Cardiac electrophysiological actions of captopril: lack of direct antiarrhythmic effects

Hemsworth, Paul D.; Pallandi, Regan T.; Campbell, Terence J.

doi:10.1111/j.1476-5381.1989.tb16881.x

Cited by 16 publications

(4 citation statements)

References 21 publications

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“…Finally, the antidisrhythmic effect of ACE inhibitors, which is likely to be independent of any established direct electrophysiological action, 39 may be of greater therapeutic benefit in preventing complex VA and possibly sudden death in patients with cardiac hypertrophy than traditional antiaiThythmic drugs, which can potentially have proarrhythmic effects. …”

Section: Discussionmentioning

confidence: 99%

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

et al. 1991

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To evaluate the effects of hypertension on cardiac hypertrophy, on myocardial structure, and on ventricular arrhythmias, 27 3-month-old spontaneously hypertensive rats were treated with enalapril (10 ing/kg) daily for 11 months and compared with 26 untreated control rats. Systolic arterial pressure was significantly decreased in treated rats, and at the end of the experiment, it was 199±3 mm Hg (treated) versus 237±3 mm Hg (controls) (p<0.001). At this time, spontaneous arrhythmias and induced arrhythmias either by programmed electrical stimulation (train of stimuli +1 or 2 extrastimuli) or by trains of eight stimuli at decreasing coupling intervals were observed in isolated heart preparations.

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Section: Discussionmentioning

confidence: 99%

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

et al. 1991

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“…In the present study, we did not evaluate whether benazepril had a direct electrophysiological effect on cardiac myocytes. However, a previous study by Hemsworth et al showing that ACEI have no effects on the maximum rate of depolarization and duration of the ventricular action potential in ventricular cells using microelectrode techniques makes this possibility unlikely 36 …”

Section: Discussionmentioning

confidence: 98%

Effect of Benazepril on Heart Rate Turbulence in Patients With Dilated Cardiomyopathy

Zhong

Chen

Chunfang

et al. 2007

Clin Exp Pharma Physio

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1. Heart rate (HR) turbulence describes short-term sinus rhythmic fluctuation after a single premature ventricular beat. Turbulence onset (TO) and turbulence slope (TS) are two essential parameters in HR turbulence. Turbulence onset and TS have been used to evaluate cardiac autonomic nerve function. 2. In the present study, we measured the HR turbulence in dilated cardiomyopathy (DCM) and determined the possible role of benazepril, an angiotensin-converting enzyme inhibitor (ACEI), on these parameters. There were three groups: control, DCM and DCM treated with benazepril. The control group consisted of normal subjects with PVB, but no structural heart disease. Ambulatory electrocardiogram, blood pressure and echocardiography were analysed. 3. There was an increase in TO and a decrease in TS in DCM patients. Benazepril treatment (10 mg/day, p.o.) reduced those changes. There were no significant differences in blood pressure and left ventricular ejection fraction (LVEF) between DCM patients and DCM patients treated with benazepril. 4. Linear regression analysis showed that TO was negatively correlated with LVEF, whereas TS was positively correlated with LVEF, in the DCM group. After benazepril treatment, the correlations between TO and TS and LVEF disappeared. 5. It is concluded that the TO and TS of HR turbulence are altered in patients with DCM. These alterations indicate a dysfunction of the autonomic control of cardiac electrophysiology in DCM patients. Although TO and TS are correlated with LVEF in DCM patients, the effect of benazepril in improving HR turbulence parameters is not a result of its action on heart function, which suggests a new beneficial effect of ACEI in the treatment of DCM patients.

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“…ACE inhibitors, unlike traditional antiarrhythmic drugs, do not alter the action potential duration (37,60). The most likely explanation for the antiarrhythmic effect of ACE inhibitors is their ability to prevent the breakdown of bradykinin.…”

Section: Antiarrhythmic Effectmentioning

confidence: 99%

Protection of the Cardiovascular System by Imidapril, a Versatile Angiotensin‐Converting Enzyme Inhibitor

Hosoya

Ishimitsu

2002

Cardiovascular Drug Reviews

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Imidapril hydrochloride (imidapril) is a long-acting, non-sulfhydryl angiotensin-converting enzyme (ACE) inhibitor, which has been used clinically in the treatment of hypertension, chronic congestive heart failure (CHF), acute myocardial infarction (AMI), and diabetic nephropathy. It has the unique advantage over other ACE inhibitors in causing a lower incidence of dry cough. After oral administration, imidapril is rapidly converted in the liver to its active metabolite imidaprilat. The plasma levels of imidaprilat gradually increase in proportion to the dose, and decline slowly. The time to reach the maximum plasma concentration (T max ) is 2.0 h for imidapril and 9.3 h for imidaprilat. The elimination half-lives (t 1/2 ) of imidapril and imidaprilat is 1.7 and 14.8 h, respectively. Imidapril and its metabolites are excreted chiefly in the urine. As an ACE inhibitor, imidaprilat is as potent as enalaprilat, an active metabolite of enalapril, and about twice as potent as captopril. In patients with hypertension, blood pressure was still decreased at 24 h after imidapril administration. The antihypertensive effect of imidapril was dose-dependent. The maximal reduction of blood pressure and plasma ACE was achieved with imidapril, 10 mg once daily, and the additional effect was not prominent with higher doses. When administered to patients with AMI, imidapril improved left ventricular ejection fraction and reduced plasma brain natriuretic peptide (BNP) levels. In patients with mild-to-moderate CHF [New York Heart Association (NYHA) functional class II-III], imidapril increased exercise time and physical working capacity and decreased plasma atrial natriuretic peptide (ANP) and BNP levels in a dose-related manner. In patients with diabetic nephropathy, imidapril decreased urinary albumin excretion. Interestingly, imidapril improved asymptomatic dysphagia in patients with a history of stroke. In the same patients it 93

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Cardiac electrophysiological actions of captopril: lack of direct antiarrhythmic effects

Cited by 16 publications

References 21 publications

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

Effect of Benazepril on Heart Rate Turbulence in Patients With Dilated Cardiomyopathy

Protection of the Cardiovascular System by Imidapril, a Versatile Angiotensin‐Converting Enzyme Inhibitor

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