(per in' doe pril)
P / L : Contraindicated in pregnancy and caution during lactation (breast feeding)
WARNING: AVOID USE IN PREGNANCY
Treatment of hypertension.
Treatment of symptomatic heart failure.
Reduction of risk of cardiac events in patients with a history of myocardial infarction and/or revascularisation.
Dosage & Administration
The dose should be individualised according to the patient profile and blood pressure response.
Perindopril may be used in monotherapy or in combination with other classes of antihypertensive therapy.
The recommended starting dose is 5 mg given once daily in the morning.
Patients with a strongly activated renin-angiotensin-aldosterone system (in particular, renovascular hypertension, salt and/or volume depletion, cardiac decompensation or severe hypertension) may experience an excessive drop in blood pressure following the initial dose. A starting dose of 2.5 mg is recommended in such patients and the initiation of treatment should take place under medical supervision.
The dose may be increased to 10 mg once daily after one month of treatment.
Symptomatic hypotension may occur following initiation of therapy with Perindopril; this is more likely in patients who are being treated concurrently with diuretics. Caution is therefore recommended since these patients may be volume and/or salt depleted.
If possible, the diuretic should be discontinued 2 to 3 days before beginning therapy with Perindopril.
In hypertensive patients in whom the diuretic cannot be discontinued, therapy with Perindopril should be initiated with a 2.5 mg dose. Renal function and serum potassium should be monitored. The subsequent dosage of Perindopril should be adjusted according to blood pressure response. If required, diuretic therapy may be resumed.
In elderly patients treatment should be initiated at a dose of 2.5 mg which may be progressively increased to 5 mg after one month then to 10 mg if necessary depending on renal function (see table below).
- Symptomatic heart failure:
It is recommended that Perindopril, generally associated with a non-potassium-sparing diuretic and/or digoxin and/or a beta-blocker, be introduced under close medical supervision with a recommended starting dose of 2.5 mg taken in the morning. This dose may be increased after 2 weeks to 5 mg once daily if tolerated. The dose adjustment should be based on the clinical response of the individual patient.
In severe heart failure and in other patients considered to be at high risk (patients with impaired renal function and a tendency to have electrolyte disturbances, patients receiving simultaneous treatment with diuretics and/or treatment with vasodilating agents), treatment should be initiated under careful supervision.
Patients at high risk of symptomatic hypotension e.g. patients with salt depletion with or without hyponatraemia, patients with hypovolaemia or patients who have been receiving vigorous diuretic therapy should have these conditions corrected, if possible, prior to therapy with Perindopril. Blood pressure, renal function and serum potassium should be monitored closely, both before and during treatment with Perindopril.
- Stable coronary artery disease:
Perindopril should be introduced at a dose of 5 mg once daily for two weeks, then increased to 10 mg once daily, depending on renal function and provided that the 5 mg dose is well tolerated.
Elderly patients should receive 2.5 mg once daily for one week, then 5 mg once daily the next week, before increasing the dose up to 10 mg once daily depending on renal function (see Table 1 'Dosage adjustment in renal impairment'). The dose should be increased only if the previous lower dose is well tolerated.
Patients with renal impairment:
Dosage in patients with renal impairment should be based on creatinine clearance as outlined in table 1 below:
Table 1: Dosage adjustment in renal impairment
* Dialysis clearance of perindoprilat is 70 ml/min.
For patients on haemodialysis, the dose should be taken after dialysis.
Patients with hepatic impairment:
No dosage adjustment is necessary in patients with hepatic impairment.
The efficacy and safety of use in children and adolescents (less than 18 years) have not been established. Therefore, use in children and adolescents is not recommended.
Method of administration
For oral use.
Perindopril is recommended to be taken once daily in the morning before a meal.
Limited data are available for overdosage in humans. Symptoms associated with overdosage of ACE inhibitors may include hypotension, circulatory shock, electrolyte disturbances, renal failure, hyperventilation, tachycardia, palpitations, bradycardia, dizziness, anxiety, and cough.
The recommended treatment of overdosage is intravenous infusion of sodium chloride 9 mg/ml (0.9%) solution. If hypotension occurs, the patient should be placed in the shock position. If available, treatment with angiotensin II infusion and/or intravenous catecholamines may also be considered. Perindopril may be removed from the general circulation by haemodialysis. Pacemaker therapy is indicated for therapy-resistant bradycardia. Vital signs, serum electrolytes and creatinine concentrations should be monitored continuously.
:: Hypersensitivity to the active substance, to any of the excipients or to any other ACE inhibitor;
:: History of angioedema associated with previous ACE inhibitor therapy;
:: Hereditary or idiopathic angioedema;
:: Second and third trimesters of pregnancy;
:: Concomitant use with Aliskiren in patients with diabetes mellitus or renal impairment (GFR < 60 ml/min/1.73m²).
Stable coronary artery disease:
If an episode of unstable angina pectoris (major or not) occurs during the first month of perindopril treatment, a careful appraisal of the benefit/risk should be performed before treatment continuation.
ACE inhibitors may cause a fall in blood pressure. Symptomatic hypotension is seen rarely in uncomplicated hypertensive patients and is more likely to occur in patients who have been volume-depleted e.g. by diuretic therapy, dietary salt restriction, dialysis, diarrhoea or vomiting, or who have severe renin-dependent hypertension. In patients with symptomatic heart failure, with or without associated renal insufficiency, symptomatic hypotension has been observed. This is most likely to occur in those patients with more severe degrees of heart failure, as reflected by the use of high doses of loop diuretics, hyponatraemia or functional renal impairment. In patients at increased risk of symptomatic hypotension, initiation of therapy and dose adjustment should be closely monitored. Similar considerations apply to patients with ischaemic heart or cerebrovascular disease in whom an excessive fall in blood pressure could result in a myocardial infarction or cerebrovascular accident.
If hypotension occurs, the patient should be placed in the supine position and, if necessary, should receive an intravenous infusion of sodium chloride 9 mg/ml (0.9%) solution. A transient hypotensive response is not a contraindication to further doses, which can be given usually without difficulty once the blood pressure has increased after volume expansion.
In some patients with congestive heart failure who have normal or low blood pressure, additional lowering of systemic blood pressure may occur with Perindopril. This effect is anticipated and is usually not a reason to discontinue treatment. If hypotension becomes symptomatic, a reduction of dose or discontinuation of Perindopril may be necessary.
Aortic and mitral valve stenosis / hypertrophic cardiomyopathy:
As with other ACE inhibitors, Perindopril should be given with caution to patients with mitral valve stenosis and obstruction in the outflow of the left ventricle such as aortic stenosis or hypertrophic cardiomyopathy.
In cases of renal impairment (creatinine clearance < 60 ml/min) the initial perindopril dosage should be adjusted according to the patient's creatinine clearance and then as a function of the patient's response to treatment. Routine monitoring of potassium and creatinine are part of normal medical practice for these patients.
In patients with symptomatic heart failure, hypotension following the initiation of therapy with ACE inhibitors may lead to some further impairment in renal function. Acute renal failure, usually reversible, has been reported in this situation.
In some patients with bilateral renal artery stenosis or stenosis of the artery to a solitary kidney, who have been treated with ACE inhibitors, increases in blood urea and serum creatinine, usually reversible upon discontinuation of therapy, have been seen. This is especially likely in patients with renal insufficiency. If renovascular hypertension is also present there is an increased risk of severe hypotension and renal insufficiency. In these patients, treatment should be started under close medical supervision with low doses and careful dose titration. Since treatment with diuretics may be a contributory factor to the above, they should be discontinued and renal function should be monitored during the first weeks of Perindopril therapy.
Some hypertensive patients with no apparent pre-existing renal vascular disease have developed increases in blood urea and serum creatinine, usually minor and transient, especially when Perindopril has been given concomitantly with a diuretic. This is more likely to occur in patients with pre-existing renal impairment. Dosage reduction and/or discontinuation of the diuretic and/or Perindopril may be required.
Anaphylactoid reactions have been reported in patients dialysed with high flux membranes, and treated concomitantly with an ACE inhibitor. In these patients consideration should be given to using a different type of dialysis membrane or different class of antihypertensive agent.
There is no experience regarding the administration of Perindopril in patients with a recent kidney transplantation.
Angioedema of the face, extremities, lips, mucous membranes, tongue, glottis and/or larynx has been reported rarely in patients treated with ACE inhibitors, including Perindopril. This may occur at any time during therapy. In such cases, Perindopril should promptly be discontinued and appropriate monitoring should be initiated and continued until complete resolution of symptoms has occurred. In those instances where swelling was confined to the face and lips the condition generally resolved without treatment, although antihistamines have been useful in relieving symptoms.
Angioedema associated with laryngeal oedema may be fatal. Where there is involvement of the tongue, glottis or larynx, likely to cause airway obstruction, emergency therapy should be administered promptly. This may include the administration of adrenaline and/or the maintenance of a patent airway. The patient should be under close medical supervision until complete and sustained resolution of symptoms has occurred.
Patients with a history of angioedema unrelated to ACE inhibitor therapy may be at increased risk of angioedema while receiving an ACE inhibitor.
Intestinal angioedema has been reported rarely in patients treated with ACE inhibitors. These patients presented with abdominal pain (with or without nausea or vomiting); in some cases there was no prior facial angioedema and C-1 esterase levels were normal. The angioedema was diagnosed by procedures including abdominal CT scan, or ultrasound or at surgery and symptoms resolved after stopping the ACE inhibitor. Intestinal angioedema should be included in the differential diagnosis of patients on ACE inhibitors presenting with abdominal pain.
Anaphylactoid reactions during low-density lipoproteins (LDL) apheresis:
Rarely, patients receiving ACE inhibitors during low-density lipoprotein (LDL) apheresis with dextran sulphate have experienced life-threatening anaphylactoid reactions. These reactions were avoided by temporarily withholding ACE inhibitor therapy prior to each apheresis.
Anaphylactic reactions during desensitisation:
Patients receiving ACE inhibitors during desensitisation treatment (e.g. hymenoptera venom) have experienced anaphylactoid reactions. In the same patients, these reactions have been avoided when the ACE inhibitors were temporarily withheld, but they reappeared upon inadvertent rechallenge.
Rarely, ACE inhibitors have been associated with a syndrome that starts with cholestatic jaundice and progresses to fulminant hepatic necrosis and (sometimes) death. The mechanism of this syndrome is not understood. Patients receiving ACE inhibitors who develop jaundice or marked elevations of hepatic enzymes should discontinue the ACE inhibitor and receive appropriate medical follow-up.
Neutropenia/agranulocytosis, thrombocytopenia and anaemia have been reported in patients receiving ACE inhibitors. In patients with normal renal function and no other complicating factors, neutropenia occurs rarely. Perindopril should be used with extreme caution in patients with collagen vascular disease, immunosuppressant therapy, treatment with allopurinol or procainamide, or a combination of these complicating factors, especially if there is pre-existing impaired renal function. Some of these patients developed serious infections, which in a few instances did not respond to intensive antibiotic therapy. If perindopril is used in such patients, periodic monitoring of white blood cell counts is advised and patients should be instructed to report any sign of infection (e.g. sore throat, fever).
ACE inhibitors cause a higher rate of angioedema in black patients than in non-black patients.
As with other ACE inhibitors, perindopril may be less effective in lowering blood pressure in black people than in non-blacks, possibly because of a higher prevalence of low-renin states in the black hypertensive population.
Cough has been reported with the use of ACE inhibitors. Characteristically, the cough is non-productive, persistent and resolves after discontinuation of therapy. ACE inhibitor-induced cough should be considered as part of the differential diagnosis of cough.
In patients undergoing major surgery or during anaesthesia with agents that produce hypotension, Perindopril may block angiotensin II formation secondary to compensatory renin release. The treatment should be discontinued one day prior to the surgery. If hypotension occurs and is considered to be due to this mechanism, it can be corrected by volume expansion.
Elevations in serum potassium have been observed in some patients treated with ACE inhibitors, including perindopril. Risk factors for the development of hyperkalaemia include those with renal insufficiency, worsening of renal function, age (> 70 years), diabetes mellitus, intercurrent events, in particular dehydration, acute cardiac decompensation, metabolic acidosis and concomitant use of potassium-sparing diuretics (e.g. spironolactone, eplerenone, triamterene, or amiloride), potassium supplements or potassium-containing salt substitutes; or those patients taking other drugs associated with increases in serum potassium (e.g. heparin). The use of potassium supplements, potassium-sparing diuretics, or potassium-containing salt substitutes particularly in patients with impaired renal function may lead to a significant increase in serum potassium. Hyperkalaemia can cause serious, sometimes fatal arrhythmias. If concomitant use of the above-mentioned agents is deemed appropriate, they should be used with caution and with frequent monitoring of serum potassium.
In diabetic patients treated with oral antidiabetic agents or insulin, glycaemic control should be closely monitored during the first month of treatment with an ACE inhibitor.
The combination of lithium and perindopril is generally not recommended.
Potassium-sparing drugs, potassium supplements or potassium-containing salt substitutes:
The combination of perindopril and potassium-sparing drugs, potassium supplements or potassium-containing salt substitutes is generally not recommended.
Dual blockade of the renin-angiotensin-aldosterone system (RAAS):
Hypotension, syncope, stroke, hyperkalaemia, and changes in renal function (including acute renal failure) have been reported in susceptible individuals, especially if combining medicinal products that affect this system. Dual blockade of the renin-angiotensin-aldosterone system by combining an angiotensin converting enzyme inhibitor (ACEI) with an angiotensin II receptor blocker (ARB) or aliskiren is therefore not recommended.
Combination with aliskiren is contraindicated in patients with diabetes mellitus or renal impairment (GFR < 60 ml/min/1.73 m2) .
ACE inhibitors should not be initiated during pregnancy. Unless continued ACE inhibitor therapy is considered essential, patients planning pregnancy should be changed to alternative anti-hypertensive treatments which have an established safety profile for use in pregnancy. When pregnancy is diagnosed, treatment with ACE inhibitors should be stopped immediately, and, if appropriate, alternative therapy should be started.
Due to the presence of lactose, patients with rare hereditary problems of galactose intolerance, glucose-galactose malabsorption, or the Lapp lactase deficiency should not take this medicinal product.
Headache, dizziness, sleep disorders, depression, fever, nervousness, somnolence; cough, upper respiratory tract infection, sinusitis, rhinitis, pharyngitis; oedema, chest pain, abnormal ECG, palpitation; rash; hyperkalaemia, elevated triglycerides, menstrual disorder; nausea, diarrhoea, vomiting, dyspepsia, abdominal pain, flatulence: UTI, sexual dysfunction; increased LFTs; weakness, musculoskeletal pain, upper and lower extremity pain, hypertonia, paraesthesia; proteinuria; tinnitus, ear infection; viral infection, allergy.
Excessive BP reduction may occur in patients on diuretics. Increased risk of hyperkalaemia with potassium supplements, potassium-sparing diuretics,trimethoprim. May increase lithium levels/toxicity. May increase hypersensitivity reactions to allopurinol. Effects may be reduced by aspirin or other NSAIDs and/or adverse renal effects may be increased. May increase nephrotoxicity ofciclosporin. May increase the adverse/toxic effects (nitritoid reaction) of gold sodium thiomalate. Increased risk of hypoglycaemia with insulin. Increased risk of neutropenia with mercaptopurine.
Conversion to active form reduced with food. Ephedra, yohimbe and ginseng may worsen hypertension. Garlic may increase antihypertensive effect.
Pregnancy Category (FDA) and use in Specific Population
Pregnancy Category D.
Epidemiological evidence regarding the risk of teratogenicity following exposure to ACE inhibitors during the first trimester of pregnancy has not been conclusive; however a small increase in risk cannot be excluded. Unless continued ACE inhibitor therapy is considered essential, patients planning pregnancy should be changed to alternative antihypertensive treatments which have an established safety profile for use in pregnancy. When pregnancy is diagnosed, treatment with ACE inhibitors should be stopped immediately, and, if appropriate, alternative therapy should be started.
Exposure to ACE inhibitor therapy during the second and third trimesters is known to induce human foetotoxicity (decreased renal function, oligohydramnios, skull ossification retardation) and neonatal toxicity (renal failure, hypotension, hyperkalaemia) (see section 5.3). Should exposure to ACE inhibitor have occurred from the second trimester of pregnancy, ultrasound check of renal function and skull is recommended. Infants whose mothers have taken ACE inhibitors should be closely observed for hypotension (see also sections 4.3 and 4.4).
Because no information is available regarding the use of Perindopril during breast-feeding, Perindopril is not recommended and alternative treatments with better established safety profiles during breast-feeding are preferable, especially while nursing a newborn or preterm infant.
There was no effect on reproductive performance or fertility.
Mechanism of action
Perindopril is an inhibitor of the enzyme that converts angiotensin I into angiotensin II (Angiotensin Converting Enzyme ACE). The converting enzyme, or kinase, is an exopeptidase that allows conversion of angiotensin I into the vasoconstrictor angiotensin II as well as causing the degradation of the vasodilator bradykinin into an inactive heptapeptide. Inhibition of ACE results in a reduction of angiotensin II in the plasma, which leads to increased plasma renin activity (by inhibition of the negative feedback of renin release) and reduced secretion of aldosterone. Since ACE inactivates bradykinin, inhibition of ACE also results in an increased activity of circulating and local kallikrein-kinin systems (and thus also activation of the prostaglandin system). It is possible that this mechanism contributes to the blood pressure-lowering action of ACE inhibitors and is partially responsible for certain of their side effects (e.g. cough).
Perindopril acts through its active metabolite, perindoprilat. The other metabolites show no inhibition of ACE activity in vitro.
Clinical efficacy and safety
Perindopril is active in all grades of hypertension: mild, moderate, severe; a reduction in systolic and diastolic blood pressures in both supine and standing positions is observed.
Perindopril reduces peripheral vascular resistance, leading to blood pressure reduction. As a consequence, peripheral blood flow increases, with no effect on heart rate.
Renal blood flow increases as a rule, while the glomerular filtration rate (GFR) is usually unchanged.
The antihypertensive activity is maximal between 4 and 6 hours after a single dose and is sustained for at least 24 hours: trough effects are about 87-100 % of peak effects.
The decrease in blood pressure occurs rapidly. In responding patients, normalisation is achieved within a month and persists without the occurrence of tachyphylaxis.
Discontinuation of treatment does not lead to a rebound effect.
Perindopril reduces left ventricular hypertrophy.
In man, perindopril has been confirmed to demonstrate vasodilatory properties. It improves large artery elasticity and decreases the media: lumen ratio of small arteries.
An adjunctive therapy with a thiazide diuretic produces an additive-type of synergy. The combination of an ACE inhibitor and a thiazide also decreases the risk of hypokalaemia induced by the diuretic treatment.
Perindopril reduces cardiac work by a decrease in pre-load and after-load.
Studies in patients with heart failure have demonstrated:
- decreased left and right ventricular filling pressures,
- reduced total peripheral vascular resistance,
- increased cardiac output and improved cardiac index.
In comparative studies, the first administration of 2.5 mg of perindopril arginine to patients with mild to moderate heart failure was not associated with any significant reduction of blood pressure as compared to placebo.
Patients with stable coronary artery disease:
The EUROPA study was a multicentre, international, randomised, double-blind, placebo-controlled clinical trial lasting 4 years.
Twelve thousand two hundred and eighteen (12218) patients aged over 18 were randomised to 8 mg perindopril tert-butylamine (equivalent to 10 mg perindopril arginine) (n=6110) or placebo (n=6108).
The trial population had evidence of coronary artery disease with no evidence of clinical signs of heart failure. Overall, 90% of the patients had a previous myocardial infarction and/or a previous coronary revascularisation. Most of the patients received the study medication on top of conventional therapy including platelet inhibitors, lipid lowering agents and beta-blockers.
The main efficacy criterion was the composite of cardiovascular mortality, non-fatal myocardial infarction and/or cardiac arrest with successful resuscitation. The treatment with 8 mg perindopril tert-butylamine (equivalent to 10 mg perindopril arginine) once daily resulted in a significant absolute reduction in the primary endpoint of 1.9% (relative risk reduction of 20%, 95%CI [9.4; 28.6], p<0.001).
In patients with a history of myocardial infarction and/or revascularisation, an absolute reduction of 2.2% corresponding to a RRR of 22.4% (95% CI [12.0; 31.6], p<0.001) in the primary endpoint was observed by comparison to placebo.
After oral administration, the absorption of perindopril is rapid and the peak concentration is achieved within 1 hour. The plasma half-life of perindopril is equal to 1 hour.
Perindopril is a prodrug. Twenty seven percent of the administered perindopril dose reaches the bloodstream as the active metabolite perindoprilat. In addition to active perindoprilat, perindopril yields five metabolites, all inactive. The peak plasma concentration of perindoprilat is achieved within 3 to 4 hours.
As ingestion of food decreases conversion to perindoprilat, hence bioavailability, perindopril arginine should be administered orally in a single daily dose in the morning before a meal.
It has been demonstrated a linear relationship between the dose of perindopril and its plasma exposure.
The volume of distribution is approximately 0.2 l/kg for unbound perindoprilat. Protein binding of perindoprilat to plasma proteins is 20%, principally to angiotensin converting enzyme, but is concentration-dependent.
Perindoprilat is eliminated in the urine and the terminal half-life of the unbound fraction is approximately 17 hours, resulting in steady-state within 4 days.
Elimination of perindoprilat is decreased in the elderly, and also in patients with heart or renal failure. Dosage adjustment in renal insufficiency is desirable depending on the degree of impairment (creatinine clearance).
Dialysis clearance of perindoprilat is equal to 70 ml/min.
Perindopril kinetics are modified in patients with cirrhosis: hepatic clearance of the parent molecule is reduced by half. However, the quantity of perindoprilat formed is not reduced and therefore no dosage adjustment is required.
C09AA04 - perindopril; Belongs to the class of ACE inhibitors. Used in the treatment of cardiovascular disease.
Search Google: Perindopril
|Brand Name||Manufacturer/Marketer||Composition||Dosage Form||Pack Size & Price|
|COVERSYL||Servier Bangladesh Operation||Perindopril erbumine 4mg||Tablet||30's: 495.00 IP|
|PENDORIL||Renata Limited||Perindopril erbumine 2,4 & 8mg||Tablet||2mg x 10's, 4mg x 20's, 8mgx 10's: 70.20, 141.00 & 240.90 MRP|
|PERIPRIL||Incepta Pharmaceuticals Limited||Perindopril erbumine INN 4mg/tablet||Tablet||2mg x 20s pack: 140.00 MRP; 4mg x 20s pack: 240.00 MRP; 8mg x 20s pack: 480.00 MRP|
Do not take perindopril if you are pregnant. If you become pregnant while taking perindopril, call your doctor immediately. Perindopril may harm the fetus.
Why is this medication prescribed?
Perindopril is used alone or in combination with other medications to treat high blood pressure. Perindopril is in a class of medications called angiotensin-converting enzyme (ACE) inhibitors. It makes blood flow more smoothly by preventing the production of certain natural chemicals that tighten the blood vessels.
How should this medicine be used?
Perindopril comes as a tablet to take by mouth. It is usually taken once or twice a day. Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take perindopril exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor.
Your doctor may start you on a low dose of perindopril and gradually increase your dose.
Perindopril controls high blood pressure but does not cure it. Continue to take perindopril even if you feel well. Do not stop taking perindopril without talking to your doctor.
Other uses for this medicine
This medication may be prescribed for other uses; ask your doctor or pharmacist for more information.
What special precautions should I follow?Before taking perindopril,
- tell your doctor if you are allergic to perindopril, benazepril, captopril , enalapril, fosinopril, lisinopril , moexipril, quinapril, ramipril, trandolapril, or any other medications.
- tell your doctor if you have diabetes (high blood sugar) and you are taking aliskiren. Your doctor will probably tell you not to take perindopril if you have diabetes and you are also taking aliskiren.
- tell your doctor and pharmacist what prescription and nonprescription medications, vitamins, nutritional supplements, and herbal products you are taking. Be sure to mention any of the following: cyclosporine (Neoral, Sandimmune), diuretics, heparin, indomethacin, lithium, and potassium supplements. Your doctor may need to change the doses of your medications or monitor you carefully for side effects.
- tell your doctor if you are on dialysis and if have or have ever had heart failure; lupus (SLE); scleroderma; diabetes; swelling of the face, throat, tongue, lips, eyes, hands, feet, ankles, and/or lower legs (angioedema); or kidney or liver disease.
- tell your doctor if you plan to become pregnant or are breast-feeding.
- you should know that diarrhea, vomiting, not drinking enough fluids, and sweating a lot can cause a drop in blood pressure, which may cause light-headedness and fainting.
What special dietary instructions should I follow?
Talk to your doctor before using salt substitutes containing potassium. If your doctor prescribes a low-salt or low-sodium diet, follow these directions carefully.
What should I do if I forget a dose?
Take the missed dose as soon as you remember it. However, if it is almost time for the next dose, skip the missed dose and continue your regular dosing schedule. Do not take a double dose to make up for a missed one.
What side effects can this medication cause?Perindopril may cause side effects. Tell your doctor if any of these symptoms are severe or do not go away:
swelling of the face, throat, tongue, lips, eyes, hands, feet, ankles, or lower legs
difficulty swallowing or breathing
fever, sore throat, chills, and other signs of infection
irregular or rapid heartbeats
Perindopril may cause other side effects. Consult your doctor if you have any unusual problems while taking this medication.
What storage conditions are needed for this medicine?
Keep this medication in the container it came in, tightly closed, and out of reach of children. Store it at room temperature and away from excess heat and moisture (not in the bathroom). Throw away any medication that is outdated or no longer needed. Talk to your pharmacist about the proper disposal of your medication. It is important for you to keep a written list of all of the prescription and nonprescription (over-the-counter) medicines you are taking, as well as any products such as vitamins, minerals, or other dietary supplements. You should bring this list with you each time you visit a doctor or if you are admitted to a hospital. It is also important information to carry with you in case of emergencies.
Ref: U.S. Natl. Library of Medicine
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