C42-45 The Unusual Suspects: Identifying Cardiac Medication-related Causes of Drug-induced Pneumonitis

Abstract Introduction Amiodarone is an antiarrhythmic associated with well-known pulmonary toxicity. While less common, other cardiac medications have the potential to cause devastating lung injury. Case A 70-year-old male patient with past medical history including atrial fibrillation on amiodarone, tobacco use (50 pack years), and coronary artery disease (CAD) presented with acute onset hypoxic respiratory failure. The patient was recently hospitalized for syncope and falls, with cardiac workup revealing obstructive CAD. As part of his workup, a baseline CT chest was obtained (Fig 1A). He underwent drug-eluting stent placement (zotarolimus) to the left anterior descending coronary artery, was started on aspirin and clopidogrel, and discharged on room air. He was re-admitted the same day for hypoxia with rapid escalation to 10L nasal cannula. Imaging on admission was significant for acute diffuse bilateral ground-glass opacities with septal thickening and small pleural effusions (Fig 1B). The patient was empirically treated with broad spectrum antibiotics, high dose steroids, and diuresis. Amiodarone and clopidogrel were discontinued. He initially improved with escalating steroid doses, but ultimately required intubation for worsening respiratory status. The subsequent hospital course was complicated by acute respiratory distress syndrome (ARDS), ventilator-associated pneumonia, pneumomediastinum, and septic shock. Despite pulse dose steroids, the patient developed progressive respiratory failure with imaging showing persistent diffuse opacities (Fig 1C). He was ultimately unable to wean from the ventilator and expired from respiratory failure. Autopsy revealed severe diffuse alveolar damage, diffuse intra-alveolar proliferation of myofibroblasts with multifocal hyaline membranes, and negative staining for viral, fungal, or acid-fast organisms. Pulmonary edema was also noted. Lipid laden macrophages, which can be associated with amiodarone toxicity, were found in sparse amounts. Discussion Differential etiologies include drug-induced pneumonitis, acute interstitial pneumonia, or early interstitial lung disease. Of the patient’s medications, amiodarone, mTOR inhibitors eluted by stents, and clopidogrel have been associated with drug-induced pneumonitis. Temporally, the onset of rapidly progressive symptoms occurred 2 months after initiation of amiodarone and 3 days following percutaneous coronary intervention and initiation of clopidogrel. While the cause of this patient’s lung injury cannot be definitively determined, this case serves to highlight multiple common cardiac medications other than amiodarone with potential pneumotoxic complications. Figure 1: CT imaging over patient’s hospital course. A) Prior to left heart catheterization. B) 3 days after percutaneous intervention, when the patient became acutely hypoxic on hospital discharge and was readmitted with escalating oxygen requirements. C) Progression of extensive bilateral ground-glass opacities, ARDS. This abstract is funded by: None