Amiodarone Study

Torsades de pointes in amiodarone-associated acquired long-QT syndrome

Amiodarone was developed in Belgium in 1961 and became popular in Europe for the treatment of angina. Based on Dr. Bramah Singh's investigation, (1) the Argentine physician Dr. Mauricio Rosenbaum started using amiodarone for the treatment of ventricular and supraventricular arrhythmias with good outcomes. (2, 3) This drug is a class III agent in the Vaughan Williams scheme, with class I. II and IV antiarrhytmic effects. Amiodarone produces bradycardia, prolongs myocardial action potential and delays ventricular repolarization. Due to this three pharmacological properties amiodarone prolongs the QT-interval, predisposing to torsade de pointes (TDP), a polymorphic ventricular

Figure 1 shows the electrocardiogram (ECG) after the angiography. A carotid endarterectomy was performed 5 months before due to an atheroembolic stroke. During the postoperative period, she presented atrial fibrillation with rapid ventricular response and amiodarone was added to her habitual treatment. Her current treatment is ASA 325 mg/day, atenolol 50 mg bid, enalapril 20 mg bid and amiodarone 200 mg bid. One month before the event she attended the outpatient clinic and an echocardiogram was performed, which showed: normal left ventricular dimensions, wall thickness mildly increased, normal left atrium and aorta, mild left ventricular dysfunction with an estimated ejection fraction of 50%, hypokinetic basal inferior and mid inferior segments and mitral inflow filling pattern of delayed relaxation (according to her age). Right chambers dimensions and right ventricular function were normal (TAPSE of 20 mm Hg), a calcific trileaflet aortic valve with normal leaflet excursion was observed, with normal gradients and no regurgitation. Mitral valve was normal, without regurgitation, and tricuspid valve and pulmonary valve were also normal. There was absence of pericadial effusion and both septae were

It may be congenital or acquired. Several mutations have been identified distributed in 10 genes. The severe form of the disease is sporadic ,but there are a number of common polymorphisms that may confer susceptibility to the development of the disease when specific drugs are being administered. (5) Patients with long QT syndrome are predisposed to sudden death due to polymorphic VT (TDP). Torsade de pointe is a polymorphic VT associated with LQTS which may be terminated by increasing the heart rate.