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Article Synopsis
  • Amiodarone is a highly effective antiarrhythmic drug used to treat conditions like atrial fibrillation and ventricular arrhythmias, functioning across all four classes of antiarrhythmics.
  • It has a long half-life and complex pharmacokinetics, which can lead to prolonged effects even after stopping the medication, making regular monitoring for side effects like thyroid issues and lung damage essential.
  • This paper aims to offer a detailed review of amiodarone's uses, dosing guidelines, interactions with other medications, and necessary monitoring practices.
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An elderly Japanese woman developed acute decompensated heart failure caused by persistent atrial fibrillation (AF) and left ventricular systolic dysfunction. Approximately 6 days after starting intravenous administration of amiodarone (600 mg/day) for maintaining sinus rhythm after cardioversion of AF, electrocardiograms revealed a prolonged QT interval associated with torsade de pointes (TdP). The amiodarone-induced TdP disappeared after intravenous administration of landiolol plus magnesium and potassium, without discontinuation of amiodarone or overdrive cardiac pacing, although the prolonged QT interval persisted.

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A 57-year-old man on maintenance hemodialysis was admitted to a hospital after suffering from cardiac arrest. He had collapsed soon after hemodialysis and was restored to sinus rhythm after receiving direct-current shocks. Further examination revealed old myocardial infarction with triple-vessel disease, and he was referred to our hospital for surgical treatment.

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A woman with ischemic cardiomyopathy presented with recurrent syncope. Electrocardiogram showed complete heart block and torsade de pointes (TdP) secondary to amiodarone, recently started for paroxysmal atrial fibrillation. We describe a novel application of His bundle pacing that suppressed TdP and corrected the underlying left bundle branch block.

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This case involves a 55-year-old male patient with systolic heart failure and refractory atrial fibrillation due to thyrotoxicosis, who was electrically cardioverted but then developed torsade de pointes and ventricular fibrillation. Rate control was unsuccessful with digoxin, cardizem, labetalol, esmolol and amiodorone. Patient was externally cardioverted after which ECGs showed prolonged QT with frequent premature ventricular contractions.

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