Hypertensive patients often think about choosing between Enap or Enalapril, because These drugs are most popular among those who suffer from high blood pressure. But answering this question is difficult even for an experienced doctor. Enap or Enalapril - what to choose? The choice of medication depends on many factors, including: depending on the individual characteristics of the patient’s body.
Enap and Enalapril are drugs that are used at the risk of developing coronary ischemia, myocardial infarction and unstable angina.
Compound similarities
The active substance in the drugs is the same - enalapril. Once in the human body, the drug begins to gradually reduce blood pressure - diastolic and systolic. Enalapril also acts on the left ventricle, reducing its hypertrophy, and on the coronary vessels, improving blood flow in them. Both drugs dilate blood vessels.
The onset of action of Enap and Enalapril occurs 6 hours after administration and lasts for about 24 hours. Full pharmacological properties are achieved after 2-3 weeks, because the active substance must accumulate in the body.
The main indications for the use of drugs are arterial hypertension and heart failure in a chronic form.
Medicines are used both in monotherapy and together with other medicines included in combination therapy.
Both drugs are prescribed to patients with impaired left ventricular function as a preventive measure for heart failure. For the same purpose, medications are used at the risk of developing coronary ischemia, myocardial infarction and unstable angina.
Enalapril acts on the left ventricle, reducing its hypertrophy, and on the coronary vessels, improving blood flow in them.
Both medications are available in the form of oral tablets in different dosages - 5, 10 and 20 mg. Enap is produced in another dosage - 2.5 mg.
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“Blood pressure pill”: how it works
There is probably no other group of drugs that contains so many drugs. In addition, most of the drugs have a good dozen analogues, which wreaks havoc among antihypertensive drugs, beyond the control of the common mind. But the mind of a good cardiologist and professional pharmacist can comprehend not such a medicinal mess.
"A lot" does not mean "good"
The variety of antihypertensive drugs is largely due to the fact that today, along with modern ones, the drugs that were used to treat our grandmothers continue to be used. Fortunately, they are used quite rarely, but, nevertheless, they bring confusion to the treatment of hypertension. In addition, it should be borne in mind that in Russian pharmacies you can still easily buy any antihypertensive drug without a doctor’s prescription. This means that self-medication of hypertension, which cannot be called anything other than “self-torture,” continues to flourish and bear bitter fruits.
But is there really a big difference in how and with what to reduce the pressure: the main thing is that the tonometer shows the norm or numbers close to it? Of course there is, and here's why.
The fact is that many antihypertensive drugs lead to a sharp decrease in blood pressure. This does not have the best effect on the patient’s well-being, but there are much more serious consequences. If you constantly take these medications, the elasticity of the vascular wall, which regularly tenses and relaxes, decreases. As a result, heart and vascular diseases develop (or rapidly progress) - the most dangerous complications of hypertension.
Drugs that have a sharp vasodilating effect include adelfan and clonidine, beloved by many generations of hypertensive patients. Cheap bendazole and its combination with papaverine, metamizole and phenobarbital (andipal) have a less powerful effect on blood vessels. These drugs reduce cardiac output and, with long-term use, worsen ECG readings.
But herbal antihypertensive drugs, for example raunatin, should not be taken seriously at all: a more effective and safe alternative has long been found for drugs whose age has already exceeded the sixth decade.
Six groups
I have not listed all the antihypertensive drugs that continue to be produced and used, despite serious disadvantages and side effects. There are so many of them that I am afraid to completely confuse the reader. It is much easier to name those drugs that are recognized throughout the world as the drugs of choice for the treatment of hypertension. They belong to six pharmacological groups:
- Diuretics or diuretics (hydrochlorothiazide, indapamide).
- Beta blockers (atenolol, betaxolol, metoprolol, bisoprolol, nebivolol, etc.).
- Calcium channel blockers (verapamil, amlodipine, nifedipine, felodipine, etc.).
- ACE inhibitors (captopril, enalapril, lisinopril, ramipril, fosinopril, etc.).
- Angiotensin II receptor blockers (losartan, valsartan, candesartan, irbesartan, telmisartan, etc.).
- Alpha adrenergic blockers (doxazosin, urapidil, etc.).
The mechanism of action of each of these groups is different and quite complex:
- Diuretics
(diuretics) increase the excretion of salts and water from the body. As a result, the sodium content in the vessel wall is reduced, which prevents vasoconstriction and increased blood pressure. - Beta blockers
work by blocking so-called β1-adrenergic receptors located in the heart. This leads to a decrease in the frequency and strength of heart contractions and a decrease in blood pressure. - The action of calcium channel blockers
is based on the ability to block the passage of calcium ions into the cell, which reduces vascular tone, expands their lumen and improves blood circulation in them. - ACE inhibitors
block the angiotensin-converting enzyme, which converts angiotensin I to angiotensin II, which has a powerful vasoconstrictor effect. - Angiotensin II receptor blockers
act on the same mechanism as ACE inhibitors, but at a later stage. - Alpha blockers
lower blood pressure, reducing vasospasm.
By the way, there is practically no difference in efficiency between them. Among a number of drugs, nifedipine and captopril stand out, which can be taken as first aid to quickly reduce blood pressure. In addition, diuretics, calcium channel blockers and ACE inhibitors definitely reduce the risk of developing cardiovascular accidents, the likelihood of which increases significantly with hypertension.
Contraindications
Contraindications to the use of Enalapril and Enap:
- intolerance to the active or auxiliary components included in the tablets;
- tendency to allergic reactions, especially to the development of angioedema;
- porphyria (pigment metabolism disorder);
- stenosis of renal vessels;
- period of pregnancy and lactation.
Despite the same contraindications, it is recommended to take the drug prescribed by the doctor. The specialist will take into account the individual characteristics of the body and the process of development of the disease, and select the most suitable remedy.
What kind of medicines are these?
Enap and Enalapril are the most famous representatives of ACE inhibitors, the action of which is aimed at suppressing the activity of angiotensin II (a hormone that is produced by the renin-angiotensin system of the kidneys and has a vasoconstrictor effect).
Enap tablets
Suppression of the biologically active substance promotes the expansion of vascular structures at all levels, leading to a gradual decrease in blood pressure.
At the same time, ACE inhibitors do not potentiate an increase in myocardial contractility, which makes their use possible for arterial hypertension associated with heart failure.
Indications for the use of drugs from the group of ACE inhibitors are:
- high blood pressure;
- angina pectoris during exacerbation;
- arterial hypertension due to heart failure;
- congestive heart failure;
- asymptomatic left ventricular dysfunction;
- cardiac ischemia;
- prevention of acute myocardial infarction and severe cardiac arrhythmias.
Among the most pronounced positive effects of the drugs of the Enalapril and Enap series, the following should be highlighted:
- action aimed at dilating blood vessels;
- absence of influences causing changes in heart rhythm;
- Can be used at any age;
- improvement of renal blood flow, potentiating the functional activity of the kidneys.
Enap and Enalapril begin to act within an hour after taking the medications.
Their maximum effect is observed after 4 hours of stay in the human body, and the activity itself continues throughout the day.
Due to the high characteristics of ACE inhibitors, to maintain blood pressure at the proper level, the patient will need to take only 1-2 tablets per day.
The drugs are available in different dosages (from 2.5 to 20 mg), allowing their quantity to be adapted to the individual needs of each individual patient.
How to take Enap and Enalapril drugs
The tablets are taken orally, regardless of meals. It is advisable to do this at the same time of day. The medicine should be taken with a small amount of water.
The dosage and duration of therapy is selected by the doctor individually for each patient, taking into account the clinical picture of the disease and other factors.
The main indications for the use of Enap are arterial hypertension and heart failure in a chronic form.
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To summarize, we can confidently say that Enalapril and Enap are prominent representatives of effective antihypertensive drugs that gently lower blood pressure, normalize cardiac activity and prevent the development of heart failure.
It is important to remember that these drugs should not be taken without consulting a specialist who will prescribe the patient adequate dosages of the medication, taking into account the degree of complexity of his illness, the presence of contraindications to use and complications from other organs.
Reviews from doctors
Ekaterina Gromova, general practitioner, Nizhny Novgorod: “I prescribe Enap for hypertension and ischemia as a prevention of heart attack. I recommend enalapril for unstable angina in complex treatment. Patients do not always follow doctor's instructions. Arriving at the pharmacy, they buy the cheaper drug Enalapril. There are almost no complaints about side effects. Both drugs are well tolerated if the dosage is not violated.”
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Svetlana Kartashova, general practitioner, Rostov-on-Don: “I consider Enap a more effective remedy than Enalapril, but many patients prefer inexpensive drugs. I prescribe medication for grade 1-2 hypertension. If the disease is severe, I prescribe several medications. One of the side effects I can mention is a dry cough. In this case, I reduce the dosage or select another drug.”
Enap®-N (Enap®-H)
The drug Enap®-N should not be used to relieve a hypertensive crisis, and its use is not recommended in patients with acute myocardial infarction due to insufficient experience in clinical use.
Hydrochlorothiazide
Renal dysfunction
In patients with impaired renal function, hydrochlorothiazide may cause azotemia. In case of renal failure, accumulation of hydrochlorothiazide is possible.
In patients with reduced renal function, periodic monitoring of CK is necessary. If renal dysfunction progresses and/or oliguria (anuria) occurs, hydrochlorothiazide should be discontinued.
Liver dysfunction
When using thiazide diuretics in patients with impaired liver function, hepatic encephalopathy may develop. In patients with severe liver failure or hepatic encephalopathy, the use of thiazides is contraindicated. In patients with mild to moderate hepatic impairment and/or progressive liver disease, hydrochlorothiazide should be used with caution, since even slight changes in fluid and electrolyte balance and serum ammonium accumulation can cause hepatic coma. If symptoms of encephalopathy occur, diuretics should be discontinued immediately.
Water-electrolyte balance and metabolic disorders
Thiazide diuretics (including hydrochlorothiazide) can cause a decrease in blood volume (hypovolemia) and disturbances in water and electrolyte balance (including hypokalemia, hyponatremia, hypochloremic alkalosis). Clinical symptoms of water-electrolyte imbalance are dryness of the oral mucosa, thirst, weakness, lethargy, fatigue, drowsiness, anxiety, muscle pain or cramps, muscle weakness, and a marked decrease in blood pressure. oliguria, tachycardia, arrhythmia and gastrointestinal disorders (such as nausea and vomiting). In patients receiving hydrochlorothiazide therapy (especially with long-term course treatment), clinical symptoms of water and electrolyte imbalance should be identified and the content of electrolytes in the blood plasma should be regularly monitored.
Sodium
All diuretics can cause hyponatremia, sometimes leading to severe complications. Hyponatremia and hypovolemia can lead to dehydration and orthostatic hypotension. A concomitant decrease in chlorine ions can lead to secondary compensatory metabolic alkalosis, but the frequency and severity of this effect are insignificant. It is recommended to determine the content of sodium ions in the blood plasma before starting treatment and regularly monitor this indicator while taking hydrochlorothiazide.
Potassium
When using thiazide and thiazide-like diuretics, there is a risk of a sharp decrease in the potassium content in the blood plasma and the development of hypokalemia (potassium content less than 3.4 mmol/l). Hypokalemia increases the risk of developing heart rhythm disturbances (including severe arrhythmias) and enhances the toxic effect of cardiac glycosides. In addition, hypokalemia (as well as bradycardia) is a condition that contributes to the development of polymorphic ventricular tachycardia of the “pirouette” type, which can be fatal.
Hypokalemia poses the greatest danger to the following groups of patients: elderly people, patients simultaneously receiving therapy with antiarrhythmic and non-antiarrhythmic drugs that can cause polymorphic ventricular tachycardia of the "pirouette" type or increase the duration of the QT interval on the ECG, patients with impaired liver function. IHD, chronic heart failure. In addition, patients with an increased QT interval are at increased risk. It does not matter whether this increase is caused by congenital causes or the effect of drugs.
In all the cases described above, it is necessary to avoid the risk of developing hypokalemia and regularly monitor the potassium content in the blood plasma. The first measurement of the content of potassium ions in the blood must be carried out within the first week from the start of treatment. If hypokalemia occurs, appropriate treatment should be prescribed.
Hypokalemia can be corrected by using potassium-containing medications or eating foods rich in potassium (dried fruits, fruits, vegetables).
Calcium
Thiazide diuretics may reduce the excretion of calcium ions by the kidneys, leading to a slight and temporary increase in plasma calcium levels. In some patients, with long-term use of thiazide diuretics, pathological changes in the parathyroid glands were observed with hypercalcemia and hyperphosphatemia, but without the typical complications of hyperparathyroidism (nephrolithiasis, decreased bone mineral density, peptic ulcer). Severe hypercalcemia may be a manifestation of previously undiagnosed hyperparathyroidism.
Because of their effect on calcium metabolism, thiazides may interfere with laboratory parameters of parathyroid function. Thiazide diuretics (including hydrochlorothiazide) should be discontinued before testing parathyroid function.
Magnesium
Thiazides have been found to increase renal excretion of magnesium, which can lead to hypomagnesemia. The clinical significance of hypomagnesemia remains unclear.
Glucose
Treatment with thiazide diuretics may impair glucose tolerance. When using hydrochlorothiazide in patients with manifest or latent diabetes mellitus, it is necessary to regularly monitor the concentration of glucose in the blood. Dosage adjustment of hypoglycemic medications may be required.
Uric acid
In patients with gout, the frequency of attacks may increase or the course of gout may worsen. Careful monitoring of patients with gout and impaired uric acid metabolism (hyperuricemia) is necessary.
Lipids
When using hydrochlorothiazide, the concentration of cholesterol and triglycerides in the blood plasma may increase.
Choroidal effusion/acute myopia/acute angle-closure glaucoma
Hydrochlorothiazide may cause an idiosyncratic reaction leading to the development of choroidal effusion with visual field impairment, acute myopia and acute angle-closure glaucoma. Symptoms include sudden onset, sudden decrease in visual acuity, or eye pain, usually occurring within hours to weeks of starting hydrochlorothiazide therapy. If left untreated, acute angle-closure glaucoma can lead to irreversible vision loss. If symptoms appear, you should stop taking hydrochlorothiazide as soon as possible. If intraocular pressure remains uncontrolled, emergency medical treatment or surgery may be required. A risk factor for the development of acute angle-closure glaucoma is a history of an allergic reaction to sulfonamides or penicillin.
Immune system disorders
There are reports that thiazide diuretics (including hydrochlorothiazide) may cause exacerbation or progression of SLE, as well as lupus-like reactions.
In patients receiving thiazide diuretics, hypersensitivity reactions may occur even in the absence of a history of allergic reactions or bronchial asthma.
Photosensitivity
There is information about cases of the development of photosensitivity reactions when taking thiazide diuretics. If photosensitivity occurs while taking hydrochlorothiazide, treatment should be discontinued. If continued use of a diuretic is necessary, the skin should be protected from exposure to sunlight or artificial ultraviolet rays (UV rays).
NMRK
Two pharmacoepidemiological studies using data from the Danish National Cancer Registry demonstrated an association between hydrochlorothiazide use and an increased risk of NMSC basal cell carcinoma and squamous cell carcinoma. The risk of developing NMSC increased with increasing total (cumulative) dose of hydrochlorothiazide. A possible mechanism for the development of NMSC is the photosensitizing effect of hydrochlorothiazide. Patients taking hydrochlorothiazide as monotherapy or in combination with other drugs should be aware of the risk of developing NMSC. It is recommended that such patients undergo regular skin examination to identify any new suspicious lesions as well as changes in existing skin lesions.
Any suspicious skin changes should be reported to your doctor immediately. Suspicious areas of skin should be examined by a specialist. To clarify the diagnosis, histological examination of skin biopsies may be required.
To minimize the risk of developing NMSC, patients should be advised to follow preventive measures, such as limiting exposure to sunlight and UV rays, and using appropriate protective equipment.
In patients with a history of NMSC, it is recommended to reconsider the use of hydrochlorothiazide.
Alcohol
During treatment with hydrochlorothiazide, it is not recommended to drink alcoholic beverages, since ethanol enhances the antihypertensive effect of thiazide diuretics. Other
In patients with severe atherosclerosis of the cerebral and coronary arteries, hydrochlorothiazide should be used with extreme caution.
Thiazide diuretics can reduce the amount of iodine bound to plasma proteins without causing signs of thyroid dysfunction.
Enalapril
Arterial hypotension and water-electrolyte imbalance
When using antihypertensive drugs, some patients may develop symptomatic arterial hypotension. Patients should be under medical supervision to promptly identify clinical signs of fluid and electrolyte imbalance, for example, dehydration, hyponatremia, hypochloremic alkalosis, hypomagnesemia or hypokalemia, which may develop against the background of concomitant diarrhea or vomiting. In such patients, monitoring of serum electrolytes is necessary.
The drug should be prescribed with extreme caution to patients with coronary artery disease or cerebrovascular diseases, in whom a pronounced decrease in blood pressure can lead to the development of myocardial infarction or stroke.
If arterial hypotension develops, the patient should be placed in a horizontal position on his back and, if necessary, a 0.9% sodium chloride solution should be administered intravenously. Transient arterial hypotension when taking the drug Enap®-N is not a contraindication to its further use. After normalization of blood pressure and replenishment of blood volume, therapy can be resumed in smaller doses, or each of the components of the drug can be used in monotherapy.
Aortic or mitral stenosis, HOCM
Like all drugs that have a vasodilating effect, ACE inhibitors should be administered with caution to patients with left ventricular outflow tract obstruction. Should not be used in patients with cardiogenic shock and hemodynamically significant left ventricular obstruction.
Patients on hemodialysis
The use of Enap®-N is not recommended for patients with renal failure undergoing hemodialysis. Anaphylactoid reactions have been observed in patients on dialysis using high-flux membranes (such as AN69®) and concomitantly receiving ACE inhibitor therapy. In these patients, it is necessary to use a different type of dialysis membrane or other classes of antihypertensive agents.
Kidney transplant
There is no experience with the use of enalapril in patients after kidney transplantation. Treatment with enalapril in patients after kidney transplantation is not recommended.
Liver dysfunction
The use of ACE inhibitors has rarely been associated with the development of a syndrome starting with cholestatic jaundice or hepatitis and progressing to fulminant hepatic necrosis, sometimes fatal. The mechanism of this syndrome has not been studied. If jaundice appears or a significant increase in the activity of hepatic transaminases in the blood plasma during the use of ACE inhibitors, the ACE inhibitor should be discontinued and appropriate auxiliary therapy should be prescribed. The patient should be under appropriate supervision.
Surgical interventions, general anesthesia
During major surgery or general anesthesia with the use of drugs that cause an antihypertensive effect, enalaprilat blocks the formation of angiotensin II caused by the compensatory release of renin. If a pronounced decrease in blood pressure develops, explained by a similar mechanism, it can be corrected by increasing the volume of blood volume.
Hypersensitivity reactions, angioedema
When using ACE inhibitors, including enalapril, rare cases of angioedema of the face, extremities, lips, tongue, vocal folds and/or larynx have been observed, occurring at different periods of treatment. In very rare cases, the development of intestinal edema has been reported. In such cases, you should immediately stop taking enalapril and carefully monitor the patient's condition in order to monitor and correct clinical symptoms. Even in cases where only swelling of the tongue is observed without the development of respiratory distress syndrome, patients may require long-term observation, since therapy with antihistamines and corticosteroids may not be sufficient.
Death due to angioedema associated with laryngeal edema or tongue edema has been very rarely reported. Swelling of the tongue, vocal folds, or larynx can lead to airway obstruction, especially in patients who have undergone respiratory surgery. In cases where swelling is localized to the tongue, vocal folds or larynx and may cause airway obstruction, appropriate treatment should be immediately prescribed, which may include subcutaneous injection of 0.1% epinephrine (adrenaline) solution (0.3-0.5 ml), and/or ensure airway patency.
In black patients taking ACE inhibitors, angioedema was observed more often than in patients of other races.
Patients with a history of angioedema not associated with taking ACE inhibitors may be at greater risk of developing angioedema during therapy with ACE inhibitors (see section "Contraindications").
An increased risk of developing angioedema was observed in patients taking ACE inhibitors and mTOR inhibitors concomitantly.
In patients taking thiazide diuretics, hypersensitivity reactions may occur even in the absence of a history of allergic reactions or bronchial asthma. Relapses or worsening of the severity of SLE have been reported in patients taking thiazide diuretics.
When ACE inhibitors are used simultaneously with drugs containing sacubitril (neprilysin inhibitor), the risk of developing angioedema increases, and therefore the simultaneous use of these drugs is contraindicated. ACE inhibitors should be prescribed no earlier than 36 hours after discontinuation of drugs containing sacubitril. Prescription of drugs containing sacubitril is contraindicated in patients receiving ACE inhibitors, as well as within 36 hours after discontinuation of ACE inhibitors.
Tissue plasminogen activators
Observational studies have shown an increased incidence of angioedema in patients taking ACE inhibitors following the use of alteplase for thrombolytic therapy of ischemic stroke.
Patients taking concomitant use of an ACE inhibitor and mTOR inhibitors (eg, sirolimus, everolimus, temsirolimus), racecadotril, DPP-4 inhibitors (gliptins) may be at increased risk of developing angioedema (eg, swelling of the upper airway or tongue with or without breathing problems). Caution should be exercised when prescribing racecadotril, mTOR inhibitors (eg, sirolimus, everolimus, temsirolimus), and DPP-4 inhibitors (gliptins) (eg, vildagliptin) to patients already taking an ACE inhibitor.
Anaphylactoid reactions during desensitization with an allergen from Hymenoptera venom
In rare cases, patients taking ACE inhibitors have developed life-threatening anaphylactoid reactions during desensitization with hymenoptera venom allergen. Adverse reactions can be avoided if you temporarily stop taking the ACE inhibitor before starting desensitization.
Anaphylactoid reactions during LDL apheresis
Life-threatening anaphylactoid reactions have rarely been observed in patients taking ACE inhibitors during LDL apheresis using dextran sulfate. The development of these reactions can be avoided if the ACE inhibitor is temporarily discontinued before each LDL apheresis procedure.
Neutropenia/agranulocytosis
Neutropenia/agranulocytosis, thrombocytopenia and anemia have been observed in patients taking ACE inhibitors. In patients with normal renal function and in the absence of other complicating factors, neutropenia rarely developed. Enalapril should be used with extreme caution in patients with systemic connective tissue diseases, those receiving immunosuppressive therapy, allopurinol or procainamide therapy, or a combination of these complicating factors, especially if there is a history of impaired renal function. Some of these patients developed serious infectious diseases, which in some cases did not respond to intensive antibiotic therapy. If enalapril is used in such patients, periodic monitoring of the number of leukocytes in the blood is recommended. Patients should be warned to report any signs of infection.
Hypoglycemia
In patients with diabetes mellitus receiving oral hypoglycemic agents or insulin, blood glucose concentrations should be carefully monitored during the first month of treatment with an ACE inhibitor.
Cough
Cases of cough occurring during therapy with ACE inhibitors have been observed. As a rule, the cough is non-productive, persistent and stops after discontinuation of therapy. Cough associated with the use of ACE inhibitors should be taken into account in its differential diagnosis.
Hyperkalemia
ACE inhibitors may cause hyperkalemia because they inhibit the release of aldosterone. In patients with normal renal function, this effect is usually minor.
Risk factors for the development of hyperkalemia are renal failure, diabetes mellitus, hypoaldosteronism, old age (over 70 years), some concomitant conditions (decrease in blood volume, acute heart failure in the decompensation stage, metabolic acidosis), with simultaneous use of potassium-sparing diuretics (for example, spironolactone, eplerenone , triamterene, amiloride), potassium supplements or potassium-containing salt substitutes and other drugs that increase plasma potassium levels (for example, heparin, trimethoprim or co-trimoxazole (sulfamethoxazole + trimethoprim) and especially aldosterone antagonists or angiotensin receptor blockers). The use of potassium supplements, potassium-sparing diuretics and potassium-containing table salt substitutes can lead to a significant increase in serum potassium levels, especially in patients with impaired renal function. Hyperkalemia can cause serious heart rhythm problems, sometimes fatal.
The simultaneous use of ACE inhibitors and the drugs listed above should be carried out with caution under the control of potassium levels in the blood serum and monitoring of renal function.
Renovascular hypertension
When using ACE inhibitors in patients with bilateral renal artery stenosis or stenosis of the artery of a solitary kidney, there is an increased risk of developing arterial hypotension and renal failure. In patients with elevated plasma creatinine concentrations, renal function may deteriorate. In such patients, therapy with ACE inhibitors should be started with low doses strictly under the supervision of a physician, the dose of the drug should be carefully selected and renal function monitored.
Double blockade of the RAAS
Concomitant use of ACE inhibitors with aliskiren and drugs containing aliskiren is contraindicated in patients with diabetes mellitus and/or with moderate or severe renal impairment (GFR < 60 ml/min/1.73 m2 body surface area) and is not recommended in other patients . Concomitant use of ACE inhibitors with ARB II is contraindicated in patients with diabetic nephropathy and is not recommended in other patients. The risk of developing arterial hypotension, hyperkalemia and renal dysfunction (including acute renal failure) is higher in the case of double blockade of the RAAS, i.e. with the simultaneous use of ARB II and ACE inhibitors, compared to the use of a drug from one of the listed groups as monotherapy. This combination is not recommended.
If simultaneous use of drugs is necessary, it is recommended to monitor renal function (including periodic monitoring of potassium levels and creatinine concentrations in the blood serum).
Renal dysfunction
Thiazide diuretics may not be effective enough in patients with impaired renal function and are ineffective in patients with creatinine clearance <30 ml/min (i.e., moderate to severe renal impairment).
The drug Enap®-N should not be prescribed to patients with renal failure (creatinine clearance < 80 ml/min) until the selected doses of enalapril and hydrochlorothiazide, used separately, correspond to the doses of these components contained in one tablet of the combined drug.
In some patients with arterial hypertension without any evidence of a history of renal disease, when treated with enalapril concomitantly with a diuretic, there was usually a slight and transient increase in serum urea and creatinine concentrations. In such cases, treatment with Enap®-N should be discontinued. In the future, it is possible to resume therapy in lower doses or each of the components of the drug can be used in monotherapy.
In some patients with bilateral renal artery stenosis or arterial stenosis of a solitary kidney, increases in serum urea and creatinine concentrations were observed when treated with ACE inhibitors. The changes were usually reversible, with indicators returning to baseline values after cessation of treatment. This pattern of changes is most likely in patients with renal failure.
Lithium preparations
The simultaneous use of lithium, enalapril and diuretics is not recommended (see section “Interaction with other drugs”).
Ethnic characteristics
The drug Enap®-N, like other ACE inhibitors. has a less pronounced antihypertensive effect in patients of the Negroid race compared to representatives of other races.
Special information on excipients
The drug Enap®-N contains lactose, therefore the drug is contraindicated in patients with lactase deficiency, lactose intolerance, and glucose-galactose malabsorption syndrome.
Patient reviews
Valery Kravtsov, 53 years old, Krasnodar: “As soon as I turned 50 years old, many ailments appeared, incl. The pressure began to rise. I had to undergo an examination, after which the doctor diagnosed arterial hypertension and prescribed Enap. The medicine is not cheap, but I bought it and started taking it. The condition improved after about a month.
I decided to look for analogues and came across Enalapril, which is much cheaper. I bought it and started taking it in the same dosage that the doctor prescribed. There were no side effects, both drugs were equally effective, so I settled on the cheaper one.”
Irina Romanova, 47 years old, Sochi: “Enalapril was prescribed by a therapist after he diagnosed stage 2 hypertension. Due to problems with the thyroid gland, the doctor recommended the minimum dosage. There were no side effects, so the dosage was gradually increased to 10 mg. I began to feel much better, but after a few months the drug stopped working.
I went to the doctor and told about my problems. He prescribed another drug - Enap, warning that this medicine was more expensive. I started taking it. This medicine is gentler and more effective. It’s helping for now, but I don’t know what will happen in a year.”
Nina Kruglitskaya, 54 years old, Khabarovsk: “I’ve been taking Enalapril for about a year. The pressure remains normal. When I started taking the medicine, I suffered from a dry cough. I thought it was bronchitis and went to the doctor. But the doctor said that this is a side effect that often happens when taking this medication. He suggested replacing it with something else, but the cough went away, so she continued taking Enalapril. I feel good so far.”
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What is the difference?
If Enap and Enalapril are the same thing, then why do these drugs have different market prices? What is the difference between these two representatives of the ACE inhibitor group?
Enalapril tablets
As you know, domestic Enalapril costs about three times less than its well-known analogue of Slovenian origin Enap, although there is no significant difference in the dosages and composition of these two drugs. Why is this happening? Is a foreign medicine really of higher quality and more effective?
Both drugs are analogues, so there is no significant difference between them: the effect of taking them is the same, the effect is mild, and they also do not differ in composition. The main difference is hidden behind the cost of drugs, and therefore requires more in-depth study.
Enalapril is a domestic medicinal form that is produced by most Russian pharmaceutical companies.
Unfortunately, some of these enterprises have not proven themselves to be the best, so the quality of their products can be questioned.
Enalapril is also produced by German and Indian manufacturers.
But while European drugs are distinguished by their quality and effectiveness, their Indian analogues pay more attention to low prices, and therefore are inferior in their medicinal properties.
The drug Enap is a unique ACE inhibitor produced in Slovenia from the KRKA company. They are protected from all kinds of counterfeits, and are famous all over the world for their authenticity, high quality and effectiveness. Therefore, if it is possible to purchase a more expensive drug, you should give preference to it.
Despite numerous reviews that Enap or Enalapril is better, scientists still decided to conduct a number of statistical studies to confirm the effectiveness of this or that drug.
For 14 days, two groups of people suffering from high blood pressure took Enap and Enalapril, respectively.
After the specified period of time, patients were asked to change medications and use them for another two weeks.
During the experiment it was possible to establish the following:
- there is no difference in the effect of taking the drugs;
- both antihypertensive drugs are well tolerated and cause adverse reactions with the same frequency;
- Both Enap and Enalapril are perfectly accepted by the body.
Enalapril Forte
Symptomatic arterial hypotension
Symptomatic hypotension is rarely observed in patients with uncomplicated hypertension. In patients with hypertension. taking the drug Enalapril FORTE, arterial hypotension develops more often against the background of dehydration, which occurs, for example, as a result of diuretic therapy, limiting the intake of table salt, in patients on dialysis, as well as in patients with diarrhea or vomiting (see sections “Side effects” ; “Interaction with other drugs”). Symptomatic hypotension has also been observed in patients with HF with or without renal failure.
Hypotension occurs more frequently in patients with more severe heart failure with hyponatremia or impaired renal function who use higher doses of loop diuretics. These patients should begin treatment with enalapril under medical supervision, which should be especially careful when changing the dose of the drug and/or diuretic.
Similarly, patients with coronary heart disease or cerebrovascular disease, in whom an excessive decrease in blood pressure may lead to the development of myocardial infarction or stroke, should be monitored. If arterial hypotension develops, the patient should be laid down and, if necessary, a 0.9% sodium chloride solution should be administered. Transient arterial hypotension when taking the drug is not a contraindication to further use and increasing the dose of the drug, which can be continued after replenishment of fluid volume and normalization of blood pressure.
In some patients with heart failure, with normal or low blood pressure, the drug may cause an additional decrease in blood pressure. This reaction to taking the drug is expected and is not a reason to stop treatment. In cases where arterial hypotension becomes stable, the dose should be reduced and/or treatment with a diuretic and/or drug should be discontinued.
Aortic or mitral stenosis/hypertrophic obstructive cardiomyopathy
Like all drugs that have a vasodilating effect, ACE inhibitors should be administered with caution to patients with left ventricular outflow tract obstruction.
Renal dysfunction
In some patients, hypotension that develops after initiation of treatment with ACE inhibitors may lead to further deterioration of renal function. In some cases, the development of acute renal failure, which is usually reversible, has been reported.
In patients with renal failure, it may be necessary to reduce the dose and/or frequency of taking the drug (see section "Dosage and Administration"). In some patients with bilateral renal artery stenosis or arterial stenosis of a solitary kidney, increases in blood urea and serum creatinine concentrations were observed. The changes were usually reversible, and indicators returned to baseline values after cessation of treatment. This pattern of changes is most likely in patients with renal failure.
In some patients who did not have renal disease before treatment, the drug in combination with diuretics usually caused a slight and transient increase in the concentration of urea in the blood and creatinine in the serum. In such cases, it may be necessary to reduce the dose and/or discontinue the diuretic and/or Enalapril FORTE.
Kidney transplant
There is no experience of use in patients after kidney transplantation, therefore treatment with Enalapril FORTE is not recommended in patients after kidney transplantation.
Liver failure
The use of ACE inhibitors has rarely been associated with the development of a syndrome starting with cholestatic jaundice or hepatitis and progressing to fulminant hepatic necrosis, sometimes fatal. The mechanism of this syndrome has not been studied. If jaundice appears or a significant increase in the activity of “liver” transaminases during the use of ACE inhibitors, the drug should be discontinued and appropriate auxiliary therapy should be prescribed, the patient should be under appropriate supervision.
Neutropenia/agranylocytosis
Neutropenia/agranulocytosis, thrombocytopenia and anemia are observed in patients taking ACE inhibitors. Neutropenia occurs rarely in patients with normal renal function and no other complicating factors.
Enalapril FORTE should be used with extreme caution in patients with systemic connective tissue diseases (systemic lupus erythematosus, scleroderma and others) taking immunosuppressive therapy, allopurinol or procainamide, or a combination of these complicating factors, especially if there are already existing renal impairments. Some of these patients develop serious infectious diseases, which in some cases do not respond to intensive antibiotic therapy. For such patients using enalapril, regular monitoring of the number of leukocytes and lymphocytes in the blood is recommended. Patients should be warned to report any signs of infectious disease.
Hypersensitivity reactions/angioedema
When using ACE inhibitors, including Enalapril FORTE, rare cases of angioedema of the face, extremities, lips, tongue, vocal folds and/or larynx have been observed, occurring during different periods of treatment. In very rare cases, intestinal edema may develop. In such cases, you should immediately stop taking the drug and carefully monitor the patient's condition in order to monitor and correct clinical symptoms. Even in cases where only swelling of the tongue is observed without the development of respiratory distress syndrome, patients may require long-term observation, since therapy with antihistamines and corticosteroids may not be sufficient.
Death due to angioedema associated with laryngeal edema or tongue edema has been very rarely reported. Swelling of the tongue, vocal folds, or larynx can lead to airway obstruction, especially in patients who have undergone respiratory surgery. In cases where swelling is localized in the area of the tongue, vocal folds or larynx and can cause airway obstruction, appropriate treatment should be immediately prescribed, which may include subcutaneous injection of 0.1% epinephrine (adrenaline) solution (0.3-0.5 ml) and/or ensure airway patency.
In rare cases, intestinal edema (angioedema of the intestine) develops during therapy with ACE inhibitors. In this case, patients experience abdominal pain as an isolated symptom or in combination with nausea and vomiting, in some cases without previous angioedema of the face and with normal levels of C1-esterase. Diagnosis is made using abdominal computed tomography, ultrasound, or surgery. Symptoms disappeared after stopping the ACE inhibitors. The possibility of developing intestinal edema must be taken into account when carrying out the differential diagnosis of abdominal pain in patients taking ACE inhibitors.
In black patients taking ACE inhibitors, angioedema is observed more often than in patients of other races.
Patients with a history of angioedema not associated with taking ACE inhibitors may be at greater risk of developing angioedema during therapy with ACE inhibitors (see section "Contraindications").
An increased risk of developing angioedema was observed in patients taking ACE inhibitors and mTOR inhibitors concomitantly.
An increased risk of angioedema was observed in patients taking ACE inhibitors and neprilysin inhibitors concomitantly.
Anaphylactoid reactions during desensitization with an allergen from Hymenoptera venom
In rare cases, in patients taking ACE inhibitors. Life-threatening anaphylactoid reactions develop during desensitization with an allergen from the venom of Hymenoptera. Adverse reactions can be avoided if you temporarily stop taking the ACE inhibitor before starting desensitization.
Anaphylactoid reactions during LDL apheresis
Life-threatening anaphylactoid reactions are rarely observed in patients taking ACE inhibitors during LDL apheresis using dskstran sulfate. The development of these reactions can be avoided if the ACE inhibitor is temporarily discontinued before each LDL apheresis procedure.
Patients undergoing hemodialysis using high-flow membranes
Anaphylactoid reactions have been observed in patients on dialysis using high-flux membranes (such as AN 69®) and concomitantly receiving ACE inhibitor therapy. In these patients, it is necessary to use a different type of dialysis membrane or other classes of antihypertensive drugs.
Cough
Cases of cough occurring during therapy with ACE inhibitors have been observed. As a rule, the cough is non-productive, persistent and stops after discontinuation of therapy. Cough associated with the use of ACE inhibitors should be considered in the differential diagnosis of cough.
Surgery/general anesthesia
During major surgery or general anesthesia with the use of drugs that cause an antihypertensive effect, enalaprilat blocks the formation of angiotensin II caused by the compensatory release of renin. If a pronounced decrease in blood pressure develops, explained by a similar mechanism, it can be corrected by increasing the volume of circulating blood.
Hyperkalemia
The risk of developing hyperkalemia is observed with renal failure, diabetes mellitus, as well as with the simultaneous use of potassium-sparing diuretics (for example, spironolactone, eplerenone, triamterene or amiloride), potassium-containing nutritional supplements, potassium-containing table salt substitutes and other drugs that can increase the content of potassium in the blood plasma (eg, heparin, tacrolimus, cyclosporine; drugs containing co-trimoxazole [trimethoprim + sulfamethoxazole]).
The use of potassium-containing dietary supplements, potassium-containing table salt substitutes and other drugs that can increase the content of potassium in the blood plasma (for example, heparin, tacrolimus, cyclosporine; drugs containing co-trimoxazole [trimethoprim + sulfamethoxazole]), especially in patients with impaired renal function , can lead to a significant increase in serum potassium levels. Hyperkalemia can lead to serious, sometimes fatal arrhythmias.
If it is necessary to use the drug simultaneously with the drugs listed above, caution should be exercised and the potassium content in the blood serum should be regularly monitored.
Hypoglycemia
Patients with diabetes mellitus taking oral hypoglycemic agents or insulin should be informed before starting the use of ACE inhibitors of the need for regular monitoring of blood glucose concentrations (hypoglycemia), especially during the first month of simultaneous use of these drugs (see section “Interactions”) with other drugs").
Lithium preparations
The simultaneous use of lithium preparations and the drug Enalapril FORTE is not recommended (see section “Interaction with other drugs”).
Dual blockade of the renin-angiotensin-aldosterone system (RAAS)
The development of arterial hypotension, syncope, stroke, hyperkalemia and renal dysfunction (including acute renal failure) has been reported in susceptible patients, especially if combination therapy with drugs affecting the RAAS was used (see section "Interaction with other drugs"). .
Double blockade of the RAAS by combined use of ACE inhibitors with ARA II or aliskiren is not recommended.
Concomitant use of the drug with aliskiren and drugs containing aliskiren is contraindicated in patients with diabetes mellitus and/or with moderate or severe renal failure (GFR less than 60 ml/min/1.73 m2 body area) (see section "Contraindications") and not recommended in other patients.
Concomitant use of ACE inhibitors with angiotensin II receptor antagonists is contraindicated in patients with diabetic nephropathy and is not recommended in other patients.
Use in elderly patients
The effectiveness and safety of Enalapril FORTE are similar in older and younger patients with hypertension.
Race
As with the use of other ACE inhibitors, the drug Enalapril FORTE appears to be less effective in reducing blood pressure in patients of the Black race than in patients of other races, which may be explained by the higher prevalence of conditions with low plasma renin activity in the population of Black patients with AG.
