Instructions Enalapril film-coated tablets 20 mg blister No. 20
Composition
active ingredient: enalapril;
1 tablet contains enalapril maleate in terms of 100% substance 10 mg or 20 mg;
excipients: sodium bicarbonate; lactose monohydrate; corn starch; pregelatinized starch; magnesium stearate.
Dosage form
Pills.
Main physicochemical properties: round tablets, with a biconvex surface, white or almost white in color, with an imprint of "10" (for a dosage of 10 mg) or with an imprint of "20" (for a dosage of 20 mg) on one side.
Pharmacotherapeutic group
Angiotensin-converting enzyme inhibitors, monocomponent. Enalapril. ATC code C09A A02.
Pharmacological properties
Pharmacodynamics.
Enalapril is the maleic acid salt of enalapril, a derivative of two amino acids, L-alanine and L-proline.
Mechanism of action
Angiotensin-converting enzyme (ACE) is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the pressor substance angiotensin II. After absorption, enalapril is hydrolyzed to enalaprilat, which inhibits ACE. Inhibition of ACE results in a decrease in plasma angiotensin II levels, which leads to an increase in plasma renin activity (due to inhibition of the negative feedback between angiotensin II activity and renin release) and a decrease in aldosterone secretion.
ACE is identical to kininase II. Thus, enalapril may also block the cleavage of bradykinin, a potent vasodepressor peptide. However, the significance of this phenomenon for the therapeutic effect of the drug remains unclear.
The mechanism by which enalapril lowers blood pressure is primarily associated with inhibition of the renin-angiotensin-aldosterone system. Enalapril may have an antihypertensive effect even in patients with low-renin hypertension.
The use of enalapril in the treatment of hypertension causes a decrease in blood pressure in patients in the horizontal and vertical positions without a significant increase in heart rate.
Symptomatic postural hypotension occurs infrequently. In some patients, achieving optimal blood pressure control may require several weeks of therapy. Abrupt withdrawal of enalapril has not been associated with a rapid increase in blood pressure.
Effective inhibition of ACE activity is usually achieved 2-4 hours after oral administration of a single dose of enalapril. The onset of antihypertensive activity is usually observed after 1 hour, and the peak reduction in blood pressure is achieved 4-6 hours after administration. The duration of the effect is dose-dependent. However, at recommended doses, the antihypertensive and hemodynamic effects were maintained for at least 24 hours.
In hemodynamic studies in patients with essential hypertension, the reduction in blood pressure was usually accompanied by a decrease in peripheral arterial resistance with an increase in cardiac output and little or no increase in heart rate. Renal blood flow usually increases after administration of Enalapril; glomerular filtration rate is not affected. There is no evidence of sodium or water retention. However, in patients with low baseline glomerular filtration rate, this rate is usually increased.
In short-term clinical studies in patients with and without diabetes mellitus and renal disease, reductions in albuminuria, urinary IgG excretion, and total urinary protein were observed after enalapril administration.
When used concomitantly with thiazide diuretics, the hypotensive effects of Enalapril are at least additive. Enalapril may reduce or prevent the development of thiazide-induced hypokalemia.
In patients with heart failure receiving cardiac glycosides and diuretics, oral or injectable enalapril was associated with a decrease in peripheral resistance and blood pressure. Cardiac output increased and heart rate (usually increased in patients with heart failure) decreased. Pulmonary end-capillary pressure also decreased. Exercise tolerance improved and the severity of heart failure, as assessed by NYHA (New York Heart Association) criteria, decreased. These effects were maintained during long-term treatment.
A multicenter, randomized, double-blind, placebo-controlled trial (SOLVD Warning) was conducted in a population with asymptomatic left ventricular dysfunction (left ventricular ejection fraction <35%). 4228 patients were randomized to receive placebo (n = 2117) or enalapril (n = 2111). In the placebo group, 818 patients developed heart failure or died (38.6%) compared with 630 in the enalapril group (29.8%) (risk reduction 29%, 95% CI, 21-36%, p < 0.001). 518 patients in the placebo group (24.5%) and 434 in the enalapril group (20.6%) died or were hospitalized due to new or worsening heart failure (20% risk reduction, 95% CI; 9-30%, p < 0.001). The multicenter, randomized, double-blind, placebo-controlled trial (SOLVD Treatment) studied a population with symptomatic congestive heart failure associated with systolic dysfunction (ejection fraction < 35%). 2569 patients receiving conventional heart failure treatment were randomized to placebo (n = 1284) or enalapril (n = 1285). There were 510 deaths in the placebo group (39.7%) compared with 452 in the enalapril group (35.2%) (risk reduction 16%, 95% CI, 5-26%, p = 0.0036). There were 461 cardiovascular deaths in the placebo group compared with 399 in the enalapril group (risk reduction 18%, 95% CI, 6-28%, p < 0.002), mainly due to a reduction in deaths from progressive heart failure (251 in the placebo group and 209 in the enalapril group, risk reduction 22%, 95% CI, 6-35%). Fewer patients died or were hospitalized for worsening heart failure (736 in the placebo group and 613 in the enalapril group, risk reduction, 26%, 95% CI 18-34%, p < 0.0001). Overall, in the SOLVD trial, in patients with left ventricular dysfunction, enalapril reduced the risk of myocardial infarction by 23% (95% CI 11-34%, p < 0.001) and reduced the risk of hospitalization for unstable angina by 20% (95% CI, 9-29%, p < 0.001).
Clinical pharmacology in children
Experience in children aged 6 years and older with hypertension is limited. In a clinical study involving 110 hypertensive children aged 6 to 16 years with body weight ≥20 kg and glomerular filtration rate >30 ml/min/1.73 m2, patients weighing <50 kg received 0.625; 2.5 or 20 mg of enalapril per day and patients weighing ≥50 kg received 1.25; 5 or 40 mg of enalapril per day. Enalapril administered once daily reduced the lower limit of blood pressure in a dose-dependent manner. The dose-dependent antihypertensive effect of enalapril was similar in all subgroups (age, Tanner stage, gender, race). However, the lowest doses tested, 0.625 mg and 1.25 mg, corresponding to an average of 0.02 mg/kg once daily, did not provide a sustained antihypertensive effect. The highest dose tested was 0.58 mg/kg (up to 40 mg) once daily. The side effect profile in children is similar to that in adults.
Pharmacokinetics.
Absorption
After oral administration, enalapril is rapidly absorbed, with peak serum concentrations occurring within 1 hour of oral administration. The extent of absorption of enalapril from tablets is approximately 60%. The presence of food in the gastrointestinal tract does not affect the absorption of oral enalapril. Following absorption, oral enalapril is rapidly and extensively hydrolyzed to enalaprilat, a potent ACE inhibitor. Peak serum concentrations of enalaprilat occur approximately 4 hours after an oral dose of enalapril.
The effective elimination half-life (T½) of enalaprilat after multiple oral administration is 11 hours.
Distribution
Within the entire therapeutic concentration range, no more than 60% of enalaprilat binds to serum proteins.
Biotransformation
With the exception of conversion to enalaprilat, there is no further evidence of significant metabolism of enalapril.
Breeding
Enalaprilat is excreted primarily by the kidneys. The major components in the urine are enalaprilat, which accounts for approximately 40% of the dose, and unchanged enalapril (approximately 20%).
Kidney dysfunction
In patients with renal insufficiency, exposure to enalapril and enalaprilat is increased. In patients with mild to moderate renal impairment (creatinine clearance 40-60 ml/min), the AUC of enalaprilat at steady state was approximately 2-fold higher than in patients with normal renal function after administration of 5 mg once daily. In severe renal insufficiency (creatinine clearance ≤ 30 ml/min), the AUC increased approximately 8-fold. After multiple administration of enalapril maleate, the effective half-life of enalaprilat is prolonged and the time to reach steady state is increased (see section 4.2).
Enalaprilat can be removed from the general circulation by hemodialysis. The dialysis clearance of enalaprilat is 62 ml/min.
Indication
Treatment of arterial hypertension;
treatment of clinically pronounced heart failure;
prevention of clinically significant heart failure in patients with asymptomatic left ventricular dysfunction (ejection fraction ≤ 35%).
Contraindication
Hypersensitivity to enalapril, to any of the excipients or to any other ACE inhibitor.
Hereditary or idiopathic angioedema.
Pregnancy or planning to become pregnant (see section "Use during pregnancy or breastfeeding").
Enalapril should not be used with aliskiren-containing drugs in patients with diabetes mellitus or renal impairment (GFR < 60 ml/min/1.73 m2).
Enalapril should not be used in combination with sacubitril/valsartan, as this combination increases the risk of angioedema. Enalapril should not be used within 36 hours of switching from/to sacubitril/valsartan, a drug containing a neprilysin inhibitor (see sections 4.4 and 4.5).
Interaction with other medicinal products and other types of interactions
Hypotensive therapy
Concomitant use of antihypertensive drugs may enhance the hypotensive effect of enalapril. Concomitant use with nitroglycerin, other nitrates or other vasodilators may further reduce blood pressure.
Potassium-sparing diuretics, potassium supplements, or other drugs that may increase serum potassium levels
ACE inhibitors increase the potassium loss caused by diuretics. The use of potassium-sparing diuretics (e.g. spironolactone, eplerenone, triamterene or amiloride), dietary supplements, salt substitutes containing potassium, or other drugs that may increase serum potassium levels (e.g. drugs containing trimethoprim), especially in patients with impaired renal function, may lead to a significant increase in serum potassium levels. If concomitant use of enalapril with the above agents is considered appropriate, they should be used with caution and serum potassium should be monitored regularly (see section 4.4).
Diuretics (thiazide or loop diuretics)
Previous treatment with high doses of diuretics may lead to volume depletion and an increased risk of hypotension at the start of enalapril therapy (see section 4.4). Hypotensive effects may be reduced by discontinuing the diuretic, increasing salt intake, or initiating therapy with a low dose of enalapril.
Antidiabetic drugs
Epidemiological studies have shown that the concomitant use of ACE inhibitors and antidiabetic agents (insulin, oral hypoglycemic agents) may lead to a decrease in blood glucose levels with a risk of hypoglycemia. This phenomenon is most likely during the first weeks of concomitant administration and in patients with renal insufficiency (see sections "Special warnings and precautions for use", "Adverse reactions").
Serum lithium
Reversible increases in serum lithium levels and toxicity have been reported with concomitant use of ACE inhibitors and lithium. Concomitant use of ACE inhibitors and thiazide diuretics may further increase serum lithium levels and increase the risk of lithium toxicity. The use of enalapril with lithium is not recommended, but if the combination proves necessary for the patient, careful monitoring of serum lithium levels should be performed (see section 4.4).
Tricyclic antidepressants/neuroleptics/anesthetics/hypnotics
Concomitant administration of certain anesthetics, tricyclic antidepressants and neuroleptics with ACE inhibitors may lead to an additional decrease in blood pressure (see section "Special warnings and precautions for use").
Nonsteroidal anti-inflammatory drugs, including selective cyclooxygenase-2 inhibitors
Non-steroidal anti-inflammatory drugs (NSAIDs), including selective cyclooxygenase-2 inhibitors (COX-2 inhibitors), may reduce the effect of diuretics and other antihypertensive drugs. Therefore, the hypotensive effect of angiotensin II receptor antagonists or ACE inhibitors may be attenuated by non-steroidal anti-inflammatory drugs, including selective COX-2 inhibitors.
Concomitant use of NSAIDs, including COX-2 inhibitors, and angiotensin II receptor antagonists or ACE inhibitors has an additive effect on increases in serum potassium and may lead to deterioration of renal function. These effects are usually reversible.
Acute renal failure may occur rarely, especially in some patients with impaired renal function (e.g. elderly patients or patients with reduced circulating blood volume, including those taking diuretics). Therefore, this combination should be administered with caution to patients with impaired renal function. Patients should be adequately hydrated and renal function should be closely monitored at the beginning of concomitant therapy and periodically during such treatment.
Dual blockade (e.g., adding an ACE inhibitor to an angiotensin II receptor antagonist) should be limited to isolated cases with close monitoring of blood pressure, renal function, and electrolytes. In patients with established atherosclerotic vascular disease, heart failure, or diabetes with end-organ damage, dual blockade of the renin-angiotensin-aldosterone system has been reported in several studies to be associated with a higher incidence of hypotension, syncope, hyperkalemia, and worsening renal function (including acute renal failure) compared with the use of a single agent acting on the renin-angiotensin-aldosterone system.
Enalapril with aliskiren should not be used in patients with diabetes mellitus or renal impairment (GFR < 60 ml/min/1.73 m2) (see sections “Contraindications” or “Special warnings and precautions for use”).
Gold preparations
Nitritoid reactions (symptoms including facial swelling, nausea, vomiting and hypotension) have been reported rarely in patients treated with injectable gold (sodium aurothiomalate) concomitantly with an ACE inhibitor, including enalapril.
Medicines that increase the risk of angioedema
Concomitant use of ACE inhibitors with sacubitril/valsartan is contraindicated as this combination increases the risk of angioedema (see sections 4.3 and 4.4).
Concomitant use of ACE inhibitors with racecadotril, mTOR inhibitors (such as sirolimus, everolimus, temsirolimus) and vildagliptin may increase the risk of angioedema (see section 4.4).
Sympathomimetics
Sympathomimetics may reduce the antihypertensive effects of ACE inhibitors.
Alcohol
Alcohol enhances the hypotensive effect of ACE inhibitors.
Acetylsalicylic acid, thrombolytics and β-blockers
Enalapril can be safely used concomitantly with acetylsalicylic acid (in cardiological doses), thrombolytics, and β-blockers.
Application features
Symptomatic hypotension
Symptomatic hypotension is rarely observed in patients with uncomplicated hypertension. In patients with hypertension receiving enalapril, symptomatic hypotension develops more often in cases of hypovolemia, which occurs, for example, as a result of diuretic therapy, salt restriction, in patients undergoing hemodialysis, as well as in patients with diarrhea or vomiting (see sections "Interaction with other medicinal products and other forms of interaction" and "Adverse reactions"). Symptomatic hypotension has also been observed in patients with heart failure, which was accompanied or not accompanied by renal failure. Symptomatic hypotension developed more often in patients with more severe forms of heart failure, who were treated with higher doses of loop diuretics, with hyponatremia or impaired renal function. In such patients, treatment with enalapril should be initiated under medical supervision. When changing the dose of enalapril and/or diuretic, special care should be taken. Similarly, patients with ischemic heart disease and cerebrovascular disease should be monitored, in whom an excessive decrease in blood pressure could lead to myocardial infarction or stroke.
If hypotension develops, the patient should be placed in a horizontal position and, if necessary, intravenous saline should be administered. Transient hypotension while taking enalapril is not a contraindication for further administration, which can usually be continued without complications after normalization of blood pressure by restoring fluid volume.
In some patients with heart failure with normal or low blood pressure, enalapril may further reduce blood pressure. This is an expected response to the drug and is not usually a reason for discontinuation of treatment. If hypotension becomes symptomatic, it may be necessary to reduce the dose and/or discontinue the diuretic and/or enalapril.
Aortic or mitral stenosis/hypertrophic cardiomyopathy
As with all vasodilators, ACE inhibitors should be used with caution in patients with left ventricular outflow tract obstruction and outflow tract obstruction; they should be avoided in cases of cardiogenic shock and hemodynamically significant obstruction.
Kidney dysfunction
In patients with renal impairment (creatinine clearance < 80 ml/min), the initial dose of enalapril should be titrated according to creatinine clearance (see section 4.2) and then adjusted according to response to treatment. Regular monitoring of potassium and creatinine levels is standard medical practice in such patients.
In some hypertensive patients with no known pre-existing renal disease, enalapril in combination with diuretics has caused, usually minor and transient, increases in blood urea and serum creatinine. In such cases, dose reduction and/or discontinuation of the diuretic may be necessary. This situation increases the likelihood of renal artery stenosis (see section 4.4: Renovascular hypertension).
Renovascular hypertension
There is an increased risk of hypotension and renal failure when patients with bilateral renal artery stenosis or stenosis of the artery to a single functioning kidney are treated with ACE inhibitors. Loss of renal function may occur with minimal changes in serum creatinine. In such patients, treatment should be initiated at low doses under close medical supervision with careful titration and monitoring of renal function.
Kidney transplantation
There is no experience with the use of Enalapril in patients who have recently undergone kidney transplantation. Therefore, treatment with Enalapril is not recommended in these patients. Hepatic failure
Rarely, ACE inhibitors have been associated with a syndrome that begins with cholestatic jaundice or hepatitis and progresses to fulminant hepatic necrosis and (sometimes) death. The mechanism of this syndrome remains unclear. Patients taking ACE inhibitors who develop jaundice or marked elevations of liver enzymes should discontinue the ACE inhibitor and receive appropriate medical attention.
Neutropenia/agranulocytosis
Neutropenia/agranulocytosis, thrombocytopenia and anaemia have been reported in patients receiving ACE inhibitors. Neutropenia has been reported rarely in patients with normal renal function and in the absence of other complicating factors. Enalapril should be used with great caution in patients with collagen vascular disease who are receiving immunosuppressive therapy, treatment with allopurinol or procainamide, or a combination of these complicating factors, especially if there is pre-existing renal impairment. Some of these patients have developed serious infections, sometimes unresponsive to intensive antibiotic therapy. Periodic monitoring of white blood cell counts is recommended when enalapril is prescribed to such patients, and patients should be advised to report any signs of infection.
Hypersensitivity/angioedema
With the use of ACE inhibitors, including the drug Enalapril, isolated cases of angioedema of the face, extremities, lips, tongue, glottis and/or larynx have been described, which occurred at different periods of treatment. In these cases, treatment with the drug Enalapril should be discontinued immediately and the patient should be monitored closely to ensure complete resolution of symptoms. Only after this monitoring should be discontinued. Even when swelling of the tongue alone occurs without respiratory distress, patients may require prolonged monitoring, since treatment with antihistamines and corticosteroids may be insufficient.
Very rarely, deaths have been reported due to angioedema of the larynx or tongue. If the swelling is localized to the tongue, glottis or larynx, especially in patients with a history of airway surgery, airway obstruction may occur. When there is involvement of the tongue, pharynx or larynx and this may cause airway obstruction, appropriate therapy should be initiated immediately, which may include subcutaneous administration of epinephrine 1:1000 (0.3-0.5 ml) and/or measures to maintain a patent airway.
Angioedema was more common in black patients taking ACE inhibitors compared to patients of other races.
Patients with a history of angioedema unrelated to ACE inhibitor therapy may be at increased risk of developing angioedema while receiving an ACE inhibitor (see also section 4.3).
Concomitant use of ACE inhibitors with racecadotril, mTOR inhibitors (such as sirolimus, everolimus, temsirolimus) and vildagliptin may increase the risk of angioedema (e.g. swelling of the airways or tongue with or without respiratory distress) (see section 4.3). Caution should be exercised when administering racecadotril, mTOR inhibitors (such as sirolimus, everolimus, temsirolimus) and vildagliptin to patients already taking ACE inhibitors. Concomitant use of enalapril with sacubitril/valsartan is contraindicated due to an increased risk of angioedema (see section 4.3). Sacubitril/valsartan should not be initiated until 36 hours after the last dose of enalapril. If sacubitril/valsartan treatment is discontinued, enalapril therapy should not be initiated until 36 hours after the last dose of sacubitril/valsartan (see sections 4.3 and 4.5).
Rarely, patients receiving ACE inhibitors during hymenoptera venom allergen desensitization have developed anaphylactoid reactions, which may be life-threatening. Such reactions can be avoided by temporarily stopping the ACE inhibitor before the desensitization begins.
Anaphylactoid reactions during low-density lipoprotein apheresis
Rarely, patients receiving ACE inhibitors during low-density lipoprotein apheresis with dextran sulfate have experienced life-threatening anaphylactoid reactions. These reactions can be avoided by temporarily stopping ACE inhibitors before each apheresis.
Patients on hemodialysis
Anaphylactoid reactions have occasionally been reported in patients dialysed with high-flux membranes (e.g. AN 69®) and concomitantly treated with an ACE inhibitor. Therefore, consideration should be given to using a different type of dialysis membrane or a different class of antihypertensive agent in such patients.
Hypoglycemia
Diabetic patients taking oral antidiabetic agents or insulin and initiating therapy with an ACE inhibitor should be advised to monitor blood sugar levels closely, especially during the first few months of concomitant use (see section 4.5).
Cough
Cough has been reported with ACE inhibitors. The cough is usually non-productive and persistent and resolves after discontinuation of the drug. Cough due to ACE inhibitor therapy should be considered in the differential diagnosis of cough.
Performing surgeries/anesthesia
During major surgery or anesthesia with drugs that cause hypotension, enalapril blocks the formation of angiotensin II secondary to compensatory renin release. If hypotension develops, which can be explained by these mechanisms of interaction, it is corrected by increasing the volume of fluid.
Hyperkalemia
During treatment with ACE inhibitors, including enalapril, increases in serum potassium have been observed in some patients. The risk of hyperkalemia is increased in patients with renal insufficiency, with impaired renal function, age > 70 years, with diabetes mellitus, with transient conditions, in particular dehydration, acute cardiac decompensation, metabolic acidosis and concomitant use of potassium-sparing diuretics (e.g. spironolactone, eplerenone, triamterene or amiloride), food supplements, salt substitutes containing potassium, or other drugs associated with increases in serum potassium (e.g. heparin, drugs containing trimethoprim). The use of potassium supplements, potassium-sparing diuretics, salt substitutes containing potassium, or other drugs that may increase serum potassium levels, particularly in patients with impaired renal function, may lead to significant increases in serum potassium levels. Hyperkalemia may cause serious, sometimes fatal, arrhythmias. If concomitant use of enalapril and any of the above-mentioned drugs is considered necessary, they should be used with caution and with regular monitoring of serum potassium (see section 4.5).
Lithium
The combination of lithium and enalapril is generally not recommended (see section “Interaction with other medicinal products and other types of interactions”).
Concomitant therapy with an ACE inhibitor and angiotensin receptor antagonist
There is evidence that the concomitant use of ACE inhibitors, angiotensin II receptor blockers or aliskiren increases the risk of hypotension, hyperkalaemia and decreased renal function (including acute renal failure). Therefore, dual blockade of the RAAS through the combined use of ACE inhibitors, angiotensin II receptor blockers or aliskiren is not recommended (see sections 4.5 and 5.1).
If dual blockade is necessary, therapy should be under specialist supervision and with regular monitoring of renal function, electrolytes and blood pressure. ACE inhibitors and angiotensin II receptor blockers should not be used concomitantly in patients with diabetic nephropathy (see section 4.5).
Lactose
Enalapril contains lactose and therefore patients with rare hereditary conditions of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicine.
Children
Enalapril is not recommended for use in neonates and children with glomerular filtration rate < 30 ml/min/1.73 m2 due to lack of data (see section "Method of administration and dosage").
Pregnancy
The medicine should not be used by pregnant women or women planning to become pregnant.
When pregnancy is diagnosed, treatment with ACE inhibitors should be stopped immediately, and, if possible, alternative therapy should be started (see sections 4.3 and 4.4).
Ethnic features
Like other ACE inhibitors, enalapril is less effective in lowering blood pressure in black patients than in non-blacks, possibly because low-renin states are more common in this population of hypertensive patients.
Sodium content
Each tablet of the drug ENALAPRIL, tablets of 10 mg contains 1.4 mg per 1 tablet of sodium.
Each tablet of the drug ENALAPRIL, tablets of 20 mg contains 2.8 mg per 1 tablet of sodium.
Use during pregnancy or breastfeeding
Pregnancy
The drug should not be used by pregnant women or women planning to become pregnant. If pregnancy is confirmed during treatment with this drug, its use should be discontinued immediately and replaced with another drug approved for use in pregnant women.
ACE inhibitors, when used during the second and third trimesters of pregnancy, may cause fetotoxicity (decreased renal function, oligohydramnios, skull ossification retardation) or neonatal toxicity (renal failure, hypotension, hyperkalemia).
If ACE inhibitors were taken during the second trimester of pregnancy, ultrasound examination of the kidneys and skull is recommended.
Newborns whose mothers have taken ACE inhibitors should be closely observed for hypotension (see sections "Contraindications", "Special warnings and precautions for use").
Breastfeeding period
Limited pharmacokinetic data indicate very low drug concentrations in breast milk (see section 5.2). Although these concentrations are considered clinically insignificant, the use of Enalapril is not recommended during breastfeeding in premature infants and infants in the first few weeks after birth because of the hypothetical risk of cardiovascular and renal effects and because of insufficient experience in this regard. In older infants, the use of Enalapril during breastfeeding may be considered if treatment is necessary for the mother and the infant is observed for any adverse effects.
Ability to influence reaction speed when driving vehicles or other mechanisms
When driving vehicles or using other mechanisms, the possible development of dizziness or increased fatigue should be taken into account.
Method of administration and doses
Food intake does not affect the absorption of Enalapril tablets. Since the tablet is not divided, if the drug is prescribed in a dose of less than 10 mg, enalapril preparations with the possibility of such a dosage should be used.
The dosage should be individualized according to each patient's condition (see section "Special warnings and precautions for use") and blood pressure response.
Children
There is limited experience in conducting clinical trials of enalapril in the treatment of arterial hypertension in children (see sections "Special instructions for use", "Pharmacological properties").
Arterial hypertension
The dose of enalapril ranges from an initial 5 mg to a maximum of 20 mg depending on the degree of hypertension and the patient's condition (see below). Enalapril is taken once a day. In mild hypertension, the recommended initial dose of enalapril is 5-10 mg.
In patients with a strongly activated renin-angiotensin-aldosterone system (e.g. renovascular hypertension, salt and/or fluid imbalance, decompensated cardiac function or severe hypertension), an excessive fall in blood pressure may occur after the initial dose. In such patients, a starting dose of 5 mg or less of enalapril is recommended, and initiation of treatment should be under medical supervision.
Previous treatment with high doses of diuretics may lead to fluid depletion and a risk of hypotension at the start of enalapril therapy. In such patients, a starting dose of 5 mg or less of enalapril is recommended. Diuretics should be discontinued if possible.
