[Heart failure and arrhythmias: the role of ACE inhibitors]

Mortality of patients with congestive heart failure (CHF) is high; > 40% of deaths are sudden, most often due to sustained ventricular arrhythmias (VA). In such patients frequent ventricular premature beats (VPB) and non sustained ventricular tachycardia (NSVT) are common. The relationship between VA and an increased risk for sudden death has been reported for patients with recent myocardial infarction. Although such relationship is uncertain for patients affected by dilated cardiomyopathy, many authors have reported an association between the frequency and the complexity of VA and the risk of sudden death. Many factors are responsible for VA in CHF: structural abnormalities, electrolyte imbalance, hemodynamic impairment, pharmacologic therapy and abnormal activation of neurohormonal system. ACE inhibitors have reduced VA in several experimental models, suggesting that these drugs decrease heart vulnerability to arrhythmogenic stimuli such as reperfusion and electrical stimulation. Many clinical trials have demonstrated that ACE inhibitors decreased VPB frequency and the prevalence of NSVT. Although ACE inhibitors decrease VA frequency, the reduction in cardiac mortality observed in CONSENSUS31 and in SOLVD32 trials was due only to a decrease in the progression of CHF. Recently the results of V-HeFT II33 trial have shown that the reduction in VA prevalence observed in patients treated with enalapril paralleled a reduction of sudden death. Factors that may contribute to the reduction in VA by ACE inhibitors include: increase in serum potassium; unloading of the ventricle; decrease in myocardial oxygen consumption. However, the most important factor seems related to their interference on neurohormonal system whose abnormal activation is the main mechanism of CHF progression.