nt in Caucasian patients whose blood pressure was inadequately controlled by 8 weeks of monotherapy with 20 mg olmesartan medoxomil.
In patients who continued to receive only 20 mg olmesartan medoxomil, systolic/diastolic blood pressure was reduced by -10.6/ -7.8 mmHg after a further 8 weeks. The addition of 5 mg amlodipine for 8 weeks resulted in a reduction in systolic/diastolic blood pressure of -16.2/-10.6 mmHg (p = 0.0006).
The proportion of patients reaching blood pressure goal (< 140/90 mmHg for non-diabetic patients and < 130/80 mmHg for diabetic patients) was 44.5% for the 20 mg/5 mg combination compared to 28.5% for 20 mg olmesartan medoxomil.
A further study eva luated the addition of various doses of olmesartan medoxomil in Caucasian patients whose blood pressure was not adequately controlled by 8 weeks of monotherapy with 5 mg amlodipine.
In patients who continued to receive only 5 mg amlodipine, systolic/diastolic blood pressure was reduced by -9.9/ -5.7 mmHg after a further 8 weeks. The addition of 20 mg olmesartan medoxomil resulted in a reduction in systolic/diastolic blood pressure of -15.3/-9.3 mmHg and the addition of 40 mg olmesartan medoxomil resulted in a reduction in systolic/diastolic blood pressure of -16.7/-9.5 mmHg (p < 0.0001).
The proportions of patients reaching blood pressure goal (< 140/90 mmHg for non-diabetic patients and < 130/80 mmHg for diabetic patients) was 29.9% for the group who continued to receive 5 mg amlodipine alone, 53.5% for Sevikar 20 mg/5 mg and 50.5% for Sevikar 40 mg/5 mg.
Randomised data in uncontrolled hypertensive patients, comparing the use of medium dose Sevikar combination therapy versus escalation to top dose monotherapy of amlodipine or olmesartan, are not available.
The three studies performed confirmed that the blood pressure lowering effect of Sevikar once daily was maintained throughout the 24-hour dose interval, with trough-to-peak ratios of 71% to 82% for systolic and diastolic response and with 24-hour effectiveness being confirmed by ambulatory blood pressure monitoring.
The antihypertensive effect of Sevikar was similar irrespective of age and gender, and was similar in patients with and without diabetes.
In two open-label, non-randomised extension studies, sustained efficacy using Sevikar 40 mg/5 mg was demonstrated at one year for 49 - 67% of patients.
Olmesartan medoxomil (active ingredient of Sevikar)
The olmesartan medoxomil component of Sevikar is a selective angiotensin II type 1 (AT1) receptor antagonist. Olmesartan medoxomil is rapidly converted to the pharmacologically active metabolite, olmesartan. Angiotensin II is the primary vasoactive hormone of the renin-angiotensin-aldosterone system and plays a significant role in the pathophysiology of hypertension. The effects of angiotensin II include vasoconstriction, stimulation of the synthesis and release of aldosterone, cardiac stimulation and renal reabsorption of sodium. Olmesartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by blocking its binding to the AT1 receptor in tissues including vascular smooth muscle and the adrenal gland. The action of olmesartan is independent of the source or route of synthesis of angiotensin II. The selective antagonism of the angiotensin II (AT1) receptors by olmesartan results in increases in plasma renin levels and angiotensin I and II concentrations, and some decrease in plasma aldosterone concentrations.
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