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 lowe ring the safety factor for conduction by high K+ or flecainide preferential ly depresses conduction of sharply turning wavefronts. Methods and Results: In 16 Langendorff-perfused rabbit hearts, a thin layer of anisotropic ventricular myocardium was made using a cryoprocedure. In t his lever, a linear radiofrequency lesion was made parallel to the fiber or ientation. The tip of the lesion was extended by a short incision. U-turnin g wavefronts were initiated by pacing at one side of the lesion. ii mapping electrode (240 electrodes, resolution 350 to 700 mu m) 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 11 mmol/L) and flecainide (1 and 2 mg/L). On av erage, high potassium and flecainide increased the conduction times of U-tu rning wavefronts 1.6 times more than longitudinal or transverse planar wave fronts (P < 0.01). At a critical lowering of the excitatory current, functi onal conduction block occurred at the pivot point, which forced the wavefro nt to make a longer U-turn, In these cases, the total U-turn conduction tim e increased from 27 +/- 9 msec to 75 +/- 37 msec, About 40% of this delay w as caused by a shift of the pivot point and consequent lengthening of the r eturning pathway. Conclusion: Lowering the amount of excitatory current by potassium or fleca inide preferentially impairs U-turn conduction. The occurrence of long dela ys and conduction block at pivot points may explain the mode of action of C lass I drugs.