{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T05:19:04Z","timestamp":1790054344935,"version":"4.0.1"},"reference-count":34,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2014,2,22]],"date-time":"2014-02-22T00:00:00Z","timestamp":1393027200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Capital Medical Development Scientific Research Fund","award":["20091003"],"award-info":[{"award-number":["20091003"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Cardiology"],"published-print":{"date-parts":[[2014,6]]},"abstract":"ABSTRACT<\/jats:title>\n \n Background<\/jats:title>\n \n Soluble suppression of tumorigenicity (\n sST2<\/jats:styled-content>\n ) has been proposed to be a marker for biomechanical strain and a possible predictor of mortality in patients with chronic heart failure. The use of\n sST2<\/jats:styled-content>\n in pulmonary arterial hypertension (\n PAH<\/jats:styled-content>\n ) has not been well defined.\n <\/jats:p>\n <\/jats:sec>\n \n Hypothesis<\/jats:title>\n Plasma sST2 levels may correlate with the disease severity and predict clinical worsening in PAH.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n We performed a cohort study of 40 idiopathic\n PAH<\/jats:styled-content>\n patients with data on demographics, exercise capacity, echocardiographic parameters, laboratory tests, hemodynamics, and medications. Plasma\n sST2<\/jats:styled-content>\n was assessed with the high\u2010sensitivity\n ST2 ELISA<\/jats:styled-content>\n kit at diagnostic catheterization. All patients were followed up from the date of blood sampling. The endpoint was clinical worsening.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n sST2<\/jats:styled-content>\n was significantly elevated in patients with idiopathic\n PAH<\/jats:styled-content>\n compared with control subjects (28.9\u2009\u00b1\u200913.9 vs 20.7\u2009\u00b1\u20097.5\u2009ng\/\n mL<\/jats:styled-content>\n ,\n P<\/jats:italic>\n = 0.003). Pearson correlation analysis revealed that\n sST2<\/jats:styled-content>\n levels correlated with cardiac index (\n r<\/jats:italic>\n = \u22120.534,\n P<\/jats:italic>\n = 0.000) and pulmonary vascular resistance (\n r<\/jats:italic>\n = 0.350,\n P<\/jats:italic>\n = 0.027), and could reflect disease severity of\n PAH<\/jats:styled-content>\n . After a mean follow\u2010up of 14\u2009\u00b1\u20095\u2009months, 12 patients showed clinical worsening. Receiver operating characteristic analysis suggested that\n sST2<\/jats:styled-content>\n levels >31.4\u2009ng\/\n mL<\/jats:styled-content>\n discriminated clinical worsening with a sensitivity and specificity of 83.3% and 78.6%, respectively. Kaplan\u2010Meier analysis showed that higher\n sST2<\/jats:styled-content>\n levels (>31.4\u2009ng\/\n mL<\/jats:styled-content>\n ) were associated with poor clinical outcomes (\n P<\/jats:italic>\n = 0.008). Multivariate Cox regression analysis showed that\n sST2<\/jats:styled-content>\n was an independent predictor of clinical worsening (hazard ratio: 6.067, 95% confidence interval: 1.317\u201327.948,\n P<\/jats:italic>\n = 0.021).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n sST2<\/jats:styled-content>\n correlates with disease severity and is a significant predictor of clinical worsening in patients with\n PAH<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/clc.22262","type":"journal-article","created":{"date-parts":[[2014,2,24]],"date-time":"2014-02-24T12:48:14Z","timestamp":1393246094000},"page":"365-370","source":"Crossref","is-referenced-by-count":51,"title":["Plasma Soluble\n ST2<\/scp>\n Levels Correlate With Disease Severity and Predict Clinical Worsening in Patients With Pulmonary Arterial Hypertension"],"prefix":"10.1002","volume":"37","author":[{"given":"Ya\u2010Guo","family":"Zheng","sequence":"first","affiliation":[{"name":"State Key Laboratory of Cardiovascular Disease, Fuwai Hospital National Center for Cardiovascular Diseases Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tao","family":"Yang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Cardiovascular Disease, Fuwai Hospital National Center for Cardiovascular Diseases Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian\u2010Guo","family":"He","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Cardiovascular Disease, Fuwai Hospital National Center for Cardiovascular Diseases Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guo","family":"Chen","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Cardiovascular Disease, Fuwai Hospital National Center for Cardiovascular Diseases Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhi\u2010Hong","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chang\u2010Ming","family":"Xiong","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Cardiovascular Disease, Fuwai Hospital National Center for Cardiovascular Diseases Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing","family":"Gu","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Cardiovascular Disease, Fuwai Hospital National Center for Cardiovascular Diseases Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 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