Preferential depression of conduction around a pivot point in rabbit ventricular myocardium by potassium and...

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 by high K+ or flecainide preferentially depresses conduction of sharply turning wavefronts.

In 16 Langendorff-perfused rabbit 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 microm) 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 increased 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. About 40% of this delay was caused by a shift of the pivot point and consequent lengthening of the returning pathway.

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.