[Amiodarone induced pulmonary toxicity]

Antiarrhythmic therapy with class III drug amiodarone (Cordarex(R)) for supraventricular and ventricular tachycardia is commonly used because of its high efficacy and absent negative inotropy. Pulmonary toxicity of amiodarone possibly leading to lung fibrosis is a rare, but severe side effect of chronic therapy. In contrast to patients with coronary artery disease, there are only a few data about pulmonary toxicity in patients with dilated cardiomyopathy.

We report on two patients with dilated cardiomyopathy who received amiodarone because of symptomatic non-sustained or sustained ventricular tachycardia. After 6 weeks resp. 8 months of treatment with amiodarone both patients developed pulmonary toxicity. Other causes of pulmonary toxicity were ruled out by bronchoscopy, bronchoalveolar lavage and biopsy. Pulmonary function improved in both patients within some weeks after discontinuation of amiodarone.

This report deals with two cases of amiodarone induced pulmonary toxicity in dilated cardiomyopathy leading to respiratory insufficiency. Pulmonary toxicity is a rare, but potentially lethal side effect of amiodarone. Reversibility of pulmonary changes in case of an early drug discontinuation is shown. Because of severe reduced left ventricular function in dilated cardiomyopathy, heart failure symptoms could conceal clinical signs of pulmonary amiodarone toxicity. Therefore, pulmonary function should be controlled periodically during amiodarone therapy including bronchoscopy, bronchoalveolar lavage, biopsy and measurement of diffusion capacity.