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Pneumologie 2002; 56(1): 31-35
DOI: 10.1055/s-2002-19567
Kasuistik
Georg Thieme Verlag Stuttgart · New York

Amiodaron-induzierte Pneumonitis bei dilatativer Kardiomyopathie

Amiodarone Induced Pulmonary ToxicityP.  Alter1 , W.  Grimm1 , B.  Maisch1
  • 1Zentrum für Innere Medizin - Kardiologie, Philipps-Universität Marburg/Lahn
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Publication History

Publication Date:
16 January 2002 (online)

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Zusammenfassung

Hintergrund: Amiodaron (Cordarex®) ist ein Klasse-III-Antiarrhythmikum, das zur Behandlung von ventrikulären und supraventrikulären Tachykardien eingesetzt wird. Eine seltene, aber potentiell lebensbedrohliche Nebenwirkung von Amiodaron ist die pulmonale Toxizität, die zur Lungenfibrose führen kann. Kasuistik: Wir berichten über zwei Patienten mit dilatativer Kardiomyopathie (DCM), die wegen symptomatischer nicht anhaltender Kammertachykardien bzw. anhaltender Kammertachykardien mit Amiodaron behandelt wurden. Nach 6 Wochen bzw. 8 Monaten Behandlungsdauer entwickelten beide Patienten eine Amiodaron-induzierte Pneumonitis mit progredienter Dyspnoe. Andere Ursachen für eine Pneumonitis wurden bei beiden Patienten mittels Bronchoskopie, broncho-alveolärer Lavage und transbronchialer Biopsie ausgeschlossen. In beiden Fällen waren die Lungenveränderungen nach Absetzen der Amiodarontherapie weitgehend reversibel. Schlussfolgerungen: Amiodaron-induzierte Lungenveränderungen sind seltene, aber möglicherweise lebensbedrohliche Komplikationen dieser Therapie. Bei Patienten mit DCM und fortgeschrittener Herzinsuffizienz sind Amiodaron-induzierte Lungenveränderungen klinisch nur schwer zu erkennen, da die Symptome kaum von einer Progredienz der Herzinsuffizienz zu unterscheiden sind. Bei einer Verschlechterung der regelmäßig zu kontrollierenden Lungendiffusionskapazität sollten weiterführende diagnostische Maßnahmen einschließlich Bronchoskopie mit broncho-alveolärer Lavage und Biopsie durchgeführt werden.

Abstract

Background: Antiarrhythmic therapy with class III drug amiodarone (Cordarex®) 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. Case report: 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. Conclusions: 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.

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Dr. med. P. Alter

Philipps-Universität Marburg/Lahn
Klinik für Innere Medizin - Kardiologie

Baldingerstraße

35033 Marburg

Email: alter@mailer.uni-marburg.de

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