先心病心脏重构患者血清血管紧张素转化酶2水平研究

The Serum Levels of Angiotensin-converting Enzyme2 in Patients of Congenital Heart Disease with Cardiac Remodeling

目的观察先心病(congenital heart disease,CHD)伴心脏重构(Cardiac remodeling)患者血管紧张素转化酶2(angiotensin-converting enzyme 2,ACE2)含量和活性的变化,探讨它们与心脏重构的关系.方法收集被确诊为先心病的患者104例,(其中无心脏重构组80例,合并心脏重构组24例),正常对照组33例.抽取受试者静脉血,应用酶联免疫吸附法(ELISA)检测血清ACE2酶含量,用比色法检测ACE2酶活性的水平,所得实验数据使用SPSS统计软件进行分析.结果 (1)正常对照组、先心病无心脏重构组、先心病心脏重构组ACE2酶含量测定值分别为(15.79±5.03)U/L、(18.85±6.46)U/L、(14.80±4.58)U/L.正常对照组与先心病无心脏重构组比较,ACE2含量差异有统计学意义(P<0.05);正常对照组与先心病心脏重构组比较,ACE2含量无差异(P>0.05);先心病无心脏重构组与心脏重构组比较,ACE2含量差异有统计学意义(P<0.01);(2)正常对照组、先心病无心脏重构组、先心病心脏重构组ACE2酶活性测定值分别为(1.75±0.82)U/L、(1.85±0.62)U/L、(1.58±0.52)U/L,3组间比较差异无统计学意义(P>0.05).结论 (1)先心病无心脏重构患者血清中的ACE2酶含量显著升高;(2)先心病无心脏重构患者与心脏重构患者血清中ACE2酶活性无变化.

Objective To observe the Angiotensin-converting enzyme2 （ACE2） protein contents and activity in the serum of patients with Congenital Heart Disease （CHD） combined with cardiac remodeling （CR） , and investigate the correlation of those with cardiac remodeling. Methods 104 patients with Congenital Heart Disease and 33 normal control patients were collected. The patients with congenital heart disease were divided into 80 cases of non-cardiac remodeling group, and 24 cases of cardiac remodeling group. The serum levels of ACE2 protein were detected by enzyme-linked immunosorbent assay （ELISA） , ACE2 activity was detected by colorimetric method. Statistical analysis was performed by using SPSS software. Results （1） The ACE2 protein contents in serum measured by enzyme-linked immunosorbent assay were （15.79 ± 5.03） U/L, （18.85 ± 6.46） U /L, （14.80 ± 4.58） U/L in normal control group, Congenital Heart Disease with non-cardiac remodeling group, Congenital Heart Disease with cardiac remodeling group.The levels of ACE2 protein showed significant difference between normal control group and Congenital Heart Disease with non-cardiac remodeling group （P〈0.05）. The levels of ACE2 protein showed no significant difference between normal control group and Congenital Heart Disease with cardiac remodeling group （P〉0.05）. The levels of ACE2 protein showed significant difference between Congenital Heart Disease with non-cardiac remodeling group and Congenital Heart Disease with cardiac remodeling group （P〈0.01）. （2） The ACE2 activities in plasma measured by activity colorimetric were （1.75± 0.82） U/L, （1.85 ±0.62） U/L, （1.58 ±0.52） U/L in normal control group, Congenital Heart Disease with non-cardiac remodeling group, and Congenital Heart Disease with cardiac remodeling group. There were no significant differences among three groups （P 〉0.05）. Conclusions （1） ACE2 protein contents in the patients with Congenital Heart Disease combined with non-cardiac remodeling have significantly increased. （2） ACE2 activity has no differences in the patients with Congenital Heart Disease combined with non-cardiac remodeling and Congenital Heart Disease combined with cardiac remodeling.