What is the clinical evidence from this study?

Study design: Case Report. Population: Amiodarone pulmonary toxicity (n=1). Intervention: Amiodarone.

What does this research mean for the field?

Clinically significant amiodarone pulmonary toxicity can develop within one month at standard maintenance doses, and its diagnosis can be heavily confounded by concurrent heart failure with preserved ejection fraction. Novelty: ClaimNovelty.CONFIRMATORY. Consensus alignment: ConsensusAlignment.CHALLENGES_CONSENSUS.

What question did this study set out to answer?

This case aims to highlight early-onset pulmonary toxicity due to amiodarone at standard doses, complicating heart failure diagnoses.

May 27, 2026Open Access

Early-Onset Amiodarone Pulmonary Toxicity at a Standard Maintenance Dose Masquerading as Decompensated Heart Failure: A Case Report and Literature Review

Key Result

Amiodarone at a standard maintenance dose of 400 mg/day induced early-onset pulmonary toxicity within one month of initiation, which was successfully treated with drug discontinuation and corticosteroids.

Key Points

This case aims to highlight early-onset pulmonary toxicity due to amiodarone at standard doses, complicating heart failure diagnoses.
Case report of a 71-year-old male with paroxysmal atrial fibrillation and heart failure who received standard amiodarone treatment.
Clinical assessment included chest CT imaging and BNP level measurements, alongside symptom monitoring.
Patient developed pulmonary toxicity after one month of standard amiodarone treatment, with symptoms resembling heart failure.
Intravenous methylprednisolone led to significant clinical improvement, with normalization of symptoms and BNP at follow-up.

Study Design

Type

Case Report (n=1)

Multicenter

Structured PICO

Population

71-year-old male with paroxysmal atrial fibrillation, nonischemic cardiomyopathy, and multiple comorbidities including decompensated heart failure with preserved ejection fraction (HFpEF)

Intervention

Amiodarone 400 mg/day

Outcome

Development of early-onset amiodarone pulmonary toxicity (APT)safety

Clinically significant amiodarone pulmonary toxicity can occur at standard maintenance doses within a short timeframe and can be diagnostically challenging when coexisting with HFpEF.

Limitations

Diagnosis of APT remains presumptive, as bronchoscopy, BAL, pulmonary function testing, and histopathological confirmation were not obtained.
Baseline pulmonary imaging and spirometry prior to amiodarone initiation were unavailable, precluding formal exclusion of pre-existing lung disease.
As a single case report, generalizability is inherently limited, and causal inference must be interpreted with caution.

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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