Ischemia Versus Amiodarone Induced Polymorphic Ventricular Tachycardia

September 2002 PACE, Vol. 25, No. 9 An 88-year-old woman was admitted with enterococcal bacteremia complicated by endocarditis and lumbar osteomyelitis for which she was treated with a 6-week regimen of intravenous ampicillin and gentamicin. Her medical background included paroxysmal atrial fibrillation, moderate to severe aortic stenosis and hypertension. At the time of admission, her medications included amiodarone 100 mg daily, enalapril 10 mg daily, lansoprazole 30 mg daily, and ferrous sulfate 325 mg daily. Electrocardiogram (ECG) before admission showed normal sinus rhythm with a heart rate of 63 beats/min and normal QRS duration with a QT interval of 432 ms and U waves (Fig. 1). She had been receiving amiodarone therapy for paroxysmal atrial fibrillation for more than 6 months prior to this admission. One week into her admission, she developed progressive shortness of breath and was found to be in pulmonary edema. The ECG showed sinus tachycardia with a rate related left bundle branch block (LBBB). Serial cardiac enzymes were found to be elevated, and ECGs following the resolution of LBBB showed marked ST-segment changes with deep symmetrical T wave inversion, consistent with global subendocardial ischemia. QT interval was prolonged at 628 ms (Fig. 2). Electrolytes including serum magnesium were within normal limits and the average heart rate was 60–70 beats/min. The following day she reported sudden onset light-headedness with presyncope. The arrhythmia recorded at this time is shown in Figure 3. Subsequently, a 12lead ECG showed a further prolongation of QT interval to 699 ms. What caused the above ECG changes in this patient? How would you treat this patient, keeping in mind that a few weeks later her QT interval had returned to normal? Commentary There was a treatment dilemma in this case because the mechanisms responsible for marked QT prolongation were unclear. Amiodarone alone at such a low dose (100 mg, daily) is unlikely to have a significant effect on the QT interval, particularly under conditions of essentially normal serum electrolytes. Even at doses where it significantly prolongs the QT interval, amiodarone induced polymorphic ventricular tachycardia is rare. Endocardial or subendocardial ischemia alone is usually not associated with such marked QT prolongation, and ischemia induced polymorphic ventricular tachycardia is mostly triggered by extrasystoles with a short coupling interval and is not pause dependent. In clinical practice, fortunately, marked QT prolongation causing torsades de pointes (TP) is readily identifiable and is usually drug induced or secondary to electrolyte imbalance. Classical TP due to ischemia alone is uncommon as shown by Halkin et al. in a recent study where they encountered this arrhythmia in only 8 of 434 patients with uncomplicated myocardial infarction, and they referred to this as “infarct-related long QT syndrome. ” Previous studies have demonstrated that ventricular myocardium is composed of three intrinsically distinct cell layers, epicardium, mid-myocardium (M cells), and endocardium. Endocardial ischemia may electrically uncouple injured cells with intrinsically short action potential duration (endocardium) from those with intrinsically long-action potential duration (M cells), resulting in QT prolongation. However, whether amiodarone can exaggerate the QT prolongation under certain pathophysiological conditions like endocardial ischemia is unproven. In view of the difficulty in deciding between ischemia and amiodarone as the cause of polymorphic ventricular tachycardia in this patient, treatment was directed to include both. Lidocaine and bblockers treated a presumed ischemic etiology. Coronary revascularization was considered, but, unfortunately, because of advanced age and associated comorbid factors, she was not thought to be a suitable candidate. Polymorphic ventricular tachycarEP ROUNDS