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Abstract: Slide Presentations |

REDUCTION OF AMIODARONE PULMONARY TOXICITY IN PATIENTS TREATED WITH ANGIOTENSIN CONVERTING ENZYME INHIBITORS AND ANGIOTENSIN RECEPTOR BLOCKERS FREE TO VIEW

Semaan G. Kosseifi, MD*; Ahmad Halawa, MD; Beth Bailey, PhD; Melinda Micklewright, RPh; Thomas Roy, MD; Ryland R. Byrd, MD
Author and Funding Information

East Tennessee State University, Johnson City, TN


Chest


Chest. 2007;132(4_MeetingAbstracts):457b-458. doi:10.1378/chest.132.4_MeetingAbstracts.457b
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Abstract

PURPOSE: Amiodarone is a widely used anti-arrhythmic medication. Its utility is, however, limited by adverse side effects. The mechanism of amiodarone toxicity in the lungs is attributed primarily to stimulation of the angiotensin enzyme leading to lung cell apoptosis and subsequent cell death. This mechanism has been demonstrated in vitro experimentation and in animal studies. To date, however, no in vivo human studies have confirmed this mechanism for amiodarone pulmonary toxicity. This study was undertaken to determine whether angiotensin converting enzyme inhibitor (ACE-I) or angiotensin receptor blockers (ARB) offer a protective effects against amiodarone-induced pulmonary toxicity in humans. Demonstration of a protective effect of an ACE-I or ARB would suggest that stimulation of the angiotensin enzyme is a key process in amiodarone-induced toxicity in humans.

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

RESULTS: A total of 895 patients on amiodarone were identified. Five hundred-thirty-three patients were simultaneously on an ACE-I or ARB. The remaining 362 patients were not. The pulmonary toxicity rate attributed to amiodarone was 3.5% for the entire patient sample. Amiodarone-induced pulmonary toxicity occurred in 2.6% (n=14) of patients on an ACE-I or ARB and in 4.7% (n=17) of patients not taking an ACE-I or ARB. This observed difference in pulmonary toxicity rates was statistically significant (χ2=2.76, p<0.05).

CONCLUSION: The concomitant use of ACE-I or ARB in patients on amiodarone appears to offer a protective effect against amiodarone-induced pulmonary toxicity. This observation suggests stimulation of the angiotensin enzyme may play an important role in amiodarone-induced pulmonary toxicity in humans.

CLINICAL IMPLICATIONS: This retrospective analysis suggests that placing patients on an ACE-I or an ARB may offer a protection from amiodarone-induced pulmonary toxicity. The exact clinical significance of this obseravtion, however, requires further study.

DISCLOSURE: Semaan Kosseifi, No Financial Disclosure Information; No Product/Research Disclosure Information

Tuesday, October 23, 2007

10:30 AM - 12:00 PM


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