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Comparative Study
Journal Article
Multicenter Study
Randomized Controlled Trial
Carotid intima-media thickness and plaque volume changes following 2-year angiotensin II-receptor blockade. The Multicentre Olmesartan atherosclerosis Regression Evaluation (MORE) study.
Therapeutic Advances in Cardiovascular Disease 2007 December
OBJECTIVE: The Multicentre Olmesartan atherosclerosis Regression Evaluation (MORE) study was a double-blind trial in patients with hypertension at increased cardiovascular risk with carotid wall thickening and a defined atherosclerotic plaque that used non-invasive 2- and 3-dimensionaL (D) ultrasound (US), to compare the effects of a 2-year treatment based on either olmesartan medoxomil or atenolol on common carotid (CC) intima-media thickness (IMT) and plaque volume (PV).
METHODS: A total of 165 patients (with systolic/diastolic blood pressure 140-180/ 90-105 mmHg) were randomized to receive either olmesartan (20-40 mg/day) or atenolol (50-100 mg/day). US was performed at baseline and 28, 52 and 104 weeks. The primary efficacy outcome was the change from baseline ( Delta) in CC-IMT assessed by 2D US. Secondary outcomes included Delta PV assessed by 3D US and blood pressure (BP).
RESULTS: Olmesartan and atenolo produced comparable significant reductions in CC-IMT; mean Delta IMT (SEM) was -0.090 (0.015) mm for oLmesartan and -0.082 (0.014) mm for atenolol. Mean Delta PV was -4.4 (2.3) microl and 0.1 (1.5) microl in the olmesartan and atenolol treated subjects, respectively, without significant between-treatment differences. In the subgroup of patients with baseLine PV > or = median (33.7 microl), significant between-treatment differences existed in Delta PV (p = 0.023), because PV regressed significantly with olmesartan (Delta PV: -11.5 (4.4) microl) but not with atenolol ( Delta PV: 0.6 (2.5) microl). In these patients BP reductions were comparabLe.
CONCLUSIONS: Carotid IMT and BP decreased similarly with olmesartan and atenolol, but only olmesartan reduced the volume of larger atherosclerotic plaques.
METHODS: A total of 165 patients (with systolic/diastolic blood pressure 140-180/ 90-105 mmHg) were randomized to receive either olmesartan (20-40 mg/day) or atenolol (50-100 mg/day). US was performed at baseline and 28, 52 and 104 weeks. The primary efficacy outcome was the change from baseline ( Delta) in CC-IMT assessed by 2D US. Secondary outcomes included Delta PV assessed by 3D US and blood pressure (BP).
RESULTS: Olmesartan and atenolo produced comparable significant reductions in CC-IMT; mean Delta IMT (SEM) was -0.090 (0.015) mm for oLmesartan and -0.082 (0.014) mm for atenolol. Mean Delta PV was -4.4 (2.3) microl and 0.1 (1.5) microl in the olmesartan and atenolol treated subjects, respectively, without significant between-treatment differences. In the subgroup of patients with baseLine PV > or = median (33.7 microl), significant between-treatment differences existed in Delta PV (p = 0.023), because PV regressed significantly with olmesartan (Delta PV: -11.5 (4.4) microl) but not with atenolol ( Delta PV: 0.6 (2.5) microl). In these patients BP reductions were comparabLe.
CONCLUSIONS: Carotid IMT and BP decreased similarly with olmesartan and atenolol, but only olmesartan reduced the volume of larger atherosclerotic plaques.
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