Cardiac effects of angiotensin converting enzyme inhibitors

Sharpe, Norman

doi:10.1007/bf01857639

Cited by 3 publications

(4 citation statements)

References 38 publications

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“…Experimental and clinical studies have suggested that ACE inhibitors may also prevent the occurrence of ischaemic heart disease and exert cardioprotection following acute myocardial infarction (Pfeffer et al 1985;Sharpe 1990). So far, there is no epidemiological evidence that these drugs decrease the incidence of coronary heart disease.…”

Section: Indications For Usementioning

confidence: 98%

“…Any primary protection with these agents could theoretically be related to the fact that they decrease blood pressure, do not affect lipid metabolism and may improve insulin sensitivity and cause regression of left ventricular hypertrophy. With regard to secondary protection, ACE inhibition is associated with an increase in coronary blood flow and antianginal effects in patients with symptomatic coronary insufficiency (Sharpe 1990).…”

Section: Indications For Usementioning

confidence: 99%

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Pharmacokinetic Optimisation of Angiotensin Converting Enzyme (ACE) Inhibitor Therapy

Burnier¹,

Biollaz²

1992

Clinical Pharmacokinetics

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Angiotensin converting enzyme (ACE) inhibitors are increasingly used to treat hypertension and congestive heart failure. Recently, several new ACE inhibitors with pharmacokinetic features different from earlier agents such as captopril or enalapril have come into use. This review discusses the use of pharmacokinetics to optimise ACE inhibitory therapy in various patient groups. Among the pharmacokinetic characteristics of ACE inhibitors the route of excretion and to a lesser degree the half-life appear to be the most clinically relevant. There is no evidence that being a prodrug offers a significant clinical advantage. The importance of varying tissue penetration also remains to be determined. Knowledge of ACE inhibitor pharmacokinetics is particularly important in patients with renal or hepatic dysfunction in whom the major route of excretion of these agents is impaired. This might also be the case in elderly patients or those with severe congestive heart failure. However, for most ACE inhibitors, major changes in the drug dosage (amount or interval) are necessary only when the glomerular filtration rate falls below 30 ml/min (1.80 L/h). The occurrence of adverse effects due to overdosage or drug interactions may be prevented by adapting the prescription of an ACE inhibitor to its pharmacokinetic characteristics.

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Section: Indications For Usementioning

confidence: 98%

Section: Indications For Usementioning

confidence: 99%

Pharmacokinetic Optimisation of Angiotensin Converting Enzyme (ACE) Inhibitor Therapy

Burnier¹,

Biollaz²

1992

Clinical Pharmacokinetics

View full text Add to dashboard Cite

show abstract

“…In addition to reducing the preload and afterload (92), an inhibitory effect of ACE inhibitors on the cardiac renin-angiotensin system (20) was suggested to be a contributing factor.…”

Section: Congestive Heart Failurementioning

confidence: 98%

“…ACE inhibitors became first-line drugs for the treatment of CHF because of the favorable results from large-scale prospective studies such as the SOLVD study (109) and the VHeFT-II study (12). In addition to reducing the preload and afterload (92), an inhibitory effect of ACE inhibitors on the cardiac renin-angiotensin system (20) was suggested to be a contributing factor.…”

Section: Congestive Heart Failurementioning

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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Prolonging Action of Imidapril on the Lifespan Expectancy of Cardiomyopathic Hamsters

Narita¹,

Kaburaki²,

Doi³

et al. 1996

Journal of Cardiovascular Pharmacology

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We studied the effect of imidapril, a novel angiotensin-converting enzyme (ACE) inhibitor, on lifespan expectancy of cardiomyopathic (CM) hamsters of BIO 14.6 strain, one of the representative models of congestive heart failure (CHF). Imidapril was consecutively administered to hamsters by mixing it in their diet at a concentration of 480 ppm (approximately 30 mg/kg/day) or 1,600 ppm (approximately 120 mg/kg/day) from age 26 weeks. Only several control hamsters died before age 54 weeks, but their survival rate decreased to 23.7% at age 73 weeks. The survival rates of 480-ppm and 1,600-ppm imidapril groups at age 73 weeks were as high as 75.7 and 68.4%, respectively (p < 0.01 vs. control hamsters). Macroscopic and microscopic pathology in imidapril-treated groups was milder than that in control animals in general, but differences were not statistically significant when animals were divided into survivors and fatalities except for the presence of mural thrombus in the heart. We further studied the effects of imidapril on blood pressure (BP), in vivo cardiac function, cardiac beta-adrenoceptor distribution, and plasma catecholamine levels after dietary treatment with 480 ppm imidapril for 8-10 weeks from age 37 weeks. Imidapril-treated animals showed improved cardiac function under urethane anesthesia. These results indicate that imidapril prolongs lifespan expectancy of CM hamsters and suggest that a hemodynamic effect of imidapril is involved in its beneficial effect.

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Cardiac effects of angiotensin converting enzyme inhibitors

Cited by 3 publications

References 38 publications

Pharmacokinetic Optimisation of Angiotensin Converting Enzyme (ACE) Inhibitor Therapy

Pharmacokinetic Optimisation of Angiotensin Converting Enzyme (ACE) Inhibitor Therapy

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

Prolonging Action of Imidapril on the Lifespan Expectancy of Cardiomyopathic Hamsters

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