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Original Research: Carotid intima-media thickness and plaque volume changes following 2-year angiotensin II-receptor blockade. The Multicentre Olmesartan atherosclerosis Regression Evaluation (MORE) study

University of Bonn, Centre of Preventive Medicine, Herwarthstraße 36, D-53115 Bonn, Germany, stumpe{at}uni-bonn.de

Enrico Agabiti-Rosei

Department of Medical and Surgical Sciences, University of Brescia, Brescia, Italy

Tomasz Zielinski

Klinika Niewydolnosci Serca i Transplantologii, Instytut Kardiologii, Warszawa, Poland

Dieter Schremmer

GKM Gesellschaft für Therapieforschung mbH, Munich, Germany

Jürgen Scholze

Medizinische Poliklinik, Charité-Universitätsmedizin, Berlin, Germany

Petra Laeis

Daiichi Sankyo Europe GmbH, Munich, Germany

Peter Schwandt

Institute for Atherosclerosis Prevention, Munich, Germany

Malte Ludwig

University of Bonn, Benediktus Krankenhaus, Tutzing, Germany

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 ( ) in CC-IMT assessed by 2D US. Secondary outcomes included PV assessed by 3D US and blood pressure (BP).

Results Olmesartan and atenolo produced comparable significant reductions in CC-IMT; mean IMT (SEM) was -0.090 (0.015) mm for oLmesartan and -0.082 (0.014) mm for atenolol. Mean PV was -4.4 (2.3) µl and 0.1 (1.5) µl in the olmesartan and atenolol treated subjects, respectively, without significant between-treatment differences. In the subgroup of patients with baseLine PV median (33.7 µl), significant between-treatment differences existed in PV (p = 0.023), because PV regressed significantly with olmesartan ( PV: -11.5 (4.4) µl) but not with atenolol ( PV: 0.6 (2.5) µl). 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.

Key Words: carotid arteries • atherosclerosis • hypertension • olmesartan • atenolol

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