Symptomatic heart failure

Active Ingredient: Perindopril

Indication for Perindopril

Population group: only adults (18 years old or older)
Therapeutic intent: Curative procedure

For this indication, competent medicine agencies globally authorize below treatments:

2.5 mg once daily for 2 weeks and thereafter 2.5-5 mg once daily

For:

Dosage regimens

Oral, 2.5 milligrams perindopril, once daily at morning, over the duration of 2 weeks. Afterwards, oral, between 2.5 milligrams perindopril and 5 milligrams perindopril, once daily at morning, over the duration of 2 weeks.

Detailed description

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.

Dosage considerations

It is recommended to be taken once daily in the morning before a meal.

Active ingredient

Perindopril

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).

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