Tuininga YS. Wiesfeld AC. van Veldhuisen DJ. van Gelder IC. Crijns HJ.
Thoraxcenter, Department of Cardiology, University Hospital Groningen, The Netherlands.
Electrophysiological changes of angiotensin-converting enzyme inhibition after myocardial infarction.[comment].
Journal of Cardiac Failure. 6(2):77-9, 2000 Jun.
To investigate whether prevention of remodeling would translate into a more stable electrophysiological profile, the investigators randomized 56 patients to treatment with angiotensin-converting enzyme (ACE) inhibition or placebo for 3 months after myocardial infarction. Programmed electrical stimulation revealed no significant differences in inducibility of monomorphic sustained ventricular tachycardia (VT), whereas ventricular fibrillation (VF) tended to be lower in the ACE-inhibitor group. Effective refractory periods were consistently longer, and dispersion of refractoriness was significantly shorter in the ACE-inhibitor group. The investigators conclude that in this small patient group ACE inhibition may mildly add to a more stable electrophysiological profile.
Hattori Y. Atsushi S. Hiroaki F. Toyama J.
Department of Cardiology, Nakatsugawa Municipal Hospital, Gifu, Japan.
Effects of cilazapril on ventricular arrhythmia in patients with congestive heart failure.
Clinical Therapeutics. 19(3):481-6, 1997 May-Jun.
Angiotensin-converting enzyme (ACE) inhibitors reduce mortality and morbidity in patients with congestive heart failure. These effects may be mediated, at least in part, by suppression of lethal ventricular tachycardia (VT). The aims of this study were to examine whether the ACE inhibitor cilazapril reduces ventricular arrhythmia in patients with congestive heart failure and, if cilazapril does reduce ventricular arrhythmia, to determine whether this reduction is associated with suppression of sympathetic nerve activity in these patients. Thirty-two congestive heart failure patients (left ventricular ejection fraction, 35 +/- 6%; New York Heart Association class II or III) with VTs (Lown grade IVa or IVb) were randomly assigned to receive either conventional therapy, consisting of diuretics and digitalis (control group), or conventional therapy plus cilazapril (cilazapril group). Twenty-four-hour ambulatory electrocardiographic monitoring was performed at baseline and after 2 months of therapy. Plasma norepinephrine levels and heart rate variability (standard deviation about the mean RR interval) were compared at baseline and after 2 months of treatment. The control group demonstrated no significant change in arrhythmia frequency after 2 months of treatment. In the cilazapril group, however, the number of ventricular couplets and VT runs was significantly decreased. In association with this reduction, plasma norepinephrine levels were decreased, and heart rate variability was increased. These results suggest that cilazapril has antiarrhythmic effects, which may be produced by suppressing high sympathetic activity, in patients with congestive heart failure. It should be noted that the study group was small and that, although ventricular dysrhythmia was reduced with therapy, it remained substantial. Further study is needed to verify these results and to determine the exact causes of the reduction.