摘要
目的目的观察先天性心脏病介入治疗术前后血清心肌肌钙蛋白I(cTnI)的变化并分析其相关因素。方法按不同临床类型分成室间隔缺损(VSD)组35例,动脉导管未闭(PDA)组31例,房间隔缺损(ASD)组24例,于介入治疗术前、术后6小时、12小时、24小时、5天测量血清cTnI浓度。又按cTnI是否超过0.48mg/L分为cTnI升高组68例,不升高组22例,分析不同类型的先心病与升高组和不升高组的影响因素。结果各组术后6小时、12小时、24小时cTnI水平较术前明显升高(P<0.05),高峰均出现在术后6小时;血清cTnI峰值水平与年龄、肺动脉压力、手术时间、释放封堵器次数、造影剂量具有相关性;VSD组6小时、12小时、24小时血清cTnI水平明显高于其他两组(P<0.05),ASD组最低(P<0.05)。结论先心病介入治疗术可以引起可逆性的心肌微损伤,因此先心病介入治疗术是安全、有效、创伤小的治疗方法;cTnI升高程度与年龄、肺动脉压、手术时间、释放封堵器次数、造影剂量、临床类型有关。
Objective To investigate changes in the level of serum troponin Ⅰ（cTnⅠ） after catheterization to treat congenital heart diseases（CHD） and to analyse its correlative factors. Methods Ninety patients,included 35 patients with ventricular septal defect （VSD）, 31 patients with patent ductus arteriosus （PDA）, 24 patients with atrial septal defect （ASD） ,were treated with the occluders successfully,and the levels of cTnI were measured before,and 6 h, 12 h, 24 h,5 d after intervention. According to cTnI levels,there were 68 elevated cTnI patients and 22 non-elevated cTnI patients. To analyse correlative factors of the type of CHD and elevated cTnI group. Results cTnI levels significantly evelated at 6 h.12 h.24 h（ P G0.05）,the peak levels of cTnI occurred at 6 h（ P G0.05）. The eTnI peak levels correlated with age,the purssure of pulmonary artery, total time of intervention application, the times of releasing the occluder devices,the dose of constrast agent; The cTnI levels of VSD were significantly higher than the other two groups at 6 h.12 h and 24 h after intervention（ P G0.05） and the cTnl levels of ASD were the lowest（ P G0. 05）. Conclusion Catheterization to treat CHD may result in reversible,minor myocardial damage. However it is a safe, effective and ideal method, cTnI peak levels correlated with age, the purssure of pulmonary artery, total time of intervention application,the times of releasing the occluders,the dose of constrast agent,the type of disease.
出处
《临床荟萃》
CAS
北大核心
2007年第9期622-625,共4页
Clinical Focus
基金
先天性心脏病介入治疗临床技术应用示范GL200624
关键词
心脏缺损
先天性
肌钙蛋白Ⅰ
介入治疗
heart defects
cogenital
Troponin Ⅰ
percutaneous coronary intervention
