Ramires F J, Mansur A, Coelho O, Maranhão M, Gruppi C J, Mady C, Ramires J A
InCor-Heart Institute, University of São Paulo-Medical School, São Paulo-SP, Brazil.
Am J Cardiol. 2000 May 15;85(10):1207-11. doi: 10.1016/s0002-9149(00)00729-3.
Epidemiologic studies have shown an important increase in the high mortality of patients with congestive heart failure (CHF) despite optimal medical management. Ventricular arrhythmia was recognized as the most common cause of death in this population. Electrolyte imbalance, myocardial fibrosis, left ventricular dysfunction, and inappropriate neurohumoral activation are presumed responsible for sudden cardiac death. In this study, we focused on the deleterious effects of the overproduction of aldosterone that occurs in patients with CHF. Secondary hyperaldersteronism can be part of several factors thought to be responsible for sudden cardiac death. We randomized 35 patients (32 men, aged 48 +/- 9 years) with systolic dysfunction (ejection fraction 33 +/- 5%) and New York Heart Association class III CHF secondary to dilated or ischemic cardiomyopathy into 2 groups. The treatment group received spironolactone, an aldosterone receptor antagonist, along with standard medical management using furosemide, angiotensin-converting enzyme inhibitors, and digoxin. The control group received only the standard medical treatment. Holter monitoring was used to assess the severity of ventricular arrhythmia. After 20 weeks, patients who received spironolactone had a reduced hourly frequency of ventricular premature complexes (VPCs) (65 +/- 18 VPCs/hour at week 0 and 17 +/- 9 VPCs/hour at week 16) and episodes of nonsustained ventricular tachycardia (VT) (3.0 +/- 0.8 episodes of VT/24-hour period at week 0, and 0.6 +/- 0.3 VT/24-hour period at week 16). During monitored treadmill exercise, a significant improvement in ventricular arrhythmia was found in the group receiving spironolactone (39 +/- 10 VPCs at week 0, and 6 +/- 2 VPCs at week 16). These findings suggest that aldosterone may contribute to the incidence of ventricular arrhythmia in patients with CHF, and spironolactone helps reduce this complication.
流行病学研究表明，尽管采取了最佳的药物治疗，充血性心力衰竭（CHF）患者的高死亡率仍有显著上升。室性心律失常被认为是该人群最常见的死亡原因。电解质失衡、心肌纤维化、左心室功能障碍和不适当的神经体液激活被认为是心源性猝死的原因。在本研究中，我们关注了CHF患者中醛固酮过量产生的有害影响。继发性醛固酮增多症可能是被认为导致心源性猝死的几个因素之一。我们将35例收缩功能障碍（射血分数33±5%）且因扩张型或缺血性心肌病导致纽约心脏协会III级CHF的患者（32名男性，年龄48±9岁）随机分为两组。治疗组接受醛固酮受体拮抗剂螺内酯，以及使用呋塞米、血管紧张素转换酶抑制剂和地高辛的标准药物治疗。对照组仅接受标准药物治疗。采用动态心电图监测评估室性心律失常的严重程度。20周后，接受螺内酯治疗的患者每小时室性早搏（VPC）频率降低（第0周时为65±18次VPC/小时，第16周时为17±9次VPC/小时），非持续性室性心动过速（VT）发作次数减少（第0周时为3.0±0.8次VT/24小时，第16周时为0.6±0.3次VT/24小时）。在监测的平板运动试验中，接受螺内酯治疗的组室性心律失常有显著改善（第0周时为39±
