Perindopril is a long acting angiotensin converting enzyme (ACE) inhibitor, which displays similar pharmacodynamic properties to other agents in this class. In common with enalapril, it is also a prodrug. After absorption, perindopril is hydrolysed to the active metabolite, perindoprilat, and with once daily administration adequate 24-hour inhibition of ACE is obtained. Perindopril 4 to 8mg once daily is usually effective for blood pressure control in patients with mild to moderate essential hypertension. Those patients who do not respond adequately to monotherapy with perindopril usually respond with the addition of a second agent, such as a thiazide diuretic. General practice trials indicate that perindopril is at least as effective and as well tolerated as usual therapeutic dosages of captopril, atenolol or hydrochlorothiazide plus amiloride in mild to moderate essential hypertension. Preliminary results indicate that perindopril may also be effective in patients with severe hypertension or congestive heart failure. Perindopril is generally well tolerated and has an adverse effect profile similar to that of other ACE inhibitors. It further clinical experience confirms initial findings, perindopril is likely to represent a useful alternative to other members of the ACE inhibitor class in all grades of hypertension and congestive heart failure.

Perindopril. A review of its pharmacological properties and therapeutic use in cardiovascular disorders.

Available information indicates that about 78 new molecules belonging to the class of angiotensin converting enzyme (ACE) inhibitors are under investigation, and that at least 11 or 12 of the newer ACE inhibitors will be available for clinical use. The newer ACE inhibitors can be classified, according to the zinc ion ligand of ACE, into 3 main chemical classes: sulfhydryl-, carboxyl- and phosphoryl-containing ACE inhibitors. All the newer sulfhydryl-containing ACE inhibitors differ from captopril since they are prodrugs, and among them alacepril and probably moveltipril (altiopril, MC 838) are converted in vivo to captopril. When compared with captopril, they show a slower onset and a longer duration of action, and obviously the same route of elimination. Zofenopril, a prodrug that is converted in vivo to the active diacid, shows a greater potency, a similar peak time and a longer duration of action than captopril and, unlike captopril, partial elimination through the liver. The newer carboxyl-containing ACE inhibitors are prodrugs which are converted in vivo to active diacids. Like enalaprilat, they are excreted via the kidney; the exception is spirapril, which is totally eliminated by the liver. Compared to enalapril, benazepril shows an earlier peak time and a slightly shorter terminal half-life, cilazapril and ramipril have an earlier peak time and even longer terminal half-life, perindopril shows similar peak time and terminal half-life, while delapril, quinapril and spirapril show an earlier peak time and a shorter half-life. The phosphoryl-containing ACE inhibitors belong to a new chemical class. Fosinopril is a prodrug which is converted to the active diacid in vivo, shows a relatively late peak time, a long terminal half-life, and is eliminated partially by the liver. SQ 29852, the only newly developed ACE inhibitor which is not a prodrug, seems to be more effective than captopril, with a much longer lasting effect and elimination through the kidney. When the differences in potency between these drugs are compensated by dosage adjustment, all the newer ACE inhibitors are expected to exert a similar amount of inhibition of circulating ACE, and therefore to inhibit to a similar extent the generation of circulating angiotensin II and the breakdown of bradykinin. Obviously they may differ in timing and the duration of circulating ACE inhibition according to their pharmacokinetic properties. With regard to the possibility that they may stimulate prostaglandin synthesis, it is suggested that this action, which does not seem to be specific to this drug class, plays only a minor role in their antihypertensive action; the hypothesis that the sulfhydryl group exerts an additional stimulating action remains to be proved.(ABSTRACT TRUNCATED AT 400 WORDS)

Newer ACE inhibitors. A look at the future.

The aim of this 3-month, double-blind, double-dummy, parallel group study was to compare the antihypertensive efficacy and acceptability of perindopril (4–8 mg/day) in 54 patients (30 males, 24 females, 25–68 years of age) and captopril (50–100 mg/day) in 54 patients (39 males, 15 females, 29–66 years of age) in the treatment of essential hypertension. In a subgroup of 38 patients a complete echocardiographic study was performed. The two groups had similar (ANOVA) blood pressure (BP), heart rate (HR), body mass index, and duration of hypertension. Supine and standing BP was significantly reduced by both drugs, without differences between them. Owing to poor control of BP, hydrochlorothiazide (25 mg/day) was added to 27% of patients on perindopril and to 41% of patients on captopril (p

Perindopril versus captopril : efficacy and acceptability in an Italian multicenter trial

https://www.amjmed.com/article/0002-9343(92)90153-3/pdf

Perindopril versus captopril: efficacy and acceptability in an Italian multicenter trial.

The influence of chronic perindopril treatment on digoxin pharmacokinetics was investigated in 10 patients with mild chronic heart failure under stable diuretic and digitalis treatment and normal renal function. Digoxin was administered at a dose of 0.125 mg/day (n = 2) or 0.250 mg/day (n = 8). The 24-hour steady-state digoxin profile was assessed before and after concomitant administration of perindopril for 1 month at doses of 2 mg once a day for the first 8 days and 4 mg once a day for the remaining 21 days. Chronic treatment with perindopril produced no significant effect on mean (+/- standard deviation) digoxin serum area under the curve for 24 hours (17.9 +/- 7.4 versus 16.3 +/- 4.4 ng/mL.h), peak digoxin concentration (1.3 +/- 0.54 versus 1.2 +/- 0.36 ng/mL), time to peak concentration (3 versus 4 hours), and apparent oral clearance of digoxin (237.7 +/- 109.6 versus 237.4 +/- 79.5 mL/min). Clinical and biologic tolerance of perindopril was good throughout the study. Chronic administration of perindopril did not alter steady-state digoxin kinetics in patients with mild chronic heart failure and normal renal function, indicating that no adaptation of the digoxin dose is required during co-prescription with perindopril in such patients.

Digoxin pharmacokinetics and perindopril in heart failure patients.

Perindopril is a new angiotensin converting enzyme (ACE) inhibitor which is activated after hydrolysis in vivo to a diacid(S9780). Oral administration of perindopril (1–16 mg) to groups of 6 healthy males led to a long lasting and dose-related inhibition of plasma ACE and rises in plasma renin activity with no evidence of accumulation of drug or effect. At higher doses there was a modest fall in blood pressure. S9780 given intravenously in doses of 1, 2 or 4 mg caused an immediate inhibition of plasma ACE. The concentration of S9780 in plasma which led to 50% inhibition of plasma ACE was 1.55 ± 1.14 ng/ml (mean ± S.D.). Clinical trials with 2–8 mg once daily in essential hypertension are currently in progress.

Perindopril, A New Angiotensin Converting Enzyme Inhibitor—Clinical Pharmacological Studies in Healthy Subjects

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Perindopril, A New Angiotensin Converting Enzyme Inhibitor—Clinical Pharmacological Studies in Healthy Subjects