Preferential Depression of Conduction Around a Pivot Point in Rabbit Ventricular Myocardium by Potassium and Flecainide

Preferential Depression of Conduction at Pivot Points. Introduction: During reentrant arrhythmias, the circulating wavefront often makes a sharp turn around a functional or anatomic barrier. We tested the hypothesis that lowering the safety factor for conduction hy high K + or flecainide preferentially depresses conduction of sharply turning wavefronts. Methods and Results: In 16 Langendorff‐perfused rahbit hearts, a thin layer of anisotropic ventricular myocardium was made using a cryoprocedure. In this layer, a linear radiofrequency lesion was made parallel to the fiber orientation. The tip of the lesion was extended by a short incision. U‐turning wavefronts were initiated by pacing at one side of the lesion. A mapping electrode (240 electrodes, resolution 350 to 700 μm) was used to measure conduction times and velocity of planar waves (longitudinal and transverse) and U‐turning wavefronts. The safety factor for conduction was lowered by high potassium (8, 10, and 12 mmol/L) and flecainide (1 and 2 mg/L). On average, high potassium and flecainide inereased the conduction times of U‐turning wavefronts 1.6 times more than longitudinal or transverse planar wavefronts (P < 0.01). At a critical lowering of the excitatory current, functional conduction block occurred at the pivot point, which forced the wavefront to make a longer U‐turn. In these cases, the total U‐turn conduction time increased from 27 ± 9 msec to 75 ± 37 msec. Ahout 40% of this delay was caused by a shift of the pivot point and consequent lengthening of the returning pathway. Conclusion: Lowering the amount of excitatory current by potassium or flecainide preferentially impairs U‐turn conduction. The occurrence of long delays and conduction block at pivot points may explain the mode of action of Class I drugs.