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Amiodarone is commonly used nowadays for the treatment of atrial fibrillation (AF). The wide use of this medication has led to the occurrence of adverse events, including pulmonary toxicity, hepatotoxicity, thyroid dysfunction, and many others. Higher doses of Amiodarone of ≥400 mg/day have been linked to increased complications. We present a case of a 70-year-old male with multivessel coronary artery disease (CAD) with ischemic cardiomyopathy and severe peripheral artery disease (PAD) who underwent an elective left femoral to posterior tibial bypass surgery followed by percutaneous coronary intervention (PCI) complicated by new-onset AF. The patient was loaded with 150 mg of intravenous (IV) Amiodarone followed by 360 mg infusion over six hours for chemical cardioversion. The patient was then maintained on oral Amiodarone 400 mg/day until the day of presentation when he complained of progressive dyspnea. Imaging was significant for diffuse ground glass opacities and interstitial thickening. The echocardiogram revealed an improved ejection fraction (EF) of 40% from 20%. The patient had worsening oxygenation despite adequate IV diuresis and developed severe acute respiratory distress syndrome (ARDS) requiring mechanical ventilation (MV). A bronchoscopy with bronchoalveolar lavage (BAL) showed diffuse alveolar hemorrhage (DAH) with a high lymphocyte count and negative infectious disease testing. Lab tests revealed elevated liver enzyme levels. There were also changes in thyroid function from baseline with elevated free T4 at 1.83 ng/dL (0.8-1.4 ng/dL), suppressed thyroid stimulating hormone (TSH) at 0.109 mIU/mL (0.4-4 mIU/mL), negative anti-thyroglobulin (TG) antibodies, and anti-thyroid peroxidase (TPO) antibodies indicating a type 2 Amiodarone-induced thyrotoxicosis. Unfortunately, the patient's condition deteriorated further despite appropriate treatment, and it was ultimately followed by his demise. Severe, fatal cases of Amiodarone toxicity are scarce, but more reports are being seen. We strongly believe clinicians should have a high index of suspicion for Amiodarone-related adverse events in elderly males with cardiopulmonary comorbidities. It is imperative to have an increased understanding, greater vigilance, and closer monitoring of pulmonary function tests (PFTs), laboratory tests, and imaging studies.

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Amiodarone is a commonly prescribed antiarrhythmic drug. It can cause a myriad of complications associated with its long-term use, with amiodarone induced pulmonary toxicity being the worst. Amiodarone does this through its destructive properties and its' ability to accumulate if taken for extended periods of time or in high cumulative doses. Albeit uncommon, the management of amiodarone induced pulmonary toxicity can be straightforward if recognized early. Otherwise, it can lead to severe respiratory failure causing death. In this case report, we aim to highlight the importance of vigilance with clinicians prescribing amiodarone and to spark interests into research for alternative management options of amiodarone induced pulmonary toxicity. This will be done through the description of a case of a 64-year-old male presenting with cough and dyspnoea, who has been on a large dose of amiodarone daily for the past 11 months. He was diagnosed too little, too late, which unfortunately culminated in his rapid fatality. This case is unique for two reasons. The diagnosis of amiodarone induced pulmonary toxicity was through the clinical picture - without the use of invasive investigations. In addition, the futile cessation of amiodarone and use of high dose systemic corticosteroids as a management - which to our knowledge is uncommon in literature.

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Amiodarone is a common antiarrhythmic drug that is utilised in clinical practice and is associated with pulmonary toxicity. The most common form of pulmonary complication is interstitial pneumonitis which is treated with discontinuation of amiodarone and initiation of corticosteroids. Amiodarone-induced pulmonary eosinophilia is a rare complication of amiodarone therapy, with blood and pulmonary eosinophilia the predominant features. During the COVID-19 era, the incidence of delay in treatment of pulmonary pathology is also delayed due to the effort of excluding COVID-19 infection. Here we report a case of a 64-year-old man who developed eosinophilic pneumonia after initiation of amiodarone therapy, and the investigations required to exclude other forms of pulmonary toxicity. We also reviewed the effect of COVID-19 testing in the management of patients presenting with respiratory distress.

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Amiodarone is one of the more frequently used drugs in the treatment of supraventricular and ventricular arrhythmias. Many adverse effects, more or less serious, are associated with its administration. Amiodaron-induced pulmonary toxicity (AIPT) is quite rare but represents one of the most severe adverse effects with high mortality. We present an 80 years old patient, who used amidorane due to paroxysmal atrial fibrillation for several years. Within 3 months, he was repeatedly hospitalized for a bilateral pneumonia. Eventually, AIPT was diagnosed. Early diagnosis, proper therapy of AIPT and changed antiarrhythmic therapy has significantly improved the clinical status of our patient. In this case we demonstrate typical clinical presentations of AIPT as well as the most common diagnostic procedures and recommended treatment methods. Finally, some other commonly used therapeutical options for supraventricular arrhythmias are mentioned. Future options are outlined.

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Amiodarone is an effective antiarrhythmic that frequently is used during the perioperative period. Amiodarone possesses a significant adverse reaction profile. Amiodarone-induced pulmonary toxicity (AIPT) is among the most serious adverse effects and is a leading cause of death associated with its use. Despite significant advances in the understanding of AIPT, its etiology and pathogenesis remain incompletely understood. The diagnosis of AIPT is one of exclusion. The clinical manifestations of AIPT are categorized broadly as acute, subacute, and chronic. Acute AIPT is a rarer and more aggressive form of the disease, most often encountered in cardiothoracic surgery. Acute respiratory distress syndrome (ARDS) is the predominating pattern of amiodarone's acute pulmonary toxicity. The incidence, risk factors, pathogenesis, and diagnosis of acute AIPT are speculative. Early cardiothoracic literature investigating AIPT often attributed amiodarone to the development of postoperative ARDS. Subsequent studies have found no association between amiodarone and acute AIPT and ARDS development. As a drug that is frequently prescribed to a patient population deemed most at risk for this fatal disease, the conflicting evidence on acute AIPT needs further investigation and clarification.

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Amiodarone-induced pulmonary toxicity (APT) is one of the most feared and underappreciated adverse effects of this commonly prescribed antiarrhythmic. APT has a variable presentation, among the rarest of these is amiodarone-induced diffuse alveolar hemorrhage with hemoptysis. Though previous cases confirmed with biopsy averaged a dose of 570 mg PO daily, APT can occur at any dose. Previous literature has suggested the importance of cumulative exposure to amiodarone rather than the patient's actual dose. The presented case describes amiodarone-induced hemoptysis occurring at a dose of 200 mg PO daily for five years. Additionally described is the treatment regimen which managed a patient with metabolic syndrome and elevated A1c while addressing the recommended treatment of extended high-dose steroids for APT with complicated respiratory status. To the best of the authors' knowledge, only two biopsied cases have been described at a dose this low. Furthermore, this case describes a more typical timeline for APT than those two cases.

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BACKGROUND: Amiodarone is an antiarrhythmic drug which is used to treat and prevent several dysrhythmias. This includes ventricular tachycardia and fibrillation, wide complex tachycardia, as well as atrial fibrillation (AF) and paroxysmal supraventricular tachycardia. Amiodarone may prove to be the agent of choice where the patient is hemodynamically unstable and unsuitable for direct current (DC) cardioversion. Although, it is not recommended for long-term use. The physician might encounter issues when differentiating amiodarone-induced lung toxicity with suspicion of interstitial lung disease, cancer or vasculitis. Adverse drug reactions are difficult to confirm and it leads to serious problems of pharmacotherapy. CASE PRESENTATION: A 78-year-old Caucasian male pensioner complaining of fever, dyspnea, malaise, non-productive cough, fatigue, weight loss, diagnosed with acute respiratory failure with a 16-year long history of amiodarone use and histologically confirmed temporal arteritis with long-term glucocorticosteroid (GCC) therapy. Patient was treated for temporal arteritis with GCC for ~ 1 year, then fever and dyspnea occurred, and the patient was hospitalized for treatment of bilateral pneumonia. Chest X-ray and chest high resolution computed tomography (HRCT) indicated several possible diagnoses: drug-induced interstitial lung disease, autoimmune interstitial lung disease, previously excluded pulmonary TB. Amiodarone was discontinued. Antibiotic therapy for bilateral pneumonia was started. Fiberoptic bronchoscopy with bronchial washings and brushings was performed. Acid fast bacilli (AFB) were found on Ziehl-Nielsen microscopy and tuberculosis (TB) was confirmed (later confirmed to be Mycobacterium tuberculosis in culture), initial treatment for TB was started. After a few months of treating for TB, patient was diagnosed with pneumonia and sepsis, empiric antibiotic therapy was prescribed. After reevaluation and M. Tuberculosis identification, the patient was referred to the Tuberculosis hospital for further treatment. After 6 months of TB treatment, pneumonia occurred which was complicated by sepsis. Despite the treatment, multiple organ dysfunction syndrome evolved and patient died. Probable cause of death: pneumonia and sepsis. CONCLUSIONS: The current clinical case emphasizes issues that a physician may encounter in the differential diagnostics of amiodarone-induced lung toxicity with other lung diseases.

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Pulmonary complications of long-term amiodarone use are well known. However, acute pneumonitis causing respiratory distress with short-term administration of amiodarone although rare is associated with high mortality. Early diagnosis and treatment with glucocorticoids significantly decrease associated mortality and morbidity. We are reporting one such case of amiodarone-induced pulmonary pneumonitis and its complete resolution with short-course glucocorticoid therapy. Thus, every clinician prescribing amiodarone should be well acquainted with this entity.

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UNLABELLED: Amiodarone-induced pulmonary toxicity (APT) is a serious adverse event that can lead to death. The aims of our study are to determine factors associated with mortality and to describe outcome and sequelae of patients with APT. METHODS: Forty-six patients with APT were divided into two groups according to survival at day 90 for a clinical, functional, biological and radiological comparaison. We then evaluated the evolution of 15 survivors at a median of three months [1-6 months] and/or 12 months [8-36 months]. RESULTS: Mortality of APT at day 90 was 37% (17 patients) and was linked to the speed of onset of symptoms and a high HRCT alveolar score. Angiotensin system antagonist treatment was prescribed significantly more in the survival group (p = 0.042, HR 0.34 (95% CI 0.12-0.96)). In surviving patients, dyspnea, vital capacity and HRCT alveolar score improved significantly while HRCT fibrosis score deteriorated gradually during the first six months. At the end of the study, all the surviving patients presented functional and/or radiological sequelae. CONCLUSIONS: Severity of APT is linked to the extent and speed of onset of pulmonary damage. After the initial episode, the patients who survived improved slowly but with persistent sequelae.

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The potent and efficacious anti-dysrhythmic agent amiodarone (AM) can cause potentially life-threatening lung damage (amiodarone-induced pulmonary toxicity; AIPT), which is characterized by cell death in the lungs, followed by inflammation and fibrosis. AM's major metabolite, desethylamiodarone (DEA), has a greater toxic potency than AM and it has been suggested that DEA may act synergistically with AM to cause lung toxicity. The objective of this study was to determine the type of cytotoxic interaction between AM and DEA in HPL1A human peripheral lung epithelial cells. Cytotoxicity was measured by lactate dehydrogenase release. AM and DEA caused concentration-dependent cytotoxicity in HPL1A cells. The concentration of drug causing 50% cell death (LC50) and the Hill slope factor, which represents steepness of the concentration-cell death curve, were significantly different between AM and DEA (12.4µM and 1.98; 5.07µM and 5.43, for AM and DEA, respectively) indicating that they may induce cytotoxicity through different mechanisms. A combined concentration of 7.13µM AM plus DEA, equivalent to 41% of each compound's individual LC50 value, resulted in 50% cell death. Isobolographic analysis revealed this effect to be additive, although the combined concentrations were only slightly higher than the concentrations that defined the threshold of synergy (threshold of synergy=4.21±1.98µM AM plus 1.73±1.05µM DEA; experimental data point=5.06±0.47µM AM plus 2.07±0.47µM DEA). The cytotoxic interaction between AM and DEA may be clinically relevant in the development of AIPT.

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