摘要
目的:研究扩张型心肌病(扩心病)患者血清可溶性ST2(sST2)水平与胶原代谢标志物PⅠP(Ⅰ型前胶原羧基末端前肽)、CⅠTP(Ⅰ型胶原羧基端交联肽)的关系。方法:收集苏州市立医院心内科诊治的扩心病患者31例,同期选取20例健康人作为对照组。收集一般临床资料,包括生化检验结果;ELISA检测血清中sST2、PⅠP、CⅠTP浓度;心脏超声获得心脏结构形态学特点;比较扩心病组与对照组sST2、PⅠP、CⅠTP水平;并进一步分析扩心病组sST2与胶原代谢标志物PⅠP、CⅠTP的关系。结果:扩心病组sST2浓度0.26(0.06,0.61)ng/ml,PⅠP浓度140.00(70.80,223.05)ng/ml,均明显高于对照组。扩心病组CⅠTP略高于对照组,但无统计学意义。以扩心病组PⅠP的中位数140.00ng/ml为分界,将扩心病患者分为高PⅠP组和低PⅠP组,高PⅠP组CⅠTP水平明显高于低PⅠP组,但两组sST2水平无统计学差异。同样的方法分析后发现,高CⅠTP组的PⅠP以及sST2水平均高于低CⅠTP组。偏相关分析提示sST2与CⅠTP存在正相关关系(r=0.609,P<0.01),而sST2与PⅠP之间无明确相关关系。结论:扩心病患者新型纤维化生物学标志物sST2水平高于健康人群,且sST2与I型胶原降解标志物CⅠTP密切相关,提示sST2可能调节Ⅰ型胶原降解过程而影响心肌纤维化进程。
Objective:The purpose of the study was to identify the associates of soluble ST2 in Dialated cardiomyopathy(DCM)patients,and clarify the relationship with PⅠP and CⅠTP,biomarker of collagen typeⅠsynthesis and degradation respectively.Method:In a cross-sectional study of 31 dilated cardiomyopathy patients(DCM group)and 20 healthy controls(control group),general clinical features was collected,including age,blood pressure and others;soluble ST2,PⅠP and CⅠTP was measured by ELISA;LVEDD and LVEF was measured by echo.Result:The concentration of soluble ST2 in DCM group was 0.26(0.06,0.61)ng/mL,higher than those of control group[0.08(0.06,0.12)ng/mL];PⅠP level in DCM group was higher as well.CⅠTP in DCM group was higher than control group,but no statistical differences were gotten in this research.After subgroup analaysis,we found soluble ST2 and PⅠP were higher in " high-CⅠTP group" than "low-CⅠTP group".The level of soluble ST2 was positive correlated with CⅠTP(r=0.609,P〈0.01).Conclusion:Soluble ST2 in DCM was elevated,PⅠP as well.Soluble ST2 was positively correlated with CⅠTP in DCM population.This result means that soluble ST2 participates in the progress of myocardial remodeling probably by interfering degradation of collagen typeⅠ.
作者
童敏
张强
董佳敏
陈群
蔡薇
吕克
TONG Min ZHANG Qiang DONG Jiamin CHEN Qun CAI Wei LV Ke(Department of Cariology, Suzhou Municipal Hospital, Suzhou, 215000, China)
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2016年第11期1146-1149,共4页
Journal of Clinical Cardiology