Lisinopril-Teva tablets 10 mg blister No. 60

Instructions for Lisinopril-Teva tablets 10 mg blister No. 60

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active ingredient: lisinopril;

1 tablet contains lisinopril 5 mg or 10 mg, or 20 mg in the form of lisinopril dihydrate;

excipients: mannitol (E 421), calcium hydrogen phosphate, pregelatinized corn starch, croscarmellose sodium, magnesium stearate; for 10 mg and 20 mg tablets, iron oxide yellow (E 172), iron oxide black (E 172), iron oxide red (E 172).

Dosage form

Pills.

Main physicochemical properties:

5 mg tablets: white, round, biconvex, with a break line on one side;

10 mg tablets: light pink, unevenly colored, speckled, round biconvex, with a break line on one side;

20 mg tablets: gray-red, unevenly colored, speckled, round biconvex, with a break line on one side.

Pharmacotherapeutic group

Angiotensin-converting enzyme (ACE) inhibitors are simple. ATC code C09A A03.

Pharmacological properties

Pharmacodynamics

Lisinopril is a peptidyl dipeptidase inhibitor. It inhibits ACE, which catalyzes the conversion of angiotensin I to the vasoconstrictor peptide angiotensin II. Angiotensin II also stimulates the secretion of aldosterone by the adrenal cortex. Inhibition of ACE leads to a decrease in the concentration of angiotensin II, which causes a decrease in vasoconstrictor activity and aldosterone secretion. A decrease in aldosterone secretion may lead to an increase in serum potassium. Lisinopril lowers blood pressure primarily by inhibiting the renin-angiotensin-aldosterone system (RAAS). At the same time, lisinopril has an antihypertensive effect even in patients with low renin levels. ACE is identical to kininase II, an enzyme that promotes the breakdown of bradykinin. The overall adverse reaction profile in patients treated with high or low doses of lisinopril was shown to be similar in nature and frequency. Patients treated with lisinopril had a greater reduction in urinary albumin excretion than patients treated with a calcium channel blocker, which produced a similar reduction in blood pressure. This suggests that the ACE inhibitory effect of lisinopril results in a reduction in microalbuminuria through a direct effect on renal tissue in addition to its blood pressure-lowering effect. Lisinopril therapy did not affect blood glucose control, as evidenced by its negligible effect on glycosylated hemoglobin (HbA1c).

Pharmacokinetics

Lisinopril is an orally active, non-sulfhydryl ACE inhibitor.

Absorption. After oral administration of lisinopril, maximum serum concentrations (Cmax) are reached after 7 hours, although in patients with acute myocardial infarction there is a tendency for a slight delay in reaching peak concentrations. As shown by urinary excretion, the mean extent of absorption of lisinopril is approximately 25% with interpatient variability of 6-60% over the dose range studied (5-80 mg). In patients with heart failure, absolute bioavailability is reduced by approximately 16%. Food intake does not affect the absorption of the drug.

Distribution: Lisinopril does not bind to serum proteins, except for circulating ACE. Studies in rats have shown that lisinopril penetrates the blood-brain barrier poorly.

Elimination. Lisinopril is not metabolized and is excreted unchanged in the urine. The elimination half-life in patients receiving multiple doses is 12.6 hours. The clearance of lisinopril in healthy volunteers is approximately 50 ml/min. The decline in serum concentrations demonstrates a prolonged terminal phase that is not associated with drug accumulation. This terminal phase probably reflects saturable binding to ACE and is not dose-proportional.

Patients with hepatic impairment: In patients with cirrhosis, hepatic impairment results in reduced absorption of lisinopril (approximately 30%), but due to reduced clearance, exposure is increased (approximately 50%) compared to healthy volunteers.

Renal impairment. Renal impairment reduces the elimination of lisinopril, which is excreted by the kidneys, but this decrease is clinically significant only when the glomerular filtration rate (GFR) is below 30 ml/min. In mild and moderate renal impairment (creatinine clearance 30-80 ml/min), the mean area under the pharmacokinetic concentration-time curve (AUC) increases by only 13%, while in severe renal impairment (creatinine clearance 5-30 ml/min) there is a 4.5-fold increase in the mean AUC. Lisinopril can be removed by dialysis. During 4 hours of hemodialysis, the plasma concentration of lisinopril decreases by an average of 60% with a dialysis clearance of 40-55 ml/min.

Elderly patients: Elderly patients have higher blood levels and higher AUC values (approximately 60% increase) compared to younger patients.

Indication

Arterial hypertension.

Heart failure (symptomatic treatment).

Acute myocardial infarction (short-term treatment (6 weeks) of hemodynamically stable patients no later than 24 hours after acute myocardial infarction).

Renal complications in diabetes mellitus (treatment of kidney disease in hypertensive patients with type II diabetes mellitus and initial nephropathy).

Contraindication

– Hypersensitivity to lisinopril, excipients of the drug or to other ACE inhibitors.

– History of angioedema associated with the use of ACE inhibitors.

– Concomitant use with sacubitril/valsartan: Treatment with Lisinopril should only be started 36 hours after the last dose of sacubitril/valsartan (see sections 4.5 and 4.4).

– Hereditary or idiopathic angioedema.

– II and III trimesters of pregnancy (see sections “Special precautions for use” and “Use during pregnancy or breastfeeding”).

– Concomitant use with aliskiren-containing medicinal products in patients with diabetes mellitus or renal impairment (GFR <60 ml/min/1.73 m2).

Interaction with other medicinal products and other types of interactions

Antihypertensives: Concomitant use with other antihypertensive drugs (e.g. nitroglycerin, other nitrates or other vasodilators) may further reduce blood pressure.

Clinical trial data have shown that dual blockade of the RAAS with concomitant use of ACE inhibitors, angiotensin II receptor blockers or aliskiren is characterized by a higher incidence of adverse reactions such as arterial hypotension, hyperkalemia, and renal dysfunction (including acute renal failure) compared to monotherapy.

Medicinal products that increase the risk of angioedema. Concomitant use of ACE inhibitors with sacubitril/valsartan is contraindicated due to an increased risk of angioedema (see sections 4.3 and 4.4). Concomitant use of ACE inhibitors with mammalian target of rapamycin (mTOR) inhibitors (e.g. temsirolimus, sirolimus, everolimus) or neutral endopeptidase (NEP) inhibitors (e.g. racecadotril), vildagliptin or tissue plasminogen activator may lead to an increased risk of angioedema (see section 4.4).

Diuretics. The antihypertensive effect is usually enhanced when diuretics are added to lisinopril therapy. In patients already receiving diuretics, especially those who have recently started treatment, excessive reductions in blood pressure may occasionally occur after the addition of lisinopril. The likelihood of symptomatic hypotension with lisinopril may be reduced by discontinuing diuretic therapy before initiating lisinopril therapy.

Potassium supplements, potassium-sparing diuretics, salt substitutes containing potassium, and other drugs that may increase serum potassium. Although serum potassium levels are usually within normal limits, hyperkalemia may occur in some patients taking this drug. The use of potassium-sparing diuretics (such as spironolactone, triamterene, or amiloride), potassium supplements, or salt substitutes containing potassium may lead to significant increases in serum potassium, especially in patients with impaired renal function. Caution should also be exercised when lisinopril is used concomitantly with other drugs that increase serum potassium levels, such as trimethoprim and co-trimoxazole (trimethoprim/sulfamethoxazole), since trimethoprim is known to act as a potassium-sparing diuretic, as is amiloride. Therefore, the combination of lisinopril with the above-mentioned drugs is not recommended. If concomitant use of such drugs is indicated, treatment should be carried out with caution and serum potassium should be monitored frequently. If lisinopril is used concomitantly with potassium-losing diuretics, the hypokalemia induced by the diuretic effect may be attenuated.

Cyclosporine: Concomitant use of ACE inhibitors with cyclosporine may cause hyperkalemia. Monitoring of serum potassium is recommended.

Lithium preparations. Reversible increases in serum lithium concentrations and toxic reactions have been reported with concomitant use of lithium and ACE inhibitors. Concomitant use of thiazide diuretics may increase the risk of lithium toxicity and exacerbate existing toxicity. Concomitant use of lisinopril and lithium is not recommended, but if such a combination proves necessary, serum lithium levels should be closely monitored.

Non-steroidal anti-inflammatory drugs (NSAIDs), including acetylsalicylic acid at a dose of ≥3 g/day. When ACE inhibitors are used concomitantly with NSAIDs (acetylsalicylic acid at doses that have an anti-inflammatory effect, cyclooxygenase-2 (COX-2) inhibitors and non-selective NSAIDs), attenuation of the antihypertensive effect may occur. Concomitant use of NSAIDs and ACE inhibitors may lead to an increased risk of renal dysfunction, including possible acute renal failure, and an increase in serum potassium, especially in patients with pre-existing renal dysfunction. These effects are usually reversible. The combination should be administered with caution, especially in elderly patients. Patients should be adequately hydrated and attention should be paid to monitoring renal function after initiation of concomitant therapy and periodically thereafter.

Gold preparations: Nitritoid reactions (symptoms of vasodilation including flushing, nausea, dizziness and hypotension, which may be very severe) following injections of gold preparations (e.g. sodium aurothiomalate) have been observed more frequently in patients treated with ACE inhibitors.

Tricyclic antidepressants/antipsychotics/anesthetics: Concomitant use of certain anesthetic drugs, tricyclic antidepressants, and neuroleptics with ACE inhibitors may result in further reduction in blood pressure.

Sympathomimetic drugs: Sympathomimetic drugs may reduce the antihypertensive effect of ACE inhibitors.

Antidiabetic drugs: Concomitant use of ACE inhibitors and antidiabetic drugs (insulin, oral hypoglycemic agents) may increase the blood glucose lowering effect with the risk of hypoglycemia. This effect usually occurs during the first weeks of combination therapy and in patients with renal insufficiency.

Acetylsalicylic acid, thrombolytics, β-blockers, nitrates. Lisinopril can be used concomitantly with acetylsalicylic acid (in cardiological doses), thrombolytics, β-blockers and/or nitrates.

Application features

Symptomatic hypotension. Symptomatic hypotension has been reported rarely in patients with uncomplicated hypertension. In hypertensive patients receiving lisinopril, symptomatic hypotension is more likely to occur in the setting of electrolyte and fluid imbalance, such as that caused by diuretic therapy, dialysis, salt restriction, diarrhoea or vomiting, or severe renin-dependent hypertension. Symptomatic hypotension has been reported in patients with heart failure (with or without renal insufficiency). The risk of hypotension is higher in patients with severe heart failure who are receiving high doses of loop diuretics, have hyponatraemia or have functional renal impairment. In patients at increased risk of symptomatic hypotension, initiation of therapy and subsequent dose increases should be under close medical supervision. The same warnings apply to patients with ischemic heart disease or cerebrovascular disease, in whom an excessive decrease in blood pressure could lead to myocardial infarction or stroke.

If hypotension occurs, the patient should be placed on his back and, if necessary, an intravenous infusion of saline should be given. Transient hypotension is not a contraindication to further use of the drug, and it can usually be taken without complications after the blood pressure has increased after increasing the volume of fluid in the body.

Hypotension in acute myocardial infarction. In acute myocardial infarction, treatment with lisinopril should not be initiated if there is a risk of further serious haemodynamic deterioration following treatment with a vasodilator. This applies to patients with a systolic blood pressure of 100 mm Hg or lower and patients who have developed cardiogenic shock. During the first 3 days after myocardial infarction, the dose should be reduced if the systolic blood pressure is 120 mm Hg or lower. If the systolic blood pressure is 100 mm Hg or lower, the maintenance dose should be reduced to 5 mg or temporarily to 2.5 mg. If prolonged hypotension occurs after taking lisinopril (systolic blood pressure remains below 90 mm Hg for more than 1 hour), treatment with lisinopril should be discontinued.

Aortic and mitral valve stenosis/hypertrophic cardiomyopathy: As with other ACE inhibitors, lisinopril should be used with caution in patients with mitral stenosis or obstruction in the outflow of blood from the left ventricle (as in aortic stenosis or hypertrophic cardiomyopathy).

Renal impairment: In patients with renal impairment (creatinine clearance <80 ml/min), the initial dose of lisinopril should be adjusted based on creatinine clearance (see table in section 4.2) and then according to the patient's response to treatment. In such patients, creatinine and potassium levels should be monitored regularly.

In patients with heart failure, hypotension occurring at the beginning of treatment with ACE inhibitors may lead to deterioration of renal function. In such cases, acute renal failure, usually reversible, has been reported.

In some patients with bilateral renal artery stenosis or stenosis of the artery to a solitary kidney, ACE inhibitors have been shown to increase blood urea and serum creatinine, which usually resolve after discontinuation of the drug. The risk of such events is particularly high in patients with renal insufficiency. The presence of renovascular hypertension increases the risk of severe hypotension and renal insufficiency. Treatment of such patients should be initiated under medical supervision, starting with low doses and titrating carefully. Since diuretics may precipitate the clinical events described above, they should be discontinued during the first weeks of treatment with lisinopril and renal function should be closely monitored.

In some hypertensive patients without overt renal vascular disease, the use of lisinopril, especially in combination with diuretics, has caused increases in blood urea and serum creatinine; these changes are usually minor and transient. They are more likely to occur in patients with impaired renal function. In such cases, it may be necessary to reduce the dose and/or discontinue the diuretic and/or lisinopril.

In acute myocardial infarction, lisinopril should not be initiated in patients with impaired renal function (serum creatinine >177 μmol/l and/or proteinuria >500 mg/day). If renal function deteriorates during treatment with lisinopril (serum creatinine >265 μmol/l or doubling from baseline), discontinuation of lisinopril should be considered.

Hypersensitivity/angioedema. Angioedema of the face, extremities, lips, tongue, glottis and/or larynx has been reported rarely in patients treated with ACE inhibitors, including lisinopril. Angioedema may occur at any time during treatment. In such cases, the drug should be discontinued immediately, appropriate therapy should be initiated, and the patient should be observed until symptoms resolve. Even in cases where the swelling is limited to the tongue and does not cause respiratory distress, the patient may require prolonged observation, as antihistamines and corticosteroids may be inadequate.

Fatalities have been reported very rarely as a result of angioedema of the larynx or tongue. If the swelling extends to the tongue, glottis or larynx, obstructive respiratory failure may develop, especially in patients who have previously undergone surgery on the respiratory tract. In such cases, emergency treatment should be initiated immediately, which may include the administration of adrenaline and/or the maintenance of a patent airway. The patient should be kept under close medical supervision until complete and sustained resolution of symptoms.

ACE inhibitors cause angioedema more often in black patients than in other patients.

Concomitant use of ACE inhibitors with sacubitril/valsartan is contraindicated due to an increased risk of angioedema. Sacubitril/valsartan treatment should not be started until 36 hours after the last dose of lisinopril. Lisinopril treatment should not be started until 36 hours after the last dose of sacubitril/valsartan (see sections 4.3 and 4.5).

Concomitant use of ACE inhibitors with racecadotril, mTOR inhibitors (e.g. sirolimus, everolimus, temsirolimus) and vildagliptin may lead to an increased risk of angioedema (e.g. swelling of the airways or tongue with or without respiratory distress) (see section 4.5). Caution should be exercised when initiating racecadotril, mTOR inhibitors (e.g. sirolimus, everolimus, temsirolimus) and vildagliptin in patients already taking an ACE inhibitor.

Anaphylactoid reactions in patients undergoing hemodialysis. Anaphylactoid reactions have been reported in patients undergoing hemodialysis using high-flux membranes (e.g. AN69) and receiving concomitant ACE inhibitor therapy. These patients should be offered a change of dialysis membrane type or a different class of antihypertensive drug.

Anaphylactoid reactions occurring during low-density lipoprotein (LDL) apheresis: Rarely, life-threatening anaphylactoid reactions have been observed in patients receiving ACE inhibitors during LDL apheresis with dextran sulfate. These reactions have been avoided by temporarily stopping ACE inhibitor therapy prior to each apheresis.

Desensitization: Patients taking ACE inhibitors have developed persistent anaphylactoid reactions during desensitization therapy (e.g., to hymenoptera venom). These reactions have been avoided in such patients by temporarily stopping ACE inhibitors, but the reactions have recurred after inadvertent re-administration of the drug.

Hepatic failure. Very rarely, ACE inhibitors have been associated with a syndrome that begins with cholestatic jaundice and progresses to fulminant necrosis and (sometimes) death. The mechanism of this syndrome is unknown. If patients taking lisinopril develop jaundice or marked elevations of liver enzymes, lisinopril should be discontinued and appropriate medical attention should be sought.

Neutropenia/agranulocytosis. Neutropenia/agranulocytosis, thrombocytopenia and anemia have been reported in patients receiving ACE inhibitors. Neutropenia is rare in patients with normal renal function and in the absence of other complicating factors. Neutropenia and agranulocytosis are reversible upon discontinuation of the ACE inhibitor. Lisinopril should be used with extreme caution in patients with collagen vascular disease, immunosuppressive therapy, allopurinol or procainamide, or a combination of these complicating factors, especially in patients with impaired renal function. Some such patients develop serious infections that do not always respond to intensive antibiotic therapy. When using the drug in such patients, it is recommended to periodically monitor the number of white blood cells in the blood and instruct patients to report any signs of infection.

Dual blockade of the RAAS: Concomitant use of ACE inhibitors, angiotensin II receptor blockers or aliskiren has been reported to increase the risk of hypotension, hyperkalaemia and renal impairment (including acute renal failure). Therefore, dual blockade of the RAAS through concomitant use of ACE inhibitors, angiotensin II receptor blockers or aliskiren is not recommended.

If dual blockade therapy is absolutely necessary, it should be carried out under specialist supervision and regular monitoring of renal function, electrolytes and blood pressure is recommended. The concomitant use of ACE inhibitors and angiotensin II receptor blockers is not recommended in patients with diabetic nephropathy.

Race: ACE inhibitors cause angioedema more frequently in black patients than in non-black patients. As with other ACE inhibitors, lisinopril may be less effective in lowering blood pressure in black patients than in non-black patients, possibly because of a higher prevalence of low-renin hypertension in black patients.

Surgery/Anesthesia: In patients undergoing major surgery or undergoing anesthesia with agents that produce hypotension, lisinopril may block the formation of angiotensin II secondary to compensatory renin release. If hypotension occurs due to this mechanism, it can be corrected by increasing circulating blood volume.

Hyperkalemia. ACE inhibitors may cause hyperkalemia because they inhibit aldosterone release. This effect is usually minor in patients with normal renal function. However, hyperkalemia may occur in patients with impaired renal function, diabetes mellitus, and/or in patients taking potassium supplements (including salt substitutes), potassium-sparing diuretics (e.g. spironolactone, triamterene, amiloride), other drugs that increase serum potassium (e.g. heparin, trimethoprim or co-trimoxazole, also known as trimethoprim/sulfamethoxazole), and especially aldosterone antagonists or angiotensin receptor blockers. Caution should be exercised when potassium-sparing diuretics and angiotensin receptor blockers are used in patients taking ACE inhibitors. In such patients, serum potassium levels and renal function should be monitored (see section 4.5).

Diabetic patients: In diabetic patients taking oral antidiabetic agents or insulin, close glycemic control is required during the first month of therapy with ACE inhibitors.

Lithium: The concomitant use of lithium and lisinopril is generally not recommended.

Pregnancy: ACE inhibitors should not be initiated during pregnancy (see sections 4.3 and 4.4).

Excipients

Sodium: This medicinal product contains less than 1 mmol sodium (23 mg) per tablet, i.e. essentially ‘sodium-free’.

Use during pregnancy or breastfeeding

Pregnancy: The use of ACE inhibitors is not recommended during the first trimester of pregnancy (see section "Special warnings and precautions for use"). The use of ACE inhibitors is contraindicated during the second and third trimesters of pregnancy (see sections "Contraindications" and "Special warnings and precautions for use").

Epidemiological evidence regarding the risk of teratogenicity following exposure to ACE inhibitors during the first trimester of pregnancy is inconclusive; however, a small increase in risk cannot be excluded. Unless continued ACE inhibitor therapy is considered essential, patients planning pregnancy should be changed to alternative antihypertensive treatments with an established safety profile for use in pregnancy. When pregnancy is confirmed, ACE inhibitor therapy should be stopped immediately, and, if appropriate, alternative therapy should be started. Exposure to ACE inhibitors during the second and third trimesters of pregnancy is known to induce fetotoxicity (decreased renal function, oligohydramnios, skull ossification retardation) and neonatal toxicity (renal failure, hypotension, hyperkalemia). In case of exposure to ACE inhibitors during the second trimester of pregnancy, monitoring of renal function and skull by ultrasound is recommended. Infants whose mothers have taken ACE inhibitors should be closely monitored for hypotension.

Breast-feeding: Because no information is available regarding the use of lisinopril during breast-feeding, lisinopril is not recommended and alternative treatments with better established safety profiles during breast-feeding are preferable, especially while nursing a newborn or preterm infant.

Ability to influence reaction speed when driving vehicles or other mechanisms

When driving vehicles or using other mechanisms, it should be taken into account that dizziness or fatigue may occasionally occur.

Method of administration and doses

Lisinopril should be taken orally once daily. As with other once-daily medications, lisinopril should be taken at approximately the same time each day. Food does not affect the absorption of lisinopril tablets. The dose should be individualized based on the patient's clinical status and blood pressure.

Arterial hypertension

Lisinopril can be used both as monotherapy and in combination with other classes of antihypertensive drugs.

Starting dose

The recommended starting dose for patients with hypertension is usually 10 mg. Patients with a very active RAAS (in particular, renovascular hypertension, increased salt (sodium chloride) excretion and/or decreased interstitial fluid volume, heart failure or severe arterial hypertension) may experience an excessive decrease in blood pressure after taking the initial dose. For such patients, the recommended starting dose is 2.5-5 mg, and treatment should be initiated under close medical supervision. A reduced starting dose is also recommended in the presence of renal insufficiency (see table below).

The usual effective maintenance dose is 20 mg once daily. If this dose does not provide sufficient therapeutic effect within 2-4 weeks, it can be increased. The maximum dose used in long-term controlled clinical trials was 80 mg daily.

Patients taking diuretics

Symptomatic hypotension may occur after initiation of lisinopril therapy. This is more likely in patients receiving diuretics during treatment with lisinopril. Therefore, caution is advised in such patients due to the potential for increased salt (sodium chloride) excretion and/or volume depletion. If possible, diuretic therapy should be discontinued 2-3 days before initiating lisinopril therapy. In hypertensive patients who cannot discontinue diuretic therapy, lisinopril therapy should be initiated with an initial dose of 5 mg. Renal function and serum potassium should be monitored. Subsequent doses of lisinopril should be titrated according to blood pressure response. Diuretic therapy may be resumed if necessary.

Dosage selection for patients with renal impairment

Dosage for patients with renal impairment should be based on creatinine clearance as shown in the table below.

Dosage selection for patients with renal impairment

* Dosage and/or frequency of administration should be calculated based on blood pressure readings.

The dose can be gradually increased until blood pressure control is achieved or to a maximum dose of 40 mg per day.

Use in children with arterial hypertension aged 6 to 16 years

The recommended starting dose is 2.5 mg/day for patients weighing 20 to <50 kg and 5 mg/day for patients weighing ≥50 kg. The dose should be adjusted individually to a maximum of 20 mg/day for patients weighing 20 to <50 kg and 40 mg/day for patients weighing ≥50 kg. Doses greater than 0.61 mg/kg (or greater than 40 mg) have not been studied in children.

Children with reduced renal function should be given a lower initial dose or an increased dosing interval.

Heart failure

Patients with heart failure should receive lisinopril as an adjunct to diuretics, digitalis, or β-blockers. Lisinopril therapy can be initiated at a dose of 2.5 mg once daily and should be monitored to determine the initial effect on blood pressure.

The dose of lisinopril should be increased:

increasing the dose by no more than 10 mg;

intervals between dose increases should be at least 2 weeks;

to the highest dose tolerated by the patient – up to a maximum of 35 mg once daily.

Dosage selection should be based on the clinical response of the individual patient. Patients at high risk of symptomatic hypotension, such as patients with increased salt (sodium chloride) excretion with or without hyponatremia, patients with hypovolemia, or patients who have undergone intensive diuretic therapy, should have these conditions corrected, if possible, before initiating therapy with lisinopril. Renal function and serum potassium should be monitored.

Acute myocardial infarction

Patients should receive standard recommended therapy, such as thrombolytics, acetylsalicylic acid, and β-blockers, as needed. Intravenous or transdermal nitroglycerin may be used concomitantly with lisinopril.

Initial dose (first 3 days after heart attack)

Lisinopril treatment can be started within 24 hours of symptom onset. Treatment should not be initiated if systolic blood pressure is less than 100 mm Hg. The initial dose of lisinopril is 5 mg orally, followed by 5 mg after 24 hours, 10 mg after 48 hours, and then 10 mg once daily. Patients with low systolic blood pressure (≤120 mm Hg) should be given a lower dose of 2.5 mg orally at the start of treatment or for the first 3 days after infarction.

In case of renal insufficiency (creatinine clearance below 80 ml/min), the initial dose of lisinopril should be selected according to the patient's creatinine clearance (see table above).

Maintenance dose

The maintenance dose is 10 mg once daily. In the event of hypotension (systolic blood pressure ≤100 mmHg), the maintenance dose may be 5 mg daily with a temporary reduction to 2.5 mg if necessary. In the event of prolonged hypotension (systolic blood pressure <90 mmHg for more than 1 hour), lisinopril should be discontinued.

Treatment should last 6 weeks, after which it should be repeated.