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Captopril is an orally active inhibitor of angiotensin-converting enzyme (ACE) and has been widely studied in the treatment of patients with mild to moderate essential hypertension, severe hypertension not responsive to conventional diuretic/β-adrenoceptor blocker/vasodilator regimens, and patients with chronic congestive heart failure refractory to treatment with a diuretic and digitalis.
In patients with mild or moderate essential hypertension, titrated low doses of captopril used alone or in conjunction with a diuretic are similar in efficacy to usual doses of hydrochlorothiazide, chlorthalidone, or β-adrenoceptor blocking drugs, as well as to the other ACE inhibitors. In addition, captopril improved well-being to a greater extent than methyldopa or propranolol in a study designed specifically to determine the effect of treatment on the quality of life of patients with mild or moderate essential hypertension. The earlier demonstrated efficacy of captopril, used with a diuretic and often also with a β-adrenoceptor blocking drug, in the treatment of severe hypertension refractory to conventional ‘triple therapy’ has been confirmed in more recent trials which illustrate the generally marked antihypertensive effect of captopril-containing regimens in such patients. Results of initial trials in patients with scleroderma are promising, with control of hypertension and stabilisation of renal function in these patients when treated at an early stage of the disease.
Several comparative and long term trials of captopril in patients with chronic congestive heart failure refractory to treatment with a diuretic/digitalis regimen clearly demonstrate that initial haemodynamic improvement is maintained and correlates with clinical benefit. A tendency for overall clinical response to captopril to be better than the response to prazosin, hydralazine, nisoldipine or enalapril has been reported. Results of a multicentre comparison with digoxin and placebo indicate that captopril is a suitable alternative to digoxin in patients with mild to moderate heart failure who are receiving maintenance diuretic therapy.
The tolerability of captopril has now been studied in many thousands of patients involved in formalised trials and the early impression of poor tolerability can no longer be justified. The use of generally lower dosages of captopril in patients with normal or slightly impaired renal function has resulted in a generally low incidence of rash (0.5 to 4%), dysgeusia (0.1 to 3%), proteinuria (0.5%), neutropenia (0.3% during first 3 months) and symptomatic hypotension (0.1 to 3%). Cough is an infrequent but troublesome effect resulting from ACE inhibition. The risk of these adverse effects is substantially increased when captopril is used at high dosages in patients with impaired renal function.
Thus, captopril with its generally good tolerability and proven long term efficacy warrants consideration as a ‘first line’ therapy in patients with mild or moderate essential hypertension and in patients with refractory hypertension, and as a drug of choice in patients with chronic congestive heart failure when digitalis is poorly tolerated or ineffective.
Inhibition of the renin-angiotensin-aldosterone system by pharmacological intervention produces favourable haemodynamic changes which benefit patients with hypertension or congestive heart failure. The acute effects of orally administered captopril include inhibition of angiotensin-converting enzyme (ACE) activity, decreased and increased plasma concentrations of angiotensin II and angiotensin I, respectively, increased plasma renin activity or renin concentration, and decreased aldosterone concentration or urinary aldosterone excretion. Maximal hormonal responses are usually noted after about 1 hour and return to control levels after about 6 to 8 hours, although recovery of ACE activity can take up to 12 to 14 hours. The acute changes in the renin-angiotensin-aldosterone system are generally maintained during long term captopril treatment. The blood pressure lowering effect of ACE inhibition by captopril is most pronounced in subjects with high pretreatment plasma renin activity, and response to the drug is enhanced by sodium restriction or diuretic therapy which increase dependence on plasma renin activity.
Repeated oral administration of usual therapeutic doses of captopril has reportedly decreased urinary kallikrein and increased circulating concentrations of bradykinin in some studies, but not in others. It has become increasingly evident that plasma concentrations of prostaglandin E2 and I2 (prostacyclin), or concentrations of their metabolites in urine, may be increased during treatment with captopril in patients with hypertension or congestive heart failure. That the haemodynamic responses to captopril may be partially mediated by prostaglandins is suggested by the attenuation of the antihypertensive effect of captopril by concomitant indomethacin. Adrenaline (epinephrine) plasma concentrations were not influenced by captopril treatment, while mean noradrenaline (norepinephrine) concentrations were unchanged in some studies but were decreased in individuals with high pretreatment concentrations.
The acute haemodynamic changes in hypertensive patients after a single oral dose of captopril, which are maximal within 1 hour and persist for 8 to 12 hours, consist of a decrease in systolic and diastolic blood pressure and in systemic vascular resistance, usually without clinically significant changes in heart rate or cardiac output. Maximal effects are usually produced by doses of captopril 12.5 to 25mg while increases in dose above this may increase the duration of the response.
In patients with congestive heart failure, a single dose of captopril causes a significant decrease of about 37 to 45% in right atrial pressure, pulmonary capillary wedge pressure, and pulmonary and systemic vascular resistances within 30 to 90 minutes; mean arterial and pulmonary artery pressures decrease by 24 to 30%. Cardiac output, cardiac index, stroke index and stroke work index increase by about 20 to 44%.
The beneficial haemodynamic effects of captopril are maintained during long term treatment and are accompanied by clinical improvement. Most studies have shown some degree of statistically significant correlation between high pretreatment renin levels and more marked acute haemodynamic response, although any correlation between pretreatment renin levels and long term haemodynamic or clinical response was frequently absent.
Compared with other vasodilator drugs such as hydralazine, prazosin, sodium nitroprusside or nitrates, captopril exerts a relatively weak effect in reducing pulmonary vascular resistance. However, the effect of captopril on preload and afterload is balanced and thus resembles that of prazosin, amrinone and isosorbide dinitrate, although quantitatively the effect of captopril was sometimes greater than that of prazosin and less than that of amrinone.
In healthy subjects the renal haemodynamic and functional response to ACE inhibition depends on the state of the renin-angiotensin system. Restriction of sodium intake markedly increases the renal response to captopril, resulting in increased renal blood flow, reversal of the decrease in glomerular filtration rate, decreased renal vascular resistance and a substantial natriuresis. Long term administration of captopril to patients with essential hypertension has usually resulted in little change in mean values for renal blood flow, effective renal plasma flow or glomerular filtration rate. In patients with renovascular hypertension and unilateral lesions glomerular filtration decreased (sometimes markedly) on the stenotic side, but was little changed on the non-stenotic side. Mean sodium excretion was increased in some patients with essential hypertension but not in others, while mean potassium excretion was unchanged during long term treatment. Divergent findings and considerable interindividual variation in the acute effects of captopril on renal blood flow and indices of renal function have been reported in patients with chronic congestive heart failure. Thus, both an increase and a decrease in renal blood flow have been noted, although different findings may have been related to concomitant diuretic administration in some patients. In 1 study a decrease in renal blood flow occurred when mean arterial blood pressure was reduced to below 60mm Hg. As in patients with hypertension, renal vascular resistance was consistently decreased in patients with congestive heart failure. Serum potassium concentrations have increased in some patients, but remained stable during long term captopril therapy in others receiving a thiazide diuretic plus triamterene.
Approximately 70% of an oral dose of captopril is absorbed by healthy fasting subjects and absolute bioavailability is about 60% compared with the intravenous route. Mean maximum blood concentrations after single oral doses of captopril are dose-related over the range from 10 to 100mg and are about 1.6 to 1.9 mg/L (total drug) after oral administration of 100mg. The area under the plasma concentration-time curve for free captopril was similar in healthy subjects and in patients with hypertension or congestive heart failure after repeated doses, while that for total captopril increased by around 20%. Bioavailability is decreased by 25 to 50% when captopril is coadministered with food, and is similarly decreased when the drug is given with antacids. However, food does not alter either the magnitude or timing of the antihypertensive effect of captopril. In healthy subjects the mean volume of distribution at steady state was about 0.7 L/kg; a value of 2.05 L/kg during the terminal phase indicated extensive partitioning into tissues.
The metabolism of captopril is complex and yet to be fully elucidated. In man, captopril is partially metabolised (about 50%), mainly by disulphide formation with endogenous thiol compounds including glutathione, cysteine and proteins. One of these metabolites, S-methyl captopril, is present in the circulation at concentrations of 60 to 114 µg/L after a single oral dose of captopril 100mg in healthy subjects. Most of the drug is excreted unchanged in the urine by tubular secretion, 94% of this being recovered within 6 hours. Elimination half-life has been difficult to calculate, with reported values of 0.35 to 0.66 hours and 1.7 to 1.9 hours, depending on the method used.
The pharmacokinetic properties of captopril in patients with hypertension and in the elderly are similar to those in healthy subjects. While mean pharmacokinetic values in patients with chronic congestive heart failure are not generally different, between-subject variability is more marked than in healthy subjects. Individual elimination rate constants are linearly related to endogenous creatinine clearance in patients with renal impairment, resulting in an increased half-life and reduced clearance of captopril in patients with renal impairment. Since ACE inhibition and antihypertensive response may be prolonged in patients with renal functional impairment, dosage modification according to the degree of impairment is necessary. Captopril is removed by haemodialysis more efficiently than its metabolites. Since free or total plasma captopril concentrations have not correlated well with haemodynamic or neurohormonal responses in individual patients, monitoring of plasma concentrations is of little value in establishing optimum dosage.
Captopril has been widely studied in patients with mild to moderate essential hypertension in whom, at dosages often less than 200mg daily, it has been compared with other ACE inhibitors, β-adrenoceptor blocking drugs and various diuretics. In many studies in mild to moderate essential hypertension captopril was used in conjunction with a diuretic (most often hydrochlorothiazide), which clearly resulted in enhanced antihypertensive efficacy. Most studies comparing captopril with 1 or more other antihypertensive drugs have involved relatively small numbers of patients, thus decreasing the likelihood of differences between drugs being statistically significant; however, in many studies dosages were titrated to optimum levels and results reported in the few larger studies were consistent with those in the smaller trials.
Captopril 75 to 300mg daily in 3 divided doses was closely comparable with enalapril 10 to 40mg in 2 doses daily when used in conjunction with methyldopa to reduce blood pressure to target levels. In 1 study captopril 50 to 100mg once daily was similar in efficacy to enalapril 10 to 20mg once daily, while in another study captopril 100mg daily and ramipril 10mg daily were similarly effective when both drugs were administered twice daily. In some cases enalapril was reported to be more effective than captopril at some time points during particular studies, but differences were not statistically significant at the end of the trials. Similarly, there were no significant differences in the therapeutic efficacy of captopril and various β-adrenoceptor blocking drugs or labetalol in patients with mild or moderate hypertension, either when doses were titrated to individual requirements or when fixed combinations were used. Studies comparing titrated doses or predetermined fixed doses of captopril and hydrochlorothiazide, chlorthalidone or triamterene plus hydrochlorothiazide, have noted no statistically significant differences in efficacy between treatments in patients with mild to moderately severe uncomplicated hypertension. Captopril 50 to 300mg daily was also comparable with nifedipine 40 to 80mg or minoxidil 5 to 40mg (mean 7.5mg) when added to existing ineffective treatment regimens.
While captopril alone is effective in lowering mildly or moderately elevated blood pressure in many patients, studies comparing the efficacy of captopril alone with that of captopril plus a diuretic, or occasionally other antihypertensive drugs, have clearly demonstrated an advantage for combined administration. A study in a large group of patients reported a similar decrease in blood pressure with either captopril 37.5, 75 or 150mg daily in patients allocated at random, and further improved control of blood pressure following the addition of hydrochlorothiazide. Several other studies similarly report improved efficacy with captopril used in conjunction with a diuretic or a calcium antagonist, relative to either drug alone.
The earlier reported efficacy of captopril used in conjunction with a diuretic and (usually) a β-adrenoceptor blocking drug in patients with hypertension not adequately controlled with conventional ‘triple therapy’ has been confirmed by more recent studies. These studies have demonstrated the generally marked antihypertensive effects of captopril-containing regimens in refractory hypertension. The addition of captopril to an existing diuretic/β-adrenoceptor blocker regimen resulted in a decrease in supine diastolic blood pressure of 12 to 29% over a period of several months. The decrease in blood pressure was more pronounced in patients with renovascular or renal parenchymatous hypertension than in those with essential hypertension. In small numbers of patients whose blood pressure was not controlled by maximum tolerated doses of either captopril or minoxidil added to a diuretic/β-adrenoceptor blocker regimen, treatment with captopril plus minoxidil in addition to the diuretic and β-blocker resulted in a satisfactory mean reduction in blood pressure.
Long term trials of captopril alone or in conjunction with a diuretic clearly indicate that the antihypertensive effect of titrated doses of captopril is maintained and that tolerance to this effect does not develop.
Studies undertaken to determine the effect of captopril, methyldopa and β-adrenoceptor blocking drugs on the quality of life have, with 1 notable exception, been poorly designed. However, in the best designed trial, captopril resulted in improved quality of life relative to methyldopa and relative to propranolol for some assessment criteria.
In many studies, twice daily administration of captopril alone or in conjunction with a diuretic has been effective in decreasing blood pressure to target levels in patients with mild or moderate essential hypertension. It was considered that once daily administration may provide satisfactory control in such patients, and there is some evidence that this is so. However, further trials utilising 24-hour monitoring of blood pressure and comparing once and twice daily regimens are needed.
Captopril, usually at dosages of less than 150mg daily, has proved an effective and generally well tolerated drug in elderly or diabetic patients with uncomplicated hypertension. Initial studies in children with ‘renal’ hypertension have reported captopril 0.3 to 6 mg/kg/day to effectively control blood pressure, including that not responsive to other drugs. Recent studies have described the satisfactory antihypertensive effect of captopril in conjunction with a diuretic and (usually) other drugs in the treatment of refractory hypertension associated with renal transplantation. Renal function improved in many patients in whom treatment with captopril was started less than 1 year after transplantation. Renal function appeared more likely to deteriorate in sodium-depleted patients and in those with pre-existing renal impairment and a greater than 75% narrowing of the main renal artery. Recent studies of captopril in patients with scleroderma are promising, particularly in those treated at an early stage. In such patients captopril 32 to 150 mg/day plus frusemide (furosemide) controlled hypertension and stabilised renal function where pretreatment serum creatinine was less than 442 µmol/L (5 mg/dl).
At the time that the use of captopril in chronic congestive heart failure was previously reviewed in the Journal there were few comparative studies. Subsequently, comparative data have been reported, and it has also been established that the acute haemodynamic effects of captopril are maintained during long term administration and are accompanied by clinical improvement in patients with chronic congestive heart failure refractory to diuretic and digitalis therapy. Titrated doses of captopril (37.5 to 150 mg/day) were more effective than placebo as evidenced by a reduction in NYHA functional rating or class and in symptoms, and an improvement in exercise capacity in patients with congestive heart failure not responsive to diuretics and digitalis. Similarly, in patients with mild to moderate heart failure captopril improved exercise time and NYHA functional rating relative to placebo whereas digoxin did not. Captopril 300mg daily was superior to prazosin 15mg daily when the drugs were directly compared and diuretic dosage was kept constant. Captopril has also been at least as effective as nisoldipine, hydralazine and enalapril in small groups of patients with chronic refractory heart failure. In mild heart failure, however, substitution of captopril 75mg daily for established diuretic therapy did not result in clinical improvement. Clinical responses to captopril 150mg and enalapril 40mg daily were not significantly different in patients whose pretreatment ejection fraction was below 30%, although side effects were more often a problem with enalapril. There do not appear to be any biochemical or haemodynamic characteristics that reliably predict a favourable clinical response to captopril in patients with chronic congestive heart failure. There is some evidence that the improved clinical state afforded by captopril treatment results in prolongation of survival. Over a period of 12 months treatment with captopril attenuated the progressive enlargement of the ventricular chamber in patients with symptomless left ventricular dysfunction following myocardial infarction.
Although early clinical experience with captopril in patients with severe complicated hypertension, frequently accompanied by renal impairment, and often involving higher doses than are now usually employed, suggested that captopril was not well tolerated, more recent clinical experience with many thousands of patients with mild to moderate uncomplicated hypertension or chronic congestive heart failure indicates that captopril is generally well tolerated in patients with normal or only mildly impaired renal function. Captopril at dosages lower than 150mg daily has caused rash, dysgeusia, hypotensive symptoms and proteinuria in 0.5 to 4.3, 0.1 to 2.7, 0.2 to 4.4 and 0.5% of patients, respectively. Non-productive cough has been reported in 0.2 to 4.4% of patients and appears to be a class effect of ACE inhibitors. The risk of significant side effects was greatest during the first few months of treatment, with daily dosages exceeding 150mg, and in patients with pre-existing renal disease. In post-marketing surveillance studies neutropenia has occurred in up to 0.3% of patients during the first 3 months of treatment with captopril but was not reported over the next 45 months.
Dosage and Administration
When treating hypertension or congestive heart failure it is important to titrate the dosage of captopril to suit individual patient requirements. The usual initial dosage of captopril in hypertension and congestive heart failure is 50mg daily as a single or in two divided doses. However, a much lower dosage of 6.25 or 12.5mg may be required in sodium- or volume-depleted patients. In patients with hypertension, dosage may be increased to 100 or 150mg daily if necessary, but a diuretic should be added before captopril dosage is increased further. The dosage of captopril should not exceed 450mg daily. In patients with congestive heart failure captopril should be administered with a diuretic, and once a dose of 150mg daily is reached further dosage increases should be delayed, where possible, for at least 2 weeks to determine if a satisfactory response occurs. Again, the maximum dosage of captopril should not exceed 450mg daily. In children the initial dose of captopril is 0.3 mg/kg, although 0.15 mg/kg may be appropriate in those likely to develop hypotension. The dosage in children should not exceed 6 mg/kg/day.
Patients with renal impairment should have their dosage of captopril adjusted by either decreasing the total daily dosage or by increasing the interval between each dose. When a diuretic is required in patients with severe renal impairment a loop diuretic (e.g. frusemide), rather than a thiazide, is preferred.
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