Atrial fibrillation and atrial flutter, the most frequently encountered tachyarrhythmias requiring treatment, have become a major focus for clinical and basic research in recent years. Restoration and maintenance of sinus rhythmn, having been shown to improve exercise capacity, alleviate symptoms, and reduce the incidence of thromboembolic events, may be the optimal management strategy. Identification of the safest, most efficacious and cost-effective means of restoring sinus rhythm is necessary prior to the institution of optimal antiarrhythmic therapy to maintain sinus rhythm. Potential advantages of pharmacologic compared with electrical cardioversion include lack of need for general anesthesia and likely lower cost. Pharmacologic conversion include lack of need for general anesthesia and likely lower cost. Pharmacologic conversion has been accomplished with drugs that prolong atrial refractorinerss, including class Ia (quinidine, procainamide, disopyramide), class Ic (flecainide, propafenone), and class II (sotalol, amiodarone) compounds. The so-called pure class III agents were created to overcome the blocker side effects of sotalol and the complex pharmacodynamic profile of amiodarone. Two such agents are dofetilide, which selectively blocks the rapid component of the delayed rectifier current (Ikr) and ibutilide, which augments the slow inward sodium current, with a smaller component of action mediated by the block of Ikr. Reported overall conversion rates for recent onset atrial fibrillation and atrial flutter were 31% and 54% for difetilide, respectively, and 29-31% and 38-63%, respectively, for ibutilide. Proarrhythmia, manifested as polymorphic ventricular tachycardia requiring cardioversion, was a significant early side effect of both agents. Data from clinical trtials with these new agents, combined with increasing nowledge of the electrophysiologic substrate for these arrhythmias, has renewed initerest in the development of safer, more efficacious class IIIdrugs for atrial fibrillation and atrial flutter conversion.

A 77-year-old man with no known cardiac disease has had paroxysmal atrial fibrillation for 35 years with disabling symptoms and poor exercise tolerance when not in sinus rhythm, and he did not respond to conventional therapy. Fifteen years ago he was placed on amiodarone. His arrhythmia converted to atrial flutter with a flutter rate below 200 beats/min; DC cardioversion at 3 months led to transient sinus rhythm. At 5 months he converted spontaneously to sinus rhythm and had very few recurrences until 4 years later when he began to experience further frequent recurrences when the dose was reduced from 400 mg/day to 200 mg/day. Redosing at the higher dose led to skin discoloration; amiodarone was then replaced with sotalol, which the patient did not tolerate. After 9 months with efforts to rate control with various agents, amiodarone was reintroduced at 400 mg/day, which achieved full control, but to obviate the development of skin changes, flecainide was added at a dose of 100 mg twice a day, and the dose of amiodarone was gradually reduced to 200 mg/day. This combination regimen has produced no side effects or organ toxicity, although a degree of hypogonadism developed. It responded well to testosterone replacement. On the combination regimen, there have been no symptomatic arrhythmia recurrences over 8 years. Amiodarone and flecainide may have additive or synergistic effects in maintaining sinus rhythm in atrial fibrillation; the antiarrhythmic property of amiodarone is likely to minimize or nullify the proarryhthmic reactions of flecainide during combination therapy. This combination regimen may allow the extension of the use of flecainide in controlling refractory atrial flutter and fibrillation in patients with structural cardiac disease. The efficacy and safety of the combination regimen of the two drugs should be addressed in controlled clinical trials.

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A 50-yaer-old man with hypertension had been treated for supraventricular tachycardia with several medications for nine years. In 1990, he was started on amiodarone but a year later he developed side effects causing discontinuation of amiodarone. Because of his recurrent episodes of palpitations associated with near syncope, chest pain and shortness of breath, he underwent an electrophysiology study in 1992 that showed orthodromic AVRT with the presence of a concealed left-sided accessory bypass tract. Scheduled for radiofrequency ablation the following day, after catheters were placed and during mapping of the lateralmitral annulus, his tachycardia stopped abruptly without further inducability. Isoproterenol infusion during atrial and ventricular stimulation also failed to induce his original tachycardia. A year later, the patient presented with palpitations that felt different than his previous experiences. Work-up at that point only revealed a parasystolic focus on a 24-hour ECG monitoring without any form of supraventricular tachycardia. This represents a very unusual case by which the left lateral accessory pathway was mechanically ablated with catheter manipulation. This led to the disappearance of the orthodromic tachycardia that was easily induced before due to the activity of his parasytolic focus. The latter continued for the following four years but the patient has had no recurrences of his tachycardia.