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
