摘要
目的探讨不同类型左向右分流先天性心脏病(CHD)患儿血肌钙蛋白Ⅰ(cTnⅠ)的变化。方法入选146例继发孔型房间隔缺损(ASD)、132例室间隔缺损(VSD)患儿,300例健康对照儿童,测定血cTnⅠ及脑利钠肽前体(NT-proBNP)水平,并分析其与患儿临床情况的相关性。结果 ASD组、VSD组以及对照组之间的血清cTnⅠ和NT-proBNP水平的差异均有统计学意义(H=3.89、5.27,P<0.01),VSD组患儿血清cTnⅠ和NT-proBNP水平均高于ASD组,差异有统计学意义(P均<0.05)。VSD组的肺循环/体循环压力比(Pp/Ps)、肺血管阻力指数(PVRI)以及标准化左心室舒张末期容积高于ASD组,差异有统计学意义(P均<0.05)。多元回归分析显示,在VSD患儿中Pp/Ps对cTnⅠ水平有显著影响(β=0.81,SE=0.03,P=0.000)。结论左向右分流型CHD所引起的心脏容量与压力变化可引起心肌损伤并最终导致不可逆性的心肌重塑。cTnⅠ可用于评估VSD所引起的不同程度心肌损伤。
Objective To analyze the level of cardiac troponin I （cTnI） in children with left-to-right shunt congenital heart disease （CHD）. Methods In this study, 146 children with secundum atrial septal （ASD） defect, 132 children with ventricular septal defect （VSD） and 300 healthy children were recruited. The levels of cTnI and N-terminal pro-brain natriuretic peptide （NT-proBNP） were measured and their correlation with clinical data was analyzed. Results The serum cTnI and NT-proBNP levels in both ASD and VSD patients were signiifcantly higher than those in normal children （H=3.89 and 5.27, P〈0.01）. The serum cTnI and NT-proBNP levels in VSD patients were signiifcantly higher than those in ASD patients （P〈0.05）. The ratio of pulmonary to systemic arterial pressure （Pp/Ps）, pulmonary vascular resistance index （PVRI） and standardized left ventricular end diastolic volume in VSD patients were signiifcantly higher than those in ASD patients （P〈0.05）. Multiple regression analysis showed that Pp/Ps was signiifcantly correlated with cTnI in VSD patients. （β=0.81, SE=0.03, P=0.000）. Conclusions Signiifcant volume and pressure overload due to a left-to-right shunt induce myocardial injury and could lead to irreversible myocardial remodeling in children with CHD. The serum cTnI level is a sensitive biomarker for myocardial damage in VSD patients.
出处
《临床儿科杂志》
CAS
CSCD
北大核心
2014年第9期863-866,共4页
Journal of Clinical Pediatrics
基金
2012年上海高校青年教师培养资助计划(No.ZZjdyx12116)
2013年上海市科委青年自然基金(No.13ZR1457500)
2013年上海市教委创新项目(No.14YZ039)
关键词
先天性心脏病
心肌损伤
儿童
congenital heart disease
cardiac troponin I
myocardial damage
child
