Back to Journals » Clinical Pharmacology: Advances and Applications » Volume 7

Addition of a renin-angiotensin-aldosterone system inhibitor to a calcium channel blocker ameliorates arterial stiffness

Authors Kiuchi S, Hisatake S, Kawasaki M, Hirashima O, Kabuki T, Yamazaki J, Ikeda T

Received 30 January 2015

Accepted for publication 14 May 2015

Published 8 October 2015 Volume 2015:7 Pages 97—102

DOI https://doi.org/10.2147/CPAA.S81880

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Professor Arthur Frankel


Shunsuke Kiuchi,1 Shinji Hisatake,1 Muneyasu Kawasaki,2 Osamu Hirashima,2 Takayuki Kabuki,1 Junichi Yamazaki,1 Takanori Ikeda1

1Department of Cardiovascular Medicine, Toho University Faculty of Medicine, Tokyo, 2Division of Cardiology and Cardiovascular Surgery, Misato Central General Hospital, Saitama, Japan


Background: The aim of controlling hypertension is to protect against arteriosclerosis. Calcium channel blockers (CCBs) and renin-angiotensin-aldosterone system (RAAS) inhibitors have been reported to have antihypertensive effects, but their effect on the progression of arteriosclerosis is not fully understood. The cardio-ankle vascular index (CAVI) was developed to estimate arterial stiffness, which reflects arteriosclerosis. In this study, we investigated the longer term effects of CCBs and RAAS inhibitors on the progression of arteriosclerosis by monitoring the CAVI.
Methods: Our subjects were 115 consecutive, non-smoking hypertensive patients on oral treatment with a CCB and/or RAAS inhibitor for at least 3 years in whom the CAVI was measured on two occasions approximately 1 year apart during the period from January 2009 to December 2011. Changes in CAVI were evaluated in patients administered a CCB alone (group C), an RAAS inhibitor (group R) alone, or both drugs together (group B). Changes in laboratory findings, blood pressure, and ankle-brachial index were similarly evaluated.
Results: No significant change in laboratory findings, blood pressure, or ankle-brachial index was noted in any of the groups. The CAVI decreased slightly in group R (first recording 8.80±1.03, second recording 8.57±0.97, P=0.517) and increased significantly in group C (first 8.45±0.92, second 8.95±1.04, P=0.038), but showed no significant change in group B (first 9.01±1.26, second 9.05±1.35, P=0.851).
Conclusion: Long-term administration of a CCB alone increased the CAVI, but this effect was offset by the concomitant use of a RAAS inhibitor, indicating that a RAAS inhibitor might protect against arteriosclerosis.

Keywords: cardio-ankle vascular index, renin-angiotensin-aldosterone system inhibitor, calcium channel blocker

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]