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Clinical features of and effects of angiotensin system antagonists on amiodarone-induced pulmonary toxicity.

Abstract：

BACKGROUND:Amiodarone (AMD) is a strong antiarrhythmic drug but has severe side effects such as pulmonary toxicity. There are no indicators or drugs that can prevent the development of amiodarone-induced pulmonary toxicity (AIPT). METHODS:We collected data for 96 consecutive patients treated with AMD and analyzed clinical factors related to AIPT. In addition, we examined the effect of AMD and angiotensin II (Ang II) on human lung alveolar epithelial cells (AEC) and verified the protective efficacy of an Ang II type 1 receptor blocker (ARB) in vitro. RESULTS:During a follow-up period of 33.8+/-34.6 months, AIPT developed in 11 patients (11.5%). There were no differences in the dose of AMD, left ventricular ejection fraction, serum KL-6 and %DLCO level before starting AMD between patients with and those without AIPT. However, repeated episodes of congestive heart failure (CHF) were observed more frequently in patients with AIPT than in patients without AIPT (81.8% vs. 41.2%, P<0.011). In vitro examination, AMD progressively increased apoptosis of AEC and Ang II enhanced this effect of AMD (P<0.001). However, ARB inhibited the enhancement by Ang II of the AMD-induced apoptosis effect (P<0.001). Furthermore, patients with AIPT were administrated a lower dose of angiotensin system antagonists than were those without AIPT (P<0.05). CONCLUSIONS:The results indicate that Ang II induced by CHF increases the risk of AMD-induced pulmonary toxicity. An angiotensin-converting enzyme inhibitor or ARB should be given at a sufficient dose during AMD treatment.

journal_name

Int J Cardiol

journal_title

International journal of cardiology

authors

Nikaido A,Tada T,Nakamura K,Murakami M,Banba K,Nishii N,Fuke S,Nagase S,Sakuragi S,Morita H,Ohe T,Kusano KF

doi

10.1016/j.ijcard.2008.11.106

subject

Has Abstract

pub_date

2010-04-30 00:00:00

pages

328-35

issue

3

eissn

0167-5273

issn

1874-1754

pii

S0167-5273(08)01270-9

journal_volume

140

pub_type

杂志文章

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