Effect of spironolactone on ventricular arrhythmias in congestive heart failure secondary to idiopathic dilated or to ischemic cardiomyopathy.
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.
Ramires
F J
FJ
InCor-Heart Institute, University of São Paulo-Medical School, São Paulo-SP, Brazil.
Mansur
A
A
Coelho
O
O
Maranhão
M
M
Gruppi
C J
CJ
Mady
C
C
Ramires
J A
JA
D000704:Analysis of Variance; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000150:complications / Q000188:drug therapy* / Q000209:etiology; D002311:Cardiomyopathy, Dilated / Q000150:complications*; D016757:Death, Sudden, Cardiac / Q000517:prevention & control; D004573:Electrolytes / Q000378:metabolism; D015444:Exercise; D005260:Female; D006333:Heart Failure / Q000150:complications* / Q000188:drug therapy; D006439:Hemodynamics; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications* / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use*; D013148:Spironolactone / Q000627:therapeutic use*; D018879:Ventricular Premature Complexes / Q000188:drug therapy
D000959:Antihypertensive Agents; D004573:Electrolytes; D000451:Mineralocorticoid Receptor Antagonists; D013148:Spironolactone