Perindopril arginine: instructions, synonyms, analogs, indications, contraindications, area of application and doses.

Instructions:

Clinical and pharmacological group

01.024 (ACE inhibitor)

Release form, composition and packaging

White film-coated tablets, round, biconvex.

1 tab.
perindopril arginine	2.5 mg,
which is resp. perindopril content	1.6975 mg

Excipients: lactose monohydrate, magnesium stearate, maltodextrin, hydrophobic colloidal silicon dioxide, sodium carboxymethyl starch, glycerol, hypromellose, macrogol 6000, titanium dioxide.

30 pcs. — polypropylene bottles (1) — cardboard packs with first opening control.

Light green film-coated tablets, oblong, rounded on both sides, notched on both sides and engraved with the company logo on one of the front sides.

1 tab.
perindopril arginine	5 mg,
which is resp. perindopril content	3.395 mg

Excipients: lactose monohydrate, magnesium stearate, maltodextrin, hydrophobic colloidal silicon dioxide, sodium carboxymethyl starch, glycerol, hypromellose, macrogol 6000, titanium dioxide, copper chlorophyllin dye (E141ii).

14 pcs. — polypropylene bottles (1) — cardboard packs with first opening control. 30 pcs. — polypropylene bottles (1) — cardboard packs with first opening control.

Green film-coated tablets, round, biconvex, engraved with a heart on one side and the company logo on the other.

1 tab.
perindopril arginine	10 mg,
which is resp. perindopril content	6.79 mg

30 pcs. — polypropylene bottles (1) — cardboard packs with first opening control.

pharmachologic effect

Antihypertensive drug, ACE inhibitor. ACE, or kininase, is an exopeptidase that carries out both the conversion of angiotensin I into the vasoconstrictor substance angiotensin II, and the destruction of bradykinin, which has a vasodilator effect, into an inactive heptapeptide.

Suppression of ACE leads to a decrease in the content of angiotensin II in the blood plasma, as a result of which plasma renin activity increases (due to inhibition of negative feedback, which prevents the release of renin) and aldosterone secretion decreases. Since ACE inactivates bradykinin, suppression of ACE is accompanied by an increase in the activity of both the circulating and tissue kallikrein-kinin system, while the prostaglandin system is activated. Perindopril reduces peripheral vascular resistance, which leads to a decrease in blood pressure. In this case, peripheral blood flow accelerates, but heart rate does not increase.

Perindopril has a therapeutic effect due to its active metabolite, perindoprilat. Other metabolites of the drug do not have an inhibitory effect on ACE in vitro.

Arterial hypertension

In case of arterial hypertension with the use of the drug, there is a decrease in both systolic and diastolic blood pressure in the supine and standing positions. A decrease in blood pressure is achieved quite quickly. In patients with a positive response to treatment, normalization of blood pressure occurs within a month. In this case, no addiction effect is observed.

Discontinuation of treatment is not accompanied by the development of withdrawal syndrome. Perindopril has a vasodilating effect, helps restore the elasticity of large arteries and the structure of the vascular wall of small arteries, and also reduces left ventricular hypertrophy. Concomitant administration of thiazide diuretics enhances the hypotensive effect. In addition, the combination of an ACE inhibitor and a thiazide diuretic also reduces the risk of hypokalemia while taking diuretics.

Heart failure

Perindopril normalizes heart function by reducing preload and afterload. In patients with chronic heart failure receiving perindopril, a decrease in filling pressure in the left and right ventricles of the heart was detected; decrease in OPSS; increased cardiac output and increased cardiac index. A study of the drug compared with placebo showed that changes in blood pressure after the first dose of Prestarium® A at a dose of 2.5 mg in patients with mild to moderate heart failure were not statistically significantly different from changes in blood pressure observed after taking placebo.

Cerebrovascular diseases

An international multicenter study (PROGRESS) assessed the effect of active therapy with perindopril (monotherapy or in combination with indapamide) for 4 years on the risk of recurrent stroke in patients with a history of cerebrovascular disease. After a run-in period of perindopril tert-butylamine 2 mg (equivalent to perindopril arginine 2.5 mg) once a day for 2 weeks and then 4 mg (equivalent to perindopril arginine 5 mg) once a day for the next two weeks, 6105 patients were randomized into two groups: placebo (n=3054) and perindopril tertbutylamine 4 mg (corresponding to 5 mg perindopril arginine) (monotherapy) or in combination with indapamide (n=3051). Indapamide was additionally prescribed to patients who did not have direct indications or contraindications for the use of diuretics. This therapy was prescribed in addition to standard therapy for stroke and/or arterial hypertension or other pathological conditions. All randomized patients had a history of cerebrovascular disease (stroke or transient ischemic attack) within the past 5 years. Blood pressure was not an inclusion criterion: 2916 patients had arterial hypertension and 3189 had normal blood pressure. After 3.9 years of therapy, blood pressure (systolic/diastolic) decreased by an average of 9/4 mm Hg. It also showed a significant reduction in the risk of recurrent stroke (both ischemic and hemorrhagic in nature) of about 28% (95% CI (17; 38), p < 0.0001) compared with placebo (10.1% vs 13.8%). Additionally, a significant reduction in the risk of fatal or disabling strokes was shown; major cardiovascular complications, including myocardial infarction, incl. with fatal outcome; stroke-related dementia; serious deterioration of cognitive functions.

Pharmacokinetics

Suction

After oral administration, perindopril is rapidly absorbed from the gastrointestinal tract, Cmax in blood plasma is reached after 1 hour. Approximately 27% of the total amount of absorbed perindopril is converted into perindoprilat, the active metabolite. In addition to perindoprilate, 5 more metabolites are formed during metabolism - all of them are inactive substances.

T1/2 of perindopril from plasma is 1 hour. Cmax of perindoprilate in blood plasma is achieved after 3-4 hours.

Taking the drug with food is accompanied by a decrease in the conversion of perindopril to perindoprilat, accordingly reducing the bioavailability of the drug.

Distribution

The binding of perindoprilate to plasma proteins is 20%, mainly with ACE, and is dose-dependent. The Vd of free perindoprilate is approximately 0.2 l/kg.

Removal

Perindoprilat is excreted by the kidneys and the total T1/2 of the unbound fraction is 17 hours, which ensures an equilibrium state for 4 days.

Pharmacokinetics in special clinical situations

The elimination of perindoprilate is slowed down in old age, as well as in patients with heart and renal failure. In case of renal failure, it is advisable to adjust the dose of the drug taking into account the degree of renal dysfunction.

The dialysis clearance of perindoprilate is 70 ml/min.

In patients with liver cirrhosis, the hepatic clearance of perindopril is reduced by half. However, the amount of perindoprilate formed does not decrease and no changes in the dose of the drug are required.

Dosage

The drug is prescribed orally 1 time/day in the morning, before meals.

Arterial hypertension

The recommended starting dose is 5 mg 1 time/day, in the morning. If therapy is ineffective within a month, the dose can be increased to 10 mg 1 time / day.

When prescribing ACE inhibitors to patients with severely activated RAAS (with renovascular arterial hypertension, water-salt imbalance, diuretic therapy, severe arterial hypertension, cardiac decompensation), an unpredictable sharp decrease in blood pressure may be observed, for the prevention of which it is recommended to stop taking diuretics for 2-3 days before the intended start of therapy with Prestarium® A.

If it is impossible to cancel diuretics, the initial dose of Prestarium® A is 2.5 mg. In this case, it is necessary to monitor kidney function and potassium levels in the blood serum. Subsequently, if necessary, the dose can be increased.

In elderly patients, treatment should begin with a dose of 2.5 mg/day, and then, if necessary, gradually increase it up to a maximum dose of 10 mg/day.

Heart failure

Treatment with Prestarium® A in combination with non-potassium-sparing diuretics and/or digoxin and/or beta-blockers is recommended to begin under close medical supervision, prescribing the drug at an initial dose of 2.5 mg 1 time/day, in the morning. Subsequently, depending on tolerability and response to therapy, after 2 weeks of treatment, the dose of the drug can be increased to 5 mg 1 time / day.

In patients at high risk of developing symptomatic arterial hypotension, for example, with a reduced salt intake with or without hyponatremia, hypovolemia or taking diuretics, these conditions should, if possible, be corrected before starting Prestarium® A. Indicators such as blood pressure, renal function and potassium levels in the blood plasma should be monitored both before and during therapy.

Prevention of recurrent stroke

In patients with a history of cerebrovascular disease, therapy with Prestarium® A should begin with a dose of 2.5 mg during the first 2 weeks before the administration of indapamide.

Therapy should begin at any time (from 2 weeks to several years) after a stroke.

Reducing the risk of cardiovascular complications

In case of stable coronary artery disease, therapy with Prestarium® A should be started with a dose of 5 mg 1 time/day for 2 weeks. Then the daily dose should be increased to 10 mg 1 time / day (depending on renal function).

Elderly patients should begin therapy with a dose of 2.5 mg 1 time/day for one week, then 5 mg 1 time/day for the next week before increasing the dose to 10 mg 1 time/day (depending on renal function).

If renal function is impaired, the dose of Prestarium® A should be selected taking into account the degree of renal failure and under regular monitoring of potassium and QC levels.

CC (ml/min)	Recommended dose
CC ≥ 60	5 mg/day
30 <КК< 60	2.5 mg/day
15<КК<30	2.5 mg every other day
Patients on hemodialysis * CC < 15	2.5 mg per day of dialysis

* dialysis clearance of perindoprilate: 70 ml/min

When prescribing the drug to patients with impaired liver function, no dose changes are required.

Overdose

Symptoms: marked decrease in blood pressure, shock, electrolyte imbalance (such as increased concentration of potassium ions, decreased sodium); renal failure, hyperventilation, tachycardia, dizziness, bradycardia, restlessness and cough.

Treatment: with a significant decrease in blood pressure, the patient should be placed in a supine position and the blood volume should be immediately restored, if possible, an infusion of angiotensin II and/or intravenous catecholamines should be administered. If persistent severe bradycardia develops, the use of an artificial pacemaker may be required. Constant monitoring of vital body functions, serum electrolytes and CK is required. Perindopril can be removed from the systemic circulation by hemodialysis. During dialysis, the use of high-flow polyacrylonitrile membranes should be avoided.

Drug interactions

During the initial period of treatment, some patients during diuretic therapy, especially with excessive excretion of fluid and/or salts, may experience an excessive decrease in blood pressure, the risk of which can be reduced by discontinuing the diuretic, administering increased amounts of water and/or sodium chloride, and also prescribing ACE inhibitor at lower doses. Further increases in the dose of perindopril should be carried out with caution.

During therapy with ACE inhibitors, as a rule, the potassium content in the blood serum remains within normal limits, but hyperkalemia can sometimes develop. The combined use of ACE inhibitors and potassium-sparing diuretics (spironolactone, triamterene and amiloride) and potassium preparations, potassium-containing products and nutritional supplements can lead to a significant increase in serum potassium concentrations. In this regard, their combined use with ACE inhibitors is not recommended. These combinations should be used only in case of hypokalemia, taking precautions and constantly monitoring serum potassium levels.

Co-administration of ACE inhibitors and lithium preparations can lead to a reversible increase in the concentration of lithium in the blood serum and the development of lithium toxicity. Additional administration of thiazide diuretics against the background of the combined use of lithium and ACE inhibitors increases the already existing risk of developing lithium toxicity. Concomitant use of ACE inhibitors and lithium is not recommended. If this combination cannot be avoided, then it is necessary to regularly monitor the lithium content in the blood serum.

The administration of NSAIDs may be accompanied by a weakening of the antihypertensive effect of ACE inhibitors. Moreover, NSAIDs and ACE inhibitors have been shown to have an additive effect on increasing serum potassium levels, which may also worsen renal function. As a rule, these effects are reversible. In rare cases, acute renal failure may develop, which usually occurs with pre-existing renal dysfunction in elderly patients or due to dehydration.

The antihypertensive effect of drugs may be enhanced when combined with ACE inhibitors. The use of nitroglycerin and/or other vasodilators may lead to an additional hypotensive effect.

When used simultaneously with ACE inhibitors, allopurinol, immunosuppressants, incl. cytostatic agents and systemic corticosteroids, procainamide may increase the risk of developing leukopenia.

The administration of ACE inhibitors can enhance the hypoglycemic effect of insulin and oral hypoglycemic agents, up to the development of hypoglycemia. As a rule, this phenomenon is observed in the first weeks of combined use of these drugs and in patients with renal failure.

Co-prescription of tricyclic antidepressants, antipsychotics (neuroleptics), and general anesthesia with ACE inhibitors can lead to an increased hypotensive effect.

Sympathomimetics may reduce the antihypertensive effect of ACE inhibitors. When prescribing such a combination, the effectiveness of ACE inhibitors should be regularly assessed.

Antacids reduce the bioavailability of ACE inhibitors.

Perindopril can be prescribed together with acetylsalicylic acid (as a thrombolytic), thrombolytic agents, beta-blockers and/or nitrates.

Ethanol enhances the hypotensive effect of ACE inhibitors.

Use during pregnancy and lactation

The use of Prestarium® A in the first trimester of pregnancy is not recommended. When planning or confirming pregnancy, it is necessary to switch to alternative therapy. Adequate strictly controlled clinical studies have not been conducted to study the effect of ACE inhibitors in the first trimester of pregnancy. In a limited number of cases of use of ACE inhibitors in the first trimester of pregnancy, no malformations associated with fetotoxicity were observed.

Perindopril is contraindicated in the second and third trimesters of pregnancy, because There is evidence of fetotoxicity (decreased renal function, oligohydramnios (pronounced decrease in the volume of amniotic fluid), delayed formation of skull bones) and neonatal toxicity (impaired renal function, hypotension, hyperkalemia). If perindopril therapy was carried out in the second and/or third trimesters of pregnancy, it is necessary to conduct an ultrasound examination of the function of the fetus's kidneys and skull.

It is unknown whether perindopril is excreted in breast milk in humans, therefore the use of the drug during lactation (breastfeeding) is not recommended.

Side effects

Often>1/100, <1/10	Rarely >1/1000, <1/100	Extremely rare < 1/10,000
urinary system
Decreased kidney function	Acute renal failure
Respiratory system
Cough, difficulty breathing	Bronchospasm, angioedema	Eosinophilic pneumonia, rhinitis
Digestive system
Nausea, vomiting, abdominal pain, taste disturbance, diarrhea, constipation, loss of appetite	Dry mouth	Cholestatic or cytolytic jaundice, pancreatitis
Allergic reactions
Skin rash, itchy skin	Hives	Erythema multiforme
Nervous system
Headache, asthenia, dizziness, tinnitus, visual disturbances, muscle cramps, paresthesia	Decreased mood, sleep disturbances	Confusion
Others
Sweating, sexual dysfunction

From the cardiovascular system: excessive decrease in blood pressure and associated symptoms; extremely rarely - arrhythmia, angina pectoris, myocardial infarction and stroke; in patients at risk, secondary severe arterial hypotension may develop.

From laboratory parameters: extremely rarely - decreased hemoglobin concentration and hematocrit, thrombocytopenia, leukopenia/neutropenia, isolated cases of agranulocytosis or pancytopenia; the likelihood of developing hemolytic anemia due to glucose-6-phosphate dehydrogenase deficiency; rarely - increased levels of urea and creatinine in blood plasma, transient hyperkalemia, especially against the background of renal failure, increased activity of liver enzymes and liver bilirubin.

Storage conditions and periods

The drug should be stored out of the reach of children. No special conditions are required for storing the drug. Shelf life: 3 years.

Indications

- arterial hypertension;

— chronic heart failure;

- prevention of recurrent stroke (combination therapy with indapamide) in patients who have suffered a stroke or transient ischemic cerebrovascular accident;

- stable coronary artery disease: to reduce the risk of cardiovascular complications.

Contraindications

- history of angioedema (congenital/idiopathic or reaction associated with previous treatment with an ACE inhibitor);

- pregnancy;

- lactation period (breastfeeding);

- hypersensitivity to the components of the drug;

- hypersensitivity to other ACE inhibitors;

- lactase deficiency, galactosemia, glucose/galactose malabsorption syndrome (due to the fact that the excipients of the drug include lactose monohydrate).

Use with caution when there is a decrease in blood volume (taking diuretics, a salt-free diet, vomiting, diarrhea, hemodialysis), hyponatremia, cerebrovascular diseases, angina pectoris - the risk of a sharp decrease in blood pressure; with renovascular hypertension, bilateral renal artery stenosis or the presence of only one functioning kidney - the risk of developing severe arterial hypotension and renal failure; with chronic renal failure; with systemic connective tissue diseases (SLE, scleroderma) and therapy with immunosuppressants - the risk of developing agranulocytosis and neutropenia; with hyperkalemia; with aortic valve stenosis, hypertrophic obstructive cardiomyopathy; during the hemodialysis procedure using high-flow polyacrylonitrile membranes; before the LDL apheresis procedure; in patients after kidney transplantation (no experience of clinical use); simultaneously with desensitizing therapy with allergens; surgical intervention (general anesthesia); in patients with diabetes mellitus receiving hypoglycemic agents or insulin (it is recommended to monitor blood glucose levels); in patients under the age of 18 years (the effectiveness and safety of use have not been studied).

special instructions

In patients with stable coronary artery disease, if an episode of unstable angina (significant or not) occurs during the first month of therapy with Prestarium A, the benefits and risks should be assessed before continuing treatment.

ACE inhibitors can cause a sharp decrease in blood pressure. Symptomatic arterial hypotension rarely develops in patients without concomitant diseases. The risk of an excessive decrease in blood pressure is increased in patients with reduced blood volume, which can be observed during therapy with diuretics, while following a strict salt-free diet, hemodialysis, as well as with vomiting and diarrhea. In most cases, episodes of pronounced decrease in blood pressure are observed in patients with severe heart failure, both in the presence of concomitant renal failure and in its absence. This side effect is most often observed in patients receiving loop diuretics in high doses, as well as against the background of hyponatremia or impaired renal function. In such patients, treatment should begin under close medical supervision, preferably in a hospital setting. In this case, the drug is prescribed in small doses, followed by careful titration of the dose. If possible, diuretic therapy should be temporarily discontinued. A similar approach is also used in patients with angina pectoris or cerebrovascular disease, in whom severe hypotension can lead to the development of myocardial infarction or cerebrovascular complications.

Before prescribing Prestarium® A, as well as other ACE inhibitors, and during its use, blood pressure levels, kidney function indicators and the concentration of potassium ions in the blood serum should be carefully monitored.

In order to reduce the likelihood of developing symptomatic arterial hypotension in patients receiving diuretic therapy in high doses, the dose of diuretics should, if possible, be reduced several days before starting use of the drug Prestarium® A.

If arterial hypotension develops, the patient should be placed in the supine position. If necessary, the volume of blood volume should be replenished using intravenous administration of saline solution. A pronounced decrease in blood pressure when taking the drug for the first time is not an obstacle to further prescription of the drug. After restoration of blood volume and blood pressure, treatment can be continued subject to careful selection of the dose of the drug.

In patients with symptomatic heart failure, arterial hypotension that develops during the initial period of therapy with ACE inhibitors can lead to deterioration of renal function. Sometimes acute renal failure that develops is, as a rule, reversible.

In patients with bilateral renal artery stenosis or stenosis of the artery of a single kidney (especially in the presence of renal failure), serum urea and creatinine concentrations may increase during therapy with ACE inhibitors.

The use of ACE inhibitors in patients with renovascular arterial hypertension is accompanied by an increased risk of developing severe arterial hypotension and renal failure. Treatment of such patients begins under close medical supervision with the administration of the drug in small doses and further adequate dose selection. During the first few weeks of therapy, diuretic treatment should be temporarily discontinued and renal function monitored.

In some patients suffering from arterial hypertension, in the presence of previously undetected renal failure, especially with concomitant administration of diuretics, the concentration of urea and creatinine in the blood serum may increase. These changes are usually mild and reversible. In this case, it is recommended to reduce the dose of Prestarium® A and/or discontinue the diuretic.

In patients undergoing hemodialysis using high-flow membranes, several cases of persistent, life-threatening anaphylactic reactions have been observed. Prescription of ACE inhibitors should be avoided when using this type of membrane.

There are no data on the use of Prestarium® A in kidney transplantation.

Angioedema of the face, extremities, lips, mucous membranes, tongue, glottis and/or larynx may develop in patients receiving ACE inhibitors, especially during the first few weeks of therapy. In rare cases, severe angioedema may occur during prolonged use of an ACE inhibitor. In such cases, treatment with an ACE inhibitor should be stopped immediately, and drugs of another pharmacotherapeutic group should be prescribed as a replacement.

Angioedema of the tongue, glottis, or larynx can be fatal. When it develops, emergency therapy includes, among other prescriptions, immediate subcutaneous administration of a solution of epinephrine (adrenaline) 1:1000 (1 mg/ml) 0.3-0.5 ml or slow intravenous administration (in accordance with the preparation instructions infusion solution) under ECG and blood pressure control. The patient should be hospitalized for treatment and observation for at least 12-24 hours until the symptoms of this reaction completely disappear.

When performing LDL apheresis using dextran sulfate absorption, patients may develop anaphylactic reactions when ACE inhibitors are prescribed.

There are isolated reports of the development of life-threatening anaphylactic reactions in patients receiving ACE inhibitors during desensitizing therapy with bee venom (bees, wasps). ACE inhibitors should be used with caution in patients with a predisposition to allergic reactions undergoing desensitization procedures. Avoid prescribing ACE inhibitors to patients receiving bee venom immunotherapy. However, this reaction can be avoided by temporarily stopping the ACE inhibitor before the procedure.

Taking ACE inhibitors is sometimes associated with a syndrome starting with the development of cholestatic jaundice, progressing to fulminant hepatic necrosis, and (sometimes) death. The mechanism of development of this syndrome is not clear. If symptoms of jaundice or increased liver enzyme activity occur in patients taking ACE inhibitors, discontinue drug therapy and conduct appropriate evaluation.

Neutropenia, agranulocytosis, thrombocytopenia, and anemia can develop during therapy with ACE inhibitors. With normal renal function and the absence of other complications, neutropenia rarely occurs. ACE inhibitors are prescribed only in emergency cases in the presence of systemic vasculitis, immunosuppressive therapy, taking allopurinol or procainamide, as well as when combining all of these factors, especially against the background of previous renal failure. There is a risk of developing severe infectious diseases that are resistant to intensive antibiotic therapy. When carrying out perindopril therapy in patients with the above factors, it is necessary to regularly monitor the number of leukocytes and warn the patient about the need to inform the attending physician about the appearance of any symptoms of infection.

It should be taken into account that patients of the Negroid race have a higher risk of developing angioedema. Like other ACE inhibitors, perindopril is less effective as an antihypertensive agent in black patients. This effect may be associated with a pronounced predominance of low-renin status in black patients with arterial hypertension.

During therapy with an ACE inhibitor, a dry, non-productive cough may occur, which stops after discontinuation of the drug.

The use of ACE inhibitors in patients whose condition requires surgery and/or general anesthesia may lead to the development of arterial hypotension or collapse, due to a sharp increase in the antihypertensive effect. Perindopril should be stopped the day before surgery. If arterial hypotension develops, it is necessary to maintain blood pressure by replenishing blood volume.

During therapy with ACE inhibitors, hyperkalemia may develop, especially if the patient has renal and/or heart failure or uncontrolled diabetes mellitus. It is generally not recommended to prescribe potassium supplements, potassium-sparing diuretics, and other drugs associated with a risk of potassium elevation (eg, heparin) due to the potential for severe hyperkalemia. If the combined use of these drugs is necessary, then therapy should be accompanied by regular monitoring of potassium levels in the blood serum.

In patients taking oral hypoglycemic agents or insulin, blood glucose levels should be carefully monitored during the first month of ACE inhibitor therapy.

It is not recommended to use lithium preparations, potassium-sparing diuretics, potassium preparations, potassium-containing products and nutritional supplements simultaneously with perindopril.

Due to the fact that the excipients of the drug include lactose monohydrate, Prestarium® A is contraindicated in patients with lactase deficiency, galactosemia or glucose/galactose malabsorption syndrome. Prestarium® A tablets of 2.5 mg, 5 mg and 10 mg contain 36.29 mg, 72.58 mg and 145.16 mg of lactose monohydrate, respectively.

Impact on the ability to drive vehicles and operate machinery

ACE inhibitors should be prescribed with caution to patients driving vehicles and engaging in activities that require increased concentration and speed of psychomotor reactions, due to the risk of developing arterial hypotension and dizziness.

Use for renal impairment

Use the drug with caution in bilateral renal artery stenosis or the presence of only one functioning kidney - the risk of developing severe arterial hypotension and renal failure; with chronic renal failure; during the hemodialysis procedure using high-flow polyacrylonitrile membranes.

Use for liver dysfunction

Conditions for dispensing from pharmacies

The drug is available with a prescription.

Compatibility of Perindopril and alcohol

? Perindopril is a medicine prescribed to patients with serious heart and vascular diseases. To alleviate their condition, patients should lead a measured lifestyle, excluding overload and bad habits. Drinking alcoholic beverages can not only make the treatment pointless, but also provoke a vascular accident.

The annotation for the medication states: it is recommended to exclude alcohol during the course of treatment. Combining medications with alcohol-containing drinks can have serious consequences.

Taking alcohol together with medication can cause:

exacerbation of ischemia:
hypertensive crisis;
a sharp drop in blood pressure;
cardiac conduction disorders, arrhythmias;
deterioration of the function of the excretory system.

The likelihood of complications depends on the condition and age of the sick person, the amount and strength of the alcohol-containing drink.

Perindopril and beer

It is a mistake to think that drinking beer is less dangerous. Taking a small portion of 0.25-0.3 liters may not have any consequences. If you drink more, the blood vessels expand sharply, then narrow. The heart rate increases, the pressure rises abruptly. Taking the drug simultaneously with beer can provoke an attack of angina, ischemia of the heart and brain.

To avoid a sharp deterioration in health and to make the therapy effective, simultaneous use is not allowed.

Consequences of drinking alcohol

The systematic combination of medication with strong drinks often causes a serious deterioration in the patient’s condition:

The drug causes lethargy, drowsiness, and disorientation. During intoxication, the likelihood of falling and getting injured increases.
An increase in heart rate is accompanied by a decrease in the density of cardiac muscle fibers. There is a malfunction of the sinus node.
The medicine is often prescribed to patients during rehabilitation after a heart attack or stroke. Drinking strong drinks during this difficult period can cause a second attack.
When ethanol enters the bloodstream, the blood vessels dilate, and when interacting with the drug, this leads to a drop in blood pressure. After some time, a sharp narrowing of the capillaries occurs - the pressure rises critically. Jumps in blood supply can lead to rupture of the walls of blood vessels.
Taking the drug simultaneously with alcohol is especially dangerous for older people, whose capillaries are less elastic.

Combination with ethanol reduces the therapeutic effect of the drug and increases general intoxication of the body.

Brief characteristics of the drug

This is an antihypertensive drug from the group of ACE inhibitors. Reduces the rate of synthesis of organic substances leading to vascular spasms.

Action of the drug:

normalizes blood pressure;
increases the elasticity of the vascular wall, reduces peripheral resistance;
reduces the heart's need for oxygen, improves exercise tolerance;
prevents sodium retention in the body.

Used for diseases:

arterial hypertension;
stable ischemic heart disease;
chronic cardiovascular failure;
prevention of transient ischemic attacks, repeated heart attacks, strokes.

Side effects when taken:

headache, drowsiness, coordination problems;
tachycardia, palpitations, arrhythmia;
bronchospasm.

The drug is contraindicated in case of serious pathologies of the liver and kidneys, angioedema.

https://myweak.ru/alkogolizm/lekarstva/perindopril-sovmestimost.html

Use of the drug for alcoholism

Significant difficulties during treatment arise if the patient has an alcohol addiction. Patients with chronic alcoholism do not realize the severity of the consequences and may take a large dose of alcohol.

Such patients are prone to breakdowns and serious violations of a sober lifestyle. Often alcoholics cannot adequately assess their condition.

Relatives of a person are obliged to notify the attending physician about the existing problem. The specialist weighs the advisability of using the medication, taking into account the patient’s painful craving for alcohol.

When can I take the drug? How long after?

The simultaneous use of medicine and alcohol is unacceptable. If alcohol is present in the body, you need to maintain a time interval for removing ethanol.

After how many hours you can take the medicine depends on the type and amount of alcohol taken and the severity of the disease. Beer and wine are eliminated from the body within 2-4 hours, the effect of drinks with a strength of 30-40 degrees lasts up to 10-14 hours.

Taking the medicine while intoxicated or during a hangover is contraindicated under any circumstances.

Using the drug for a hangover

The effect of the product is designed for 24 hours. In case of renal pathologies, the period of drug elimination is prolonged. The combination of a hangover syndrome with a medicine located in the body tissues against the background of a serious illness can lead to unpredictable consequences.

A hangover is a potentially life-threatening condition:

blood thickening caused by dehydration leads to the formation of blood clots;
narrowing of blood vessels can cause arterial stenosis;
severe intoxication creates additional stress on the heart;
Nausea, vertigo, and headache are typical.

Taking the drug during a hangover can provoke a severe attack of angina, increase tachycardia and arrhythmia.