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Lisinopril

A Review of its Pharmacology and Clinical Efficacy in Elderly Patients

  • Adis Drug Evaluation
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Summary

Synopsis

Lisinopril, the lysine analogue of enalaprilat, is a long-acting angiotensin converting enzyme (ACE) inhibitor which is administered once daily by mouth.

The efficacy of lisinopril in reducing blood pressure is well established in younger populations, and many trials now show it to be effective in lowering blood pressure in elderly patients with hypertension. In comparative and non-comparative clinical trials, 68.2 to 89.1 % of elderly patients responded (diastolic pressure ≤90mm Hg) to ≥8 weeks’ lisinopril treatment. Age-related differences in antihypertensive efficacy do not appear to be clinically significant, and dosages effective in elderly patients tend to range from 2.5 to 40 mg/day. Dosages usually need to be lower in patients with significant renal impairment.

In congestive heart failure, lisinopril 2.5 to 20 mg/day increases exercise duration, improves left ventricular ejection fraction and has no significant effect on ventricular ectopic beats. It is similar in efficacy to enalapril and digoxin and similar or superior to captopril on most end-points.

Data from the GISSI-3 post-myocardial infarction trial show that lisinopril reduced mortality and left ventricular dysfunction when given for 42 days starting within 24 hours of the onset of infarction symptoms. Results at 6 weeks and 6 months were similar in elderly and younger patients. Elderly patients, however, among other subgroups, exhibited a strong reduction in risk of low ejection fraction after treatment (−25.5%). Economic studies suggest that lisinopril is cost saving compared with other ACE inhibitors in some markets. When given according to the GISSI-3 protocol, lisinopril appears to be one of the less expensive of the successful ACE inhibitor regimens for acute myocardial infarction.

In other trials, patients with diabetic nephropathy and hypertension improved or did not deteriorate during lisinopril treatment. Blood pressure was controlled and reductions or trends towards reductions in albuminuria were observed. These reductions were similar to those in diltiazem, nifedipine and verapamil recipients, and greater than those in patients receiving atenolol. Lisinopril appears to reduce mortality in diabetic patients after myocardial infarction and may also improve neuropathy associated with diabetes.

Lisinopril is well tolerated and the profile of adverse events seen is typical of ACE inhibitors as a class. There is a tendency for more elderly than younger patients to discontinue treatment, but this trend is not clearly related to the incidence of adverse events in these age groups. Drug interactions occur with few other agents and are usually clinically significant only between lisinopril and either diuretics or lithium.

Lisinopril is, thus, an effective treatment for elderly patients with hypertension, congestive heart failure and acute myocardial infarction and has shown promising benefits in patients with diabetic nephropathy.

Pharmacodynamic Effects

Plasma angiotensin converting enzyme (ACE) activity is reduced in inverse proportion to plasma lisinopril concentrations. Peak effects occur 6 hours postdose and ACE activity remains low 24 hours after a dose. The different effects of lisinopril on ACE in various body sites are of unknown clinical significance. Blood pressure decreased for a mean of 30.4 hours after a lisinopril dose (vs 20.7 hours after enalapril) in one study. Lisinopril improves arterial distensibility in hypertensive patients and reduces systemic vascular resistance, left ventricular end-diastolic and end-systolic pressures, cardiac index and left ventricular mass. It does not usually alter cardiac output or glomerular filtration rate (GFR). Renal plasma flow and filtration fraction tend to increase and renal vascular resistance tends to decrease in hypertensive patients receiving lisinopril. In elderly patients, thoracic aortic blood flow and baroreceptor sensitivity improve. Haemodynamic changes similar to those seen in the elderly occur in patients with congestive heart failure (CHF), are dose-dependent and persist for >24 hours. Lisinopril does not appear to alter cerebral blood flow.

Left ventricular hypertrophy was reduced in all patients receiving lisinopril in trials that tested this variable. Reductions in left ventricular mass correlate with improved diastolic function and aortic compliance, occur in young and elderly patients, and are associated with blood pressure reductions, although the latter relationship is possibly not causal. Oxygen consumption during exercise improved with lisinopril treatment in patients with CHF or after myocardial infarction. In the GISSI-3 trial, the proportion of patients with ejection fractions ≤35% was reduced by 25.5% in elderly patients and by 23.4% in patients with anterior myocardial infarction.

Protective effects on blood vessels and the heart occurring with lisinopril treatment include reductions in vessel wall thickening, improved blood rheology, normalisation of soluble fibrin and possibly of fibrinogen levels, increased antioxidant effects, reduced myocardial fibrosis and necrosis after injury and enhancement of bradykinin activity. Lisinopril can also attenuate some sympathetic nervous system effects, although it does not alter norepinephrine (noradrenaline) or epinephrine (adrenaline) concentrations.

No changes in glycaemic control or lipid levels are seen in young nondiabetic individuals receiving lisinopril. In contrast, insulin sensitivity and glycaemia improved in elderly hypertensive patients and plasma insulin levels were reduced in obese hypertensive patients. In 3328 diabetic patients with hypertension, glycosylated haemoglobin, triglycerides, and total and low-density lipoprotein cholesterol tended to decrease during lisinopril therapy, whereas high-density lipoprotein cholesterol increased.

Antiproteinuric effects of lisinopril appear to be mediated through both post-glomerular vasodilation and altered glomerular permeability. In patients with IgA nephropathy, the DD ACE genotype may predict an antiproteinuric response to lisinopril. Low sodium diets may assist the antiproteinuric activity of lisinopril in nondiabetic patients. In hypertensive patients with impaired renal function, GFR was usually not altered during lisinopril treatment. However, dosages had to be reduced in some patients when creatinine clearance (CLCR) decreased.

Pharmacokinetics

Peak plasma lisinopril concentrations (Cmax) of 40 µg/L and 80 to 140 µg/L occur 6 hours after administration of oral dosages of 10 and 20mg, respectively. Lisinopril is not protein bound or metabolised. The 25 to 50% of an oral dose absorbed is excreted unchanged in urine, with an effective elimination half-life of 12.6 hours. Absorption is unaffected by age, but lisinopril clearance is correlated with CLcr, which tends to decline with age.

For reasons that are not clear, lisinopril concentrations may be higher and urinary recovery may be lower in patients with hepatic impairment than in healthy individuals. Lisinopril clearance is reduced in line with renal function, resulting in higher and possibly delayed Cmax values and lower urinary recovery. Population pharmacokinetic data from patients with varying degrees of renal function show that clearance can also be predicted from the combined age, bodyweight and serum creatinine concentration of individual patients. Dosage adjustments in renal failure can be made on the basis of standard methods such as the Dettli equation to achieve non-accumulating therapeutic dosages. Plasma lisinopril concentrations may be higher in CHF patients receiving this agent, possibly because of reduced heart failure-related renal function in these patients. However, bioavailability may also be reduced in this patient group, by an unknown mechanism.

Clinical Efficacy

Lisinopril has been well studied in a large number of clinical trials in elderly patients with hypertension. 80.2 and 72% of such patients in 2 noncomparative trials responded to 12 weeks of lisinopril 2.5 to 40 mg/day. Blood pressure responses were maintained after 1 to 2 years of therapy in a third study. Effective dosages varied widely across studies. In studies evaluating the effects of age, blood pressure reductions and lisinopril response rates were similar in young and elderly patients. Comparative trials show lisinopril 2.5 to 40 mg/day to be equivalent in antihypertensive efficacy to enalapril, quinapril, sustained release (SR) nifedipine and hydrochlorothiazide, superior to SR verapamil and placebo, and more effective when combined with hydrochlorothiazide.

Results of an ongoing mortality study comparing low and high doses of lisinopril in patients with CHF are expected soon. Ameta-analysis of ACE inhibitor clinical trials suggests that these agents reduce CHF mortality, a tendency that was also found in a subgroup of lisinopril trials. In clinical trials primarily in elderly patients with CHF (NYHA grades II to IV), lisinopril was superior to placebo and at least equivalent to enalapril, captopril and digoxin in improving exercise tolerance and left ventricular ejection fraction (LVEF) and was comparable to these other agents in its lack of effects on ventricular ectopic beats. Lisinopril improves Yale Scale scores of dyspnoea and fatigue significantly more than placebo or captopril. Improvements in LVEF are also significantly greater in lisinopril than captopril recipients.

ACE inhibitors have been shown in large scale trials to reduce mortality and morbidity after myocardial infarction. In the GISSI-3 trial, within 24 hours of onset of myocardial infarction symptoms 19 394 hospitalised patients received lisinopril, nitroglycerin (glyceryl trinitrate), lisinopril plus nitroglycerin, or no added treatment, in addition to standard aspirin (acetylsalicylic acid), thrombolytic and β-blocker care. Treatment continued for 6 weeks and then was withdrawn, except in the 35% of patients with an alternative indication for lisinopril use. In the 2585 elderly (>70 years) patients enrolled in the GISSI-3 trial who received lisinopril, a 12% reduction in mortality and severe left ventricular dysfunction was evident after 6 weeks (2p = 0.0039). Results in all age groups persisted, although less strongly, at 6 months. The greatest benefits were seen in patients receiving lisinopril with nitroglycerin. The effects of lisinopril on mortality were greater in the first 6 weeks of treatment, whereas effects on left ventricular dysfunction were greater later in the study.

In hypertensive diabetic patients with albuminuria, lisinopril 5 to 40 mg/day was comparable in antiproteinuric efficacy to verapamil (mean 362 mg/day) and nifedipine (20 to 80 mg/day) and superior to atenolol (50 to 100 mg/day). Effects of lisinopril on GFR in hypertensive patients with diabetic albuminuria are varied, with no changes in some studies and decreases in others. According to GISSI-3 results, there appears to be a reduction in risk of mortality in general or elderly populations of diabetic patients receiving lisinopril after myocardial infarction. Pilot studies that show improvements in diabetic neuropathy in lisinopril-treated patients require confirmation in larger well controlled clinical trials.

Tolerability

Lisinopril is generally well tolerated, with adverse events that are typical of the ACE inhibitor class. The most common adverse events in controlled clinical trials were headache (5.5%), dizziness (4.4%), cough (3%), asthenia and fatigue (2.7%) and diarrhoea (1.8%). Tolerability does not appear to be dosage related. Elderly patients may be more likely than younger patients to discontinue treatment, although it is not clear whether adverse events are more common in elderly than younger patients. Two studies suggest that they are not, while another found that cough, urticaria, hyperkalaemia, increased creatinine levels and angioedema were more frequent in elderly patients. The incidence and severity of adverse events does, however, appear to increase with progressing renal failure and more severe CHE.

Serious adverse events occur infrequently with lisinopril. Angioedema is a signal to discontinue lisinopril treatment. In some patients, hypotension may necessitate dosage reduction or stopping of lisinopril treatment. Renal dysfunction tends to occur in patients with other severe disease and is a cue to lower dosages or halt treatment.

Other adverse events sometimes occurring with lisinopril include hyperkalaemia, anaemia, reversible elevations in liver enzymes, anaphylactoid reactions during haemodialysis with high-flux membranes, and male sexual dysfunction. Lisinopril has also been associated with reports of pancreatitis, aplastic anaemia, pancytopenia, scalded mouth syndrome, purpuric rash, mania, and hypertensive crisis on lisinopril withdrawal.

Drug Interactions

Few drugs interact with lisinopril. Diuretics, N-acetylcysteine and possibly β-blockers can potentiate and indomethacin can attenuate the antihypertensive effects of lisinopril. Potassium-sparing diuretics can increase the incidence of hyperkalaemia seen with lisinopril. Lisinopril reduces lithium excretion, which can lead to toxicity. Hydralazine and digoxin can increase lisinopril bioavailability, but these interactions have not been reported to have clinical consequences.

Dosage and Administration

Dosages of lisinopril are administered orally once daily, can be given at any time in relation to meals, and must be individualised. Treatment of elderly patients should be started at lower dosages than in other adults. Lisinopril should be used with caution in patients with hyperkalaemia, renal impairment or volume or salt depletion, or those at risk of these conditions. Diuretics should be discontinued before lisinopril use if possible, or sodium intake increased, to reduce the risk of hypotension.

Lisinopril monotherapy in patients with hypertension is usually started at 10 mg/day, titrated to blood pressure response as needed up to 40 mg/day. If monotherapy does not control hypertension, a diuretic may be added. There are no specific guidelines for patients with diabetes, but a similar dosage range to that used for patients with hypertension (e.g. 5 to 40 mg/day) is likely to be appropriate, depending on renal function. Patients with renal impairment should receive lower dosages of lisinopril.

Patients with CHF are usually started on lisinopril 2.5 mg/day under close medical supervision. This dosage may be titrated upwards to a usual maximum of 20 mg/day, with regular monitoring of blood pressure and renal function before and during treatment.

After myocardial infarction in patients who are haemodynamically stable, lisinopril 5mg may be given within 24 hours of symptom onset, followed 24 hours later by another 5mg dose and 48 hours later by a 10mg dose. Thereafter, the dosage is 10 mg/day, usually for 6 weeks, when the drug may be discontinued. Patients with low systolic blood pressure (≥120mm Hg) should initially receive a dosage of 2.5mg once daily. Individuals with another indication for an ACE inhibitor, such as CHF or hypertension, may continue to take lisinopril after the first 6 weeks post-myocardial infarction.

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    Heather D. Langtry & Anthony Markham

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  1. Heather D. Langtry
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Correspondence to Heather D. Langtry.

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Various sections of the manuscript reviewed by: W.S. Aronow, Hebrew Hospital Home, Bronx, New York, USA; J. Kjekshus, Section of Cardiology, Medical Department, Rikshospitalet, Oslo, Norway; L. Lisheng, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences, Beijing, China; P. Sleight, lohn Radcliffe Hospital, University of Oxford, Oxford, England; F. Stewart, Department of Medicine, University of Auckland, Auckland, New Zealand; J. Tamargo, Consejo Superior de Investigaciones Cientificas, Universidad Complutense de Madrid, Madrid, Spain; C. Valenzuela, Consejo Superior de Investigaciones Cientificas, Universidad Complutense de Madrid, Madrid, Spain; G. Zuanetti, GISSI Coordinating Centre, Istituto Mario Negri, Milan, Italy.

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Langtry, H.D., Markham, A. Lisinopril. Drugs & Aging 10, 131–166 (1997). https://doi.org/10.2165/00002512-199710020-00006

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