Kleber F X, Niemöller L, Doering W
Division of Cardiology, Munich Schwabing Hospital, Ludwig-Maximilians-University, Federal Republic of Germany.
Br Heart J. 1992 Apr;67(4):289-96. doi: 10.1136/hrt.67.4.289.
Neurohormonal activation has major impact on the pathophysiology of congestive heart failure. The Munich Mild Heart Failure Trial was designed to test the hypothesis that interference with the renin-angiotensin system by angiotensin converting enzyme inhibition favourably influences the natural history of heart failure.
170 patients, median New York Heart Association (NYHA) class II, were randomised to double blind treatment with 25 mg captopril twice a day or placebo in addition to standard treatment for a median observation period of 2.7 years.
Progression of heart failure to NYHA class IV on an optimally adjusted standard treatment, death due to progressive heart failure, and sudden death.
Heart failure progressed to class IV in nine patients (10.8%) treated with captopril and in 23 patients (26.4%) treated with placebo (p = 0.01). The mean survival time until this end point was 223 days longer in the captopril group (Kaplan-Meier life table analysis; p = 0.02). Also, progressive deterioration to severe heart failure was a powerful predictor of total mortality and death from heart failure; 80% of deaths due to progressive heart failure occurred after this end point. There were fewer deaths caused by progressive heart failure in the captopril group than in the placebo group (4 v 11; p = 0.10) but similar numbers of sudden deaths (11 v 10). Progressive heart failure was the cause of death in 18.2% of all deaths in the captopril group and 50% in the placebo group. Total heart failure events (the end point on which power calculation was based) were also more common in the placebo group (19 v 32 events) but not significantly so. Total mortality was similar to both groups (22 of 83 v 22 of 87).
Angiotensin converting enzyme inhibition in conjunction with standard therapy early in the course of congestive heart failure slowed the progress of heart failure and thus favourably altered the natural history of the disease.
神经激素激活对充血性心力衰竭的病理生理有重大影响。慕尼黑轻度心力衰竭试验旨在检验以下假设：通过血管紧张素转换酶抑制来干扰肾素-血管紧张素系统可对心力衰竭的自然病程产生有利影响。
170例纽约心脏病协会（NYHA）心功能分级为Ⅱ级的患者，除接受标准治疗外，被随机分为两组，分别接受每天两次25毫克卡托普利的双盲治疗或安慰剂治疗，中位观察期为2.7年。
在经过最佳调整的标准治疗下，心力衰竭进展至NYHAⅣ级、因进行性心力衰竭死亡以及猝死情况。
接受卡托普利治疗的患者中有9例（10.8%）心力衰竭进展至Ⅳ级，接受安慰剂治疗的患者中有23例（26.4%）（p = 0.01）。在该终点之前，卡托普利组的平均生存时间长223天（Kaplan-Meier生存表分析；p = 0.02）。此外，进展为严重心力衰竭也是总死亡率和心力衰竭死亡的有力预测指标；80%因进行性心力衰竭导致的死亡发生在该终点之后。卡托普利组因进行性心力衰竭导致的死亡少于安慰剂组（4例对11例；p = 0.10），但猝死人数相似（11例对10例）。在卡托普利组，进行性心力衰竭是18.2%的所有死亡原因，在安慰剂组则为50%。总的心力衰竭事件（计算效能所依据的终点）在安慰剂组也更常见（19例对32例事件），但差异无统计学意义。两组的总死亡率相似（83例中有22例对87例中有22例）。
在充血性心力衰竭病程早期联合标准治疗应用血管紧张素转换酶抑制可减缓心力衰竭进展，从而有利地改变疾病的自然病程。
