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Early-Onset Amiodarone Pulmonary Toxicity at a Standard Maintenance Dose Masquerading as Decompensated Heart Failure:
M Nour Chabalout1, Afnan Chaudhry2, Ibrahim Inanc1
1Internal Medicine, Tower Health Medical Group, Phoenixville, USA.
Abstract:
Amiodarone is a widely used antiarrhythmic agent. Pulmonary toxicity is its most feared non-cardiac complication and is classically associated with high doses and prolonged duration of therapy. We report a case of early-onset amiodarone pulmonary toxicity (APT) developing after approximately one month of standard-dose amiodarone therapy (400 mg/day) in the setting of concurrent decompensated heart failure with preserved ejection fraction (HFpEF), which substantially complicated the diagnostic evaluation. A 71-year-old male with paroxysmal atrial fibrillation, nonischemic cardiomyopathy, and multiple comorbidities was initiated on amiodarone 400 mg/day in April. Within one month, he developed progressive dyspnea on exertion and productive cough. He presented to the emergency department in September with acute hypoxic respiratory failure (SpO₂ 86% on room air), weight gain, and bilateral lower extremity edema approximately five months after symptom onset. CT of the chest demonstrated bilateral ground-glass and consolidative opacities with upper lobe predominance and interlobular septal thickening. The initial working diagnosis of decompensated HFpEF was supported by elevated BNP and peripheral edema; intravenous furosemide led to the resolution of edema but no improvement in oxygenation. APT was subsequently suspected, and intravenous methylprednisolone was initiated, resulting in marked clinical improvement. The patient was discharged on room air on a prolonged prednisone taper. At the three-month follow-up, he demonstrated complete symptomatic resolution, marked radiological improvement, and normalization of BNP. This case adds to the existing evidence that clinically significant APT may occur at standard maintenance doses and within a shorter timeframe than traditionally recognized. Coexistent HFpEF poses a major diagnostic challenge given the substantial overlap in clinical and radiological features. The possibility of concurrent rather than competing pathology should always be considered. Clinicians should maintain a high index of suspicion for APT in any patient on amiodarone with progressive respiratory symptoms, irrespective of dose or duration of exposure.
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