Torsades de Pointes during Treatment of Tachycardia-Induced Cardiomyopathy

Abstract

Tachycardia-induced cardiomyopathy is caused by persistent tarchyarrhythmias and is characterized by ventricular systolic dysfunction and congestive heart failure. Tachycardia-induced cardiomyopathy is usually reversible via treatment. The cornerstone in the management of disease in these patients is to achieve a normal heart rate. We report a torsades de pointes during treatment of tachycardia-induced cardiomyopathy. Intravenous magnesium sulfate and potassium were administrated, but torsades de pointes was repeated. After overdrive right ventricular pacing, torsades de pointes was terminated. Careful monitoring of the QT interval and serum electrolyte and drug levels in such patients is warranted during treatment of tachycardia-induced cardiomyopathy.brillation of more than 48-hours duration and systolic heart failure presumed to be caused by tachycardia-induced cardio-myopathy.As we checked no thrombus in left atrium and left atrial appendage using transesophageal echocardiography, pharmacological conversion to sinus rhythm was performed by using amiodarone in addition to heparin. However, the patient's atrial fibrillation was persistent for 24 hours despite drug therapy for restoration of sinus rhythm. Electrical cardioversion also failed to terminate atrial fibrillation. Then pharmacological intervention was instituted again for two days. In short, the patient was taking digoxin for the treatment of heart failure and given amiodarone additionally for conversion to sinus rhythm.According to the 2013 American Heart Association guidelines for atrial fibrillation treatment, the combination of digoxin and amiodarone or sotalol for conversion to sinus rhythm can have harmful effects.[7] However such a warning can be oversighted in the presence of severe systolic heart failure caused by TC as described in this case.Amiodarone is an effective class III antiarrhythmic drug that prolongs repolarization period and increases QT interval up to 20% from baseline QT interval. Like Class Ia antiarrhythmic drugs, amiodarone can prolong QT interval but it can also inhibit depolarization by acting on calcium channels. As a result, it is known to be safe compared to other antiarrhythmic drugs and its incidence rate of TdP is estimated at less than 1%. [8] However, the use of amiodarone in combination with digoxin increases the risk of arrhythmia. Especially, the onset of TdP is much more likely to occur within four days when amiodarone is administered. [9] Risk factors for TdP include women gender, myocardial infarction, heart failure, cardiomyopathy, valvular heart disease, the use of antiarrhythmic drugs, bradyarrhythmias, low serum potassium, low serum magnesium, and family history of QT interval prolongation.[10] Intravenous magnesium is considered standard therapy for the onset of TdP regardless of serum concentration. Serum potassium concentration should be maintained at upper limit of the normal range (4.5-5 mmol/L).Hemodynamically unstable patients may require an immediate defibrillation. If patients does not respond to...