The antiarrhythmic effect of the ACE inhibitor captopril in patients with congestive heart failure largely is due to its potassium sparing effects.

OBJECTIVE

To evaluate the mechanisms by which the angiotensin converting enzyme (ACE) inhibitor captopril may modify the presence of ventricular arrhythmias in patients with chronic heart failure.

PATIENTS: Forty-seven patients with chronic stable congestive heart failure.

METHODS

Twenty-four hour Holter monitoring was done prior to and after one month of therapy with the ACE inhibitor captopril. In a first group of 25 patients, changes in the incidence of ventricular arrhythmias were correlated with changes in cardiac hemodynamics (assessed invasively). In a second group of 22 patients, changes in ventricular arrhythmias were correlated with changes in echocardiographic measurements. In all patients serum potassium was kept constant, and changes in exercise tolerance and serum noradrenaline levels were assessed prior to and after captopril.

RESULTS

One month of captopril therapy caused an improvement in cardiac hemodynamics and in exercise tolerance. It also led to a tendency for improved echocardiographic measurements and serum noradrenaline levels, similar to those already published by others. However, no change in the incidence or severity of ventricular arrhythmias was detected. No correlation could be found between changes in ventricular arrhythmias and any of the variables measured.

CONCLUSIONS

As the only obvious difference between this and previous studies that documented a decrease in ventricular arrhythmias when ACE inhibitors were started in patients with congestive heart failure is a lack of change in serum potassium in this study, the current results suggest that the major antiarrhythmic effect of ACE inhibitors in patients with congestive hear failure is the result of their potassium sparing effects.