先天性心脏病肺动脉高压患儿左室心肌重塑和舒张功能的临床观察

Clinical observation on the left ventricular myocardial remodel and dysfunction in children with congenital heart disease and hypoxia-induced pulmonary artery hypertension.

目的探讨肺动脉高压(pulmonary artery hypertension,PAH)对左心心肌重塑和舒张功能的影响。方法采用多普勒超声心动图检查,评价45例先天性心脏病合并PAH(PAH组)和22例单纯先天性心脏病儿童(对照组)左室重塑和舒张功能的变化情况。结果PAH组与对照组比较,其左室舒张末内径(LVDd)、右室内径(RVd)、肺动脉内径(PAd)均明显增大,且三尖瓣反流(VTR)流速增快、PASP升高,差异均有显著意义(P<0.05);而其室间隔(IVS)厚度无明显增加(P>0.05)。PAH组与对照组比较,二尖瓣口血流多普勒频谱A峰流速(AV)、速率时间积分(AVI)及肺动脉压与二尖瓣口血流频谱比值(AV/EV),AVI/EVI均逐渐明显增大,差异均有显著意义(P<0.01);左室等容舒张时间(LIVRT)明显延长(P<0.05),E峰流速(EV)、速率时间积分(EVI)及E峰减速时间(DT)无明显改变,差异均无显著意义(P>0.05)。PAH组AV/EV呈正相关(r=0.4119～0.4456,P<0.01)。结论PAH在引起右心功能异常的同时,也可能是左心室心肌重塑和肥大的发生机制之一。

Objective To investigate the affection of pulmonary artery hypertension（PAH） on the left ventricular myocardial remodel and dysfunction. Methods The Doppler echocardiography （ECH） data of 45 children of congenital heart disease with pulmonary artery hypertension were identified and compared with 22 children with simple congenital heart disease without pulmonary artery hypertension. Results Contracted with simple congenital heart disease group, the diameter of right ventricular, pulmonary artery and left ventricular end-diastolic, pulmonary artery systolic pressure and the back flow rate of atrioventricular valve in PAH group was increased significantly（P〈0.05）. However, the increased of the thickening of interventricular septum was insignificant （P〉0. 05）. In PAH group, the rnitral valve orifice blood streams, the AV of Doppler spectrum,the velocity-time integra and AV/EV, AVI/EVI were all increased significantly compared with the control group （P〈0.01）. The left ventricular isovolume diastolic time in PAH group was prolonged significantly also（P〈0.05）. But the change of EV,EVI and DT was insignificantly（P〉0.05）. In PAH group, pulmonary artery systolic pressure was positive correlation with AV/EV of the mitral valve orifice blood streams（r=0. 4119-0. 4456, P〈0.01）. Conclusion PAH may play key role in the left ventricular myocardial remodel and dysfunction while developing right cardiac abnormal.