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 fiecainide (2 mg.kg^–1)on atrial and ventricular refractoriness and conduction duringsinus rhythm, induced atrial fibrillation and atrial pacingat rates of 100, 120 and 150 ppm, in 14 patients with normalleft ventricle. Flecainide caused a significant increase inQRS 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 rates. The duration of the atrial electrogramwas significantly increased during sinus rhythm (54·9± 13·2 ms vs 64·8 ± 16·6ms, P=0·003) and at all pacing rates. The PA intervalwas also signficantly prolonged, as was the pacing stimulus-to-atrial-electrograminterval at all pacing rates. There was increased QRS durationand atrial electrogram prolongation at higher pacing rates.Atrial refractoriness was prolonged during sinus rhythm (216·4± 28·2 vs 228·6 ± 36·1, P=0·02),but not during atrial pacing at any rate. The QT interval, butnot the JT interval or ventricular refractoriness, was significantlyprolonged during sinus rhythm and at all pacing rates. Flecainideslows atrial conduction in a use-dependent manner and increasesatrial refractoriness during sinus rhythm but not during fasteratrial pacing, thus not displaying a use-dependent effect. QRSduration is prolonged in a use-dependent manner without a commensurateincrease in ventricular refractoriness. In the presence of rapidlyconducted atrial fibrillation, which was not found to be slowedby flecainide, this effect may constitute a proarrhythmic mechanismeven in patients with no apparent myocardial abnormality.