{"title":"血浆ST2和半乳糖凝集素-3是否能预测梗阻性肥厚型心肌病患者骨髓切除术后的临床结果?","authors":"","doi":"10.31829/2691-5391/jhp2020-3(1)-104","DOIUrl":null,"url":null,"abstract":"ST2 is a member of the interleukin-1 receptor family, which is expressed in a trans membrane form (ST2L) as well as in a soluble secreted form [1]. Recently, soluble ST2(sST2) was found to be elevated in patients with chronic heart failure with reduced ejection fraction (HFrEF) and regarded as a promising novel biomarkers that can improve risk stratification [2, 3]. In 2012, Broch K et al. showed that baseline sST2 was associated with death due to worsening heart failure (HF), hospitalization due to worsening HF, and all cardiovascular hospitalization in older patients with ischemic HF[4]. In a multicenter study enrolled 447 patients with acutely decompensated heart failure, sST2 was an independent predictor of mortality for 1 year follow-up, regardless of the left ventricular ejection fraction[5]. As a β-galactoside-binding lectin secreted by activated macrophages, galectin-3 (Gal-3) exists in the cytoplasm and in a secreted form, and is involved in several physiological and pathological processes that contribute to HF, including myocardial fibrosis, inflammation and cardiac remodeling [6-8]. Sub study of RELAX trial suggested that Gal-3 levels were associated with severity of renal dysfunction. De Boer et al. found that Gal-3 is an independent marker for composite end of all-cause mortality and HF hospitalization in HF and appears to be more powerful in patients with heart failure with preserved ejection fraction (HFpEF)[9]. According to results from the Aldo-DHF trial, plasma Gal-3 in HFpEF was associated with adverse outcome, independent of treatment or NT-proBNP [10].","PeriodicalId":69096,"journal":{"name":"人体生理学杂志(英文)","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2020-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Are Plasma ST2 and Galectin-3 Predictors for Clinical Outcomes After Myectomy in Patients With Obstructive Hypertrophic Cardiomyopathy?\",\"authors\":\"\",\"doi\":\"10.31829/2691-5391/jhp2020-3(1)-104\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"ST2 is a member of the interleukin-1 receptor family, which is expressed in a trans membrane form (ST2L) as well as in a soluble secreted form [1]. Recently, soluble ST2(sST2) was found to be elevated in patients with chronic heart failure with reduced ejection fraction (HFrEF) and regarded as a promising novel biomarkers that can improve risk stratification [2, 3]. In 2012, Broch K et al. showed that baseline sST2 was associated with death due to worsening heart failure (HF), hospitalization due to worsening HF, and all cardiovascular hospitalization in older patients with ischemic HF[4]. In a multicenter study enrolled 447 patients with acutely decompensated heart failure, sST2 was an independent predictor of mortality for 1 year follow-up, regardless of the left ventricular ejection fraction[5]. As a β-galactoside-binding lectin secreted by activated macrophages, galectin-3 (Gal-3) exists in the cytoplasm and in a secreted form, and is involved in several physiological and pathological processes that contribute to HF, including myocardial fibrosis, inflammation and cardiac remodeling [6-8]. Sub study of RELAX trial suggested that Gal-3 levels were associated with severity of renal dysfunction. De Boer et al. found that Gal-3 is an independent marker for composite end of all-cause mortality and HF hospitalization in HF and appears to be more powerful in patients with heart failure with preserved ejection fraction (HFpEF)[9]. According to results from the Aldo-DHF trial, plasma Gal-3 in HFpEF was associated with adverse outcome, independent of treatment or NT-proBNP [10].\",\"PeriodicalId\":69096,\"journal\":{\"name\":\"人体生理学杂志(英文)\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-03-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"人体生理学杂志(英文)\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.31829/2691-5391/jhp2020-3(1)-104\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"人体生理学杂志(英文)","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.31829/2691-5391/jhp2020-3(1)-104","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Are Plasma ST2 and Galectin-3 Predictors for Clinical Outcomes After Myectomy in Patients With Obstructive Hypertrophic Cardiomyopathy?
ST2 is a member of the interleukin-1 receptor family, which is expressed in a trans membrane form (ST2L) as well as in a soluble secreted form [1]. Recently, soluble ST2(sST2) was found to be elevated in patients with chronic heart failure with reduced ejection fraction (HFrEF) and regarded as a promising novel biomarkers that can improve risk stratification [2, 3]. In 2012, Broch K et al. showed that baseline sST2 was associated with death due to worsening heart failure (HF), hospitalization due to worsening HF, and all cardiovascular hospitalization in older patients with ischemic HF[4]. In a multicenter study enrolled 447 patients with acutely decompensated heart failure, sST2 was an independent predictor of mortality for 1 year follow-up, regardless of the left ventricular ejection fraction[5]. As a β-galactoside-binding lectin secreted by activated macrophages, galectin-3 (Gal-3) exists in the cytoplasm and in a secreted form, and is involved in several physiological and pathological processes that contribute to HF, including myocardial fibrosis, inflammation and cardiac remodeling [6-8]. Sub study of RELAX trial suggested that Gal-3 levels were associated with severity of renal dysfunction. De Boer et al. found that Gal-3 is an independent marker for composite end of all-cause mortality and HF hospitalization in HF and appears to be more powerful in patients with heart failure with preserved ejection fraction (HFpEF)[9]. According to results from the Aldo-DHF trial, plasma Gal-3 in HFpEF was associated with adverse outcome, independent of treatment or NT-proBNP [10].