“…One feature of treatment with these agents was that arrhythmia suppression was routinely accompanied by obvious and striking prolongation of P wave, PR interval, and QRS durations, evidence of marked conduction slowing across the heart. Such ECG changes had been seen with the aggressive use of high dose of quinidine to convert atrial fibrillation, 6 where they were considered a sign of drug toxicity, occasionally preceding the development of ventricular tachycardia (VT). Even during the early development of encainide and flecainide, case reports emerged that occasional patients appeared to develop “paradoxical” worsening of ventricular arrhythmias, including patients who developed incessant sustained monomorphic or polymorphic VT, some of whom who could not be resuscitated.…”