ter authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard.
4.9 Overdose
Symptoms:
There is no experience of overdose with Sevikar. The most likely effects of olmesartan medoxomil overdosage are hypotension and tachycardia; bradycardia could be encountered if parasympathetic (vagal) stimulation occurred. Amlodipine overdosage can be expected to lead to excessive peripheral vasodilatation with marked hypotension and possibly a reflex tachycardia. Marked and potentially prolonged systemic hypotension up to and including shock with fatal outcome has been reported.
Treatment:
If intake is recent, gastric lavage may be considered. In healthy subjects, the administration of activated charcoal immediately or up to 2 hours after ingestion of amlodipine has been shown to reduce substantially the absorption of amlodipine.
Clinically significant hypotension due to an overdose of Sevikar requires active support of the cardiovascular system, including close monitoring of heart and lung function, elevation of the extremities, and attention to circulating fluid volume and urine output. A vasoconstrictor may be helpful in restoring vascular tone and blood pressure, provided that there is no contraindication to its use. Intravenous calcium gluconate may be beneficial in reversing the effects of calcium channel blockade.
Since amlodipine is highly protein-bound, dialysis is not likely to be of benefit. The dialysability of olmesartan is unknown.
5. Pharmacological properties
5.1 Pharmacodynamic properties
Pharmacotherapeutic group: Angiotensin II antagonists and calcium channel blockers, ATC code C09DB02.
Mechanism of action
Sevikar is a combination of an angiotensin II receptor antagonist, olmesartan medoxomil, and a calcium channel blocker, amlodipine besilate. The combination of these active ingredients has an additive antihypertensive effect, reducing blood pressure to a greater degree than either component alone.
Clinical efficacy and safety
Sevikar
In an 8-week, double-blind, randomised, placebo-controlled factorial design study in 1940 patients (71% Caucasian and 29% non-Caucasian patients), treatment with each combination dose of Sevikar resulted in significantly greater reductions in diastolic and systolic blood pressures than the respective monotherapy components. The mean change in systolic/diastolic blood pressure was dose-dependent: -24/-14 mmHg (20 mg/5 mg combination), -25/-16 mmHg (40 mg/5 mg combination) and -30/-19 mmHg (40 mg/10 mg combination).
Sevikar 40 mg/5 mg reduced seated systolic/diastolic blood pressure by an additional 2.5/1.7 mmHg over Sevikar 20 mg/5 mg. Similarly Sevikar 40 mg/10 mg reduced seated systolic/diastolic blood pressure by an additional 4.7/3.5 mmHg over Sevikar 40 mg/5 mg.
The proportions of patients reaching blood pressure goal (< 140/90 mmHg for non-diabetic patients and < 130/80 mmHg for diabetic patients) were 42.5%, 51.0% and 49.1% for Sevikar 20 mg/5 mg, 40 mg/5 mg and 40 mg/10 mg respectively.
The majority of the antihypertensive effect of Sevikar was generally achieved within the first 2 weeks of therapy.
A second double-blind, randomised, placebo-controlled study eva luated the effectiveness of adding amlodipine to the treatme |
