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

Author:

Stumpe Klaus O.1,Agabiti-Rosei Enrico2,Zielinski Tomasz3,Schremmer Dieter4,Scholze Jürgen5,Laeis Petra6,Schwandt Peter7,Ludwig Malte8

Affiliation:

1. University of Bonn, Centre of Preventive Medicine, Herwarthstraße 36, D-53115 Bonn, Germany,

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

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

4. GKM Gesellschaft für Therapieforschung mbH, Munich, Germany

5. Medizinische Poliklinik, Charité-Universitätsmedizin, Berlin, Germany

6. Daiichi Sankyo Europe GmbH, Munich, Germany

7. Institute for Atherosclerosis Prevention, Munich, Germany

8. University of Bonn, Benediktus Krankenhaus, Tutzing, Germany

Abstract

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 ( Δ) in CC-IMT assessed by 2D US. Secondary outcomes included Δ PV assessed by 3D US and blood pressure (BP). Results Olmesartan and atenolo produced comparable significant reductions in CC-IMT; mean Δ IMT (SEM) was -0.090 (0.015) mm for oLmesartan and -0.082 (0.014) mm for atenolol. Mean Δ 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 Δ PV ( p = 0 .023), because PV regressed significantly with olmesartan ( Δ PV: -11.5 (4.4) µl) but not with atenolol ( Δ 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.

Publisher

SAGE Publications

Subject

Pharmacology (medical),Cardiology and Cardiovascular Medicine

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