This case highlights the potential for severe amiodarone-induced pulmonary toxicity in patients treated for atrial fibrillation, emphasizing the need for clinical vigilance.
APT diagnosis requires exclusion of alternatives; extends sparse case reports but leaves open need for validated criteria.
Amiodarone, a primarily class III antiarrhythmic drug is one of the most commonly used drug in atrial fibrillation. A possible rare side effect of amiodarone treatment is to develop a diffuse parenchymal lung disorder - amiodarone pulmonary toxicity (APT). There is no pathognomonic findings to diagnose APT. A 64-year-old patient with multiple comorbidities presented in our hospital with worsening a five-month history of grade 3 mMRC dyspnea, wheezing, frequent nonproductive cough, fatigue. She has a medical history of atrial fibrillation in treatment with amiodarone 400mg/day for 2 years. Her oxygen saturation was 90% on room air, chest radiography showed disseminated lung irregular opacities with a tendency to confluence in right and left lung and chest computed tomography scan showed asymmetric centrilobular nodules and asymmetrical areas of dense ground glass opacity with few consolidation. Amiodarone pulmonary toxicity was suspected, the drug was stopped and treatment with methylprednisolone started. Worsening and progression of the disease can still be noted despite stopping amiodarone because of the long persistence and elimination of the drug, with the tendency to concentrate in tissues, such as lung. In our patient case the evolution and prognosis were good even the case illustrates neglected effects of amiodarone, potential severe one.
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Mitrofan et al. (2022) studied this question.
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