EFFECT OF FLECAINIDE ON ATRIAL AND VENTRICULAR REFRACTORINESS AND CONDUCTION IN PATIENTS WITH NORMAL LEFT-VENTRICLE - IMPLICATIONS FOR POSSIBLE ANTIARRHYTHMIC AND PROARRHYTHMIC MECHANISMS

We studied the effects of intravenous flecainide (2 mg.kg(-1)) on atri al and ventricular refractoriness and conduction during sinus rhythm, induced atrial fibrillation and atrial pacing at rates of 100, 120 and 150 ppm, in 14 patients with normal left ventricle. Flecainide caused a significant increase in QRS duration during sinus rhythm (mean +/- SD; 87.2 +/- 8.4 ms vs 102.8 +/- 9.1 ms, P<0.001), atrial fibrillation (87.8 +/- 10.0 ms vs 108.8 +/- 13.7 ms, P<0.001) and at all paced rat es. The duration of the atrial electrogram was significantly increased during sinus rhythm (54.9 +/- 13.2 ms vs 64.8 +/- 16.6 ms, P = 0.003) and at all pacing rates. The PA interval was also significantly prolo nged, as was the pacing stimulus-to-atrial-electrogram interval at all pacing rates. There was increased QRS duration and atrial electrogram prolongation at higher pacing rates. Atrial refractoriness was prolon ged during sinus rhythm (216.4 +/- 28.2 v 228.6 +/- 36.1, P = 0.02), b ut not during atrial pacing at any rate. The QT interval, but not the JT interval or ventricular refractoriness, was significantly prolonged during sinus rhythm and at all pacing rates. Flecainide slows atrial conduction in a use-dependent manner and increases atrial refractorine ss during sinus rhythm but not during faster atrial pacing, thus not d isplaying a use-dependent effect. QRS duration is prolonged in a use-d ependent manner without a commensurate increase in ventricular refract oriness. In the presence of rapidly conducted atrial fibrillation, whi ch was not found to be slowed by flecainide, this effect may constitut e a proarrhythmic mechanism even in patients with no apparent myocardi al abnormality.