannapisa.it. 2. Institute of Life Sciences, Scuola Superiore Sant'Anna, Pisa, Italy. 3. Institute of Life Sciences, Scuola Superiore Sant'Anna, Pisa, Italy; Fondazione Toscana G. Monasterio, Pisa, Italy. 4. Hospital Universitari Germans Trias i Pujol, Badalona, Barcelona, Spain. 5. Department of Cardiovascular Research IRCCS-Istituto di Ricerche Farmacologiche-"Mario Negri," Milano, Italy. 6. Division of Cardiovascular Medicine, University of Minnesota, Minneapolis, Minnesota. 7. Division of Cardiovascular Medicine, University of Minnesota, Minneapolis, Minnesota; Department of Cardiology, VA Medical Centre, Minneapolis, Minnesota. 8. Department of Cardiology, Oslo University Hospital, Ullevål, Oslo, Norway; Centre for Heart Failure Research, University of Oslo, Oslo, Norway. 9. Oslo University Hospital, Rikshospitalet, Oslo, Norway. 10. Oslo University Hospital, Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway; K. G. Jebsen Thrombosis Research and Expertise Centre, University of Tromsø, Tromsø, Norway. 11. Department of Cardiology, Maastricht University Medical Centre, Maastricht, the Netherlands. 12. University Medical Centre Groningen, Groningen, the Netherlands. 13. Massachusetts General Hospital, Harvard Clinical Research Institute, Boston, Massachusetts. 14. Fondazione Toscana G. Monasterio, Pisa, Italy.
Abstract
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.
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.
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Authors: Giuseppe Vergaro; Francesco Gentile; Alberto Aimo; James L Januzzi; A Mark Richards; Carolyn S P Lam; Rudolf A de Boer; Laura M G Meems; Roberto Latini; Lidia Staszewsky; Inder S Anand; Jay N Cohn; Thor Ueland; Lars Gullestad; Pål Aukrust; Hans-Peter Brunner-La Rocca; Antoni Bayes-Genis; Josep Lupón; Akiomi Yoshihisa; Yasuchika Takeishi; Michael Egstrup; Ida Gustafsson; Hanna K Gaggin; Kai M Eggers; Kurt Huber; Greg D Gamble; Lieng H Ling; Kui Toh Gerard Leong; Poh Shuah Daniel Yeo; Hean Yee Ong; Fazlur Jaufeerally; Tze P Ng; Richard Troughton; Robert N Doughty; Gerry Devlin; Mayanna Lund; Alberto Giannoni; Claudio Passino; Michele Emdin Journal: ESC Heart Fail Date: 2022-05-05