强心合剂治疗慢性充血性心力衰竭的临床疗效观察

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60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(Ang Ⅱ)、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＜0.05),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、Ang Ⅱ和ANP水平(与治疗前及地高辛对照组比较P＜0.01),同时还能下调IVST、PWT和LVMI(P＜0.01;与地高辛对照组相比P＜0.05).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.

Clinical observation of the curative effect of Qiangxin Mixture on congestive heart failure

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 New York 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 enhancing 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.