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Author Notes:

ADDRESS FOR CORRESPONDENCE: Ronnie Ramadan, MD, Division of Cardiology, Department of Medicine, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, 1462 Clifton Rd. NE, Suite 507, Atlanta, GA 30322, Tel: (404) 727-3655, Fax: (404) 712-8785, rramadan@bidmc.harvard.edu

Conflicts of Interest: none declared.

Subjects:

Research Funding:

The work was supported by an investigator initiated research grant from Novartis, and supported by the National Center for Advancing Translational Sciences of the National Institutes of Health under Award Number UL1TR000454.

The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Cardiac & Cardiovascular Systems
  • Cardiovascular System & Cardiology
  • INTIMA-MEDIA THICKNESS
  • CARDIOVASCULAR MAGNETIC-RESONANCE
  • OXIDATIVE STRESS
  • HYPERTENSIVE PATIENTS
  • CORONARY ATHEROSCLEROSIS
  • MYOCARDIAL-INFARCTION
  • PLAQUE BURDEN
  • HEART-FAILURE
  • RISK-FACTORS
  • PART I

Effect of Angiotensin II Type I Receptor Blockade with Valsartan on Carotid Artery Atherosclerosis: A Double Blind Randomized Clinical Trial Comparing Valsartan and Placebo (EFFERVESCENT)

Tools:

Journal Title:

American Heart Journal

Volume:

Volume 174

Publisher:

, Pages 68-79

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Background Progression of atherosclerosis is associated with a greater risk for adverse outcomes. Angiotensin II plays a key role in the pathogenesis and progression of atherosclerosis. We aimed to investigate the effects of angiotensin II type-1 receptor blockade with Valsartan on carotid wall atherosclerosis, with the hypothesis that Valsartan will reduce progression of atherosclerosis. Methods Subjects (n = 120) with carotid intima-media thickness >0.65 mm by ultrasound were randomized (2:1) in a double-blind manner to receive either Valsartan or placebo for 2 years. Bilateral T2-weighted black-blood carotid magnetic resonance imaging was performed at baseline, 12 and 24 months. Changes in the carotid bulb vessel wall area and wall thickness were primary endpoints. Secondary endpoints included changes in carotid plaque thickness, plasma levels of aminothiols, C-reactive protein, fibrinogen, and endothelium-dependent and -independent vascular function. Results Over 2 years, the carotid bulb vessel wall area decreased with Valsartan (-6.7, 95% CI [-11.6, -1.9] mm2) but not with placebo (3.4, 95% CI [-2.8, 9.6] mm2), P =.01 between groups. Similarly, mean wall thickness decreased with Valsartan (-0.18, 95% CI [-0.30, -0.06] mm), but not with placebo (0.08, 95% CI [-0.07, 0.23] mm), P =.009 between groups. Furthermore, plaque thickness decreased with Valsartan (-0.35, 95% CI [-0.63, -0.08] mm) but was unchanged with placebo (+0.28, 95% CI [-0.11, 0.69] mm), P =.01 between groups. These findings were unaffected by statin therapy or changes in blood pressure. Notably, there were significant improvements in the aminothiol cysteineglutathione disulfide, and trends to improvements in fibrinogen levels and endothelium-independent vascular function. Conclusions In subjects with carotid wall thickening, angiotensin II type-1 receptor blockade was associated with regression in carotid atherosclerosis. Whether these effects translate into improved outcomes in subjects with subclinical atherosclerosis warrants investigation.

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© 2016 Elsevier Inc. All rights reserved.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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