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Reduction of amiodarone pulmonary toxicity in patients treated with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers

¹ Division of Pulmonary Diseases and Critical Care Medicine, East Tennessee State University, Johnson City, TN, USA
² Department of Internal Medicine, East Tennessee, State University, Johnson City, TN USA
³ Department of Family Medicine, East Tennessee, State University, Johnson City, TN, USA
⁴ The Veterans Affairs Medical Center, Mountain Home, TN, USA and Dept. of Pharmacy, Johnson City, TN USA
⁵ The Veterans Affairs Medical Center, Mountain Home, TN, USA; and Division of Pulmonary Diseases and Critical Care Medicine, Johnson City, TN USA

^* To whom correspondence should be addressed. E-mail: Ryland.Byrd{at}va.gov.

	Abstract

Background: Amiodarone (AM) is a widely used anti-arrhythmic medication. Its utility is, however, limited by adverse side effects. The mechanism of amiodarone-induced toxicity (APT) in the lungs is attributed primarily to stimulation of the angiotensin enzyme system leading to lung cell apoptosis and cell death. This mechanism has been demonstrated by in vitro and in vivo experimental animal studies. To date, however, no in vivo human studies have confirmed this mechanism for APT.

Purpose: This study was undertaken to determine whether angiotensin converting enzyme inhibitors (ACE-I) or angiotensin receptor blockers (ARB) offer a protective effect against APT in humans. Demonstration of a protective effect of an ACE-I or ARB would suggest that stimulation of the angiotensin enzyme system may be a key process in APT.

Design: An 8-year retrospective analysis of all patients on AM therapy at the James H. Quillen Veterans Affairs Medical Center was undertaken.

Results: A total of 1000 patients on AM were identified. One-hundred-and-seventeen were excluded from the study. Five-hundred-and-twenty-four patients were simultaneously on an ACE-I or ARB. The remaining 359 patients were not. Pulmonary toxicity attributed to AM was identified in five and 14 patients with and without concomitant ACE-I or ARB therapy, respectively. The APT rate for the entire patient sample was 2.2%. APT occurred in 1% of patients on an ACE-I or ARB and in 3.9% of patients not taking an ACE-I or ARB. This observed difference in percentage of APT was statistically significant.

Conclusion: The concomitant use of ACE-I or ARB in patients taking AM appears to offer a protective effect against APT. This observation suggests that the stimulation of the angiotensin enzyme system may play an important role in APT in humans.

First published on October 22, 2009, doi:10.1177/1753465809348015

Therapeutic Advances in Respiratory Disease 2009;3:289.

A more recent version of this article appeared on December 1, 2009


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