The role of ACE inhibitors in the treatment of arrhythmias

Abstract

Several experimental models have been studied to determine the role of angiotensin-converting enzyme (ACE) inhibitors in reducing ischemic and reperfusion arrhythmias. Studies of left main coronary artery occlusion in isolated perfused rat hearts have shown that the ACE inhibitor captopril reduced reperfusion ventricular fibrillation from 100% to 0% and was associated with a reduction in purine overflow and in norepinephrine release. These effects were abolished in the presence of indomethacin. In an anesthetized rat model of acute myocardial infarction (MI), ACE inhibition reduced mean duration of ventricular fibrillation from 1,133 to 135. ACE inhibition at programmed electrical stimulation of the heart in a closed-chest pig model of acute MI reduced the inducibility of sustained, reproducible ventricular tachycardia from a mean of 42 to 8%. In this model, ventricular tachycardia could not be provoked in animals treated with captopril from the time of acute ischemia. Studies on the rate of ventricular ectopy in patients with poor left ventricular function have demonstrated a significant reduction with ACE inhibition. However, while a protective effect has been shown, the mechanism of action is still speculative.