【摘要】 目的　验证强心合剂治疗充血性心力衰竭的临床疗效。方法　将 6 0例充血性心力衰竭患者随机分为强心合剂治疗组 ( 30例 )、地高辛对照组 ( 30例 ) ,观察临床总有效率、肾虚症状积分、NYHA心功能分级、Lee心衰评分、心肌耗氧量、心胸比例、超声心动图 [射血分数 (EF)、心输出量 (CO)、室间隔厚度 (IVST)、左室后壁厚度 (PWT)、左室重量指数 (LVMI) ]和血浆内皮素 (ET)、血管紧张素II(AngII)、心钠素 (ANP)水平等的改变。 结果　强心合剂治疗组的临床总有效率为 87% ,与治疗前比较能显著改善NYHA心功能分级和Lee心衰评分 ,提高EF和CO(P <0 .0 5 ) ,但与地高辛对照组相比无显著差异。本方还能显著改善肾虚症状积分 ,降低血浆ET、AngII和ANP水平 (与治疗前及地高辛对照组比较 P <0 .0 1) ,同时还能下调IVST、PWT和LVMI( P<0 .0 1;与地高辛对照组相比 P <0 .0 5 )。结论　强心合剂可能通过短期的加强心脏收缩功能、改善血流动力学及纠正长期的修复性指标 ,延缓心力衰竭的发生、发展。而其延缓心力衰竭进程的机制可能是降低触发重构的刺激因素 (血管紧张素等 ) ,抑制重构的细胞介质 (内皮素等 ) ,延缓或部分逆转重构的发生。更多还原

【Abstract】 Objective To investigate the efficacy of Qiangxin Mixture in patients with congestive heart failure (CHF). Methods Sixty cases of CHF were randomly divided into Qiangxin Mixture group (treatment group,n=30) and digoxin group (control group, n=30).The total clinical effective rate,integra of the symptoms of kidney deficiency, classification of functional capacity of the NewYork Heart Association (NYHA), and echocardiogram[ejection fraction (EF), cardiac output (CO), interventricular septal thickness (IVST), posterior wall thickness (PWT), left ventricular mass index (LVMI)] as well as the measurement of plasma endothelin, angiotensin II and atrial natriuretic peptide were observed in both groups. Results The total clinical effective rate of Qiangxin Mixture group was 87%, and improvement was significantly observed in the Lee CHF score, classification of functional capacity of the NYHA, EF and CO(P<0.05,vs before treatment),but no significant improvement in digoxin group (P>0.05). The integra of the symptoms of kidney deficiency, the levels of plasma ET, Ang II and ANP decreased significantly (P<0.01,vs before treatment and digoxin group respectively). IVST,PWT and LVMI were also reduced significantly(P <0.01,vs before treatment;P<0.05 vs digoxin group). Conclusion The Qiangxin Mixture is effective in enhencing cardiac contraction,improving hemodynamics in the short term and rectifying some indexes in the long term,so it could postpone the processes of CHF. This mechanism may be related to decreasing the stimulating factors (angiotensin, endothelin) which trigger the cardiac remodeling, delaying or reversing the cardiac remodeling.更多还原