OBJECTIVES

We sought to evaluate the effects of progressive shortening of the action potential duration (APD) on atrial wave front stability.

BACKGROUND

The mechanisms of conversion from atrial flutter to atrial fibrillation (AF) are unclear.

METHODS

Isolated canine right atria were perfused with 1 to 5 μmol/l of acetylcholine (ACh). We mapped the endocardium by using 477 bipolar electrodes and simultaneously recorded transmembrane potentials from the epicardium. The APD₉₀was measured during regular pacing (S₁) with cycle lengths of 300 ms. Atrial arrhythmia was induced by a premature stimulus (S₂).

RESULTS

At baseline, only short runs of repetitive beats (<10 cycles) were induced. After shortening the APD₉₀from 124 ± 15 ms to 72 ± 9 ms (p < 0.01) with 1 to 2.5 μmol/l of ACh, S₂pacing induced single, stable and stationary re-entrant wave fronts (307 ± 277 cycles). They either anchored to pectinate muscles (5 tissues) or used pectinate muscles as part of the re-entry (4 tissues). When ACh was raised to 2.5 to 5 μmol/l, the APD₉₀was further shortened to 40 ± 12 ms (p < 0.01); S₂pacing induced in vitro AF by two different mechanisms. In most episodes (n = 13), AF was characterized by rapid, nonstationary re-entry and multiple wave breaks. In three episodes with APD₉₀<30 ms, AF was characterized by rapid, multiple, asynchronous, but stationary wave fronts.

CONCLUSIONS

Progressive APD shortening modulates atrial wave front stability and converts atrial flutter to AF by two mechanisms: 1) detachment of stationary re-entry from the pectinate muscle and the generation of multiple wave breaks; and 2) formation of multiple, isolated, stationary wave fronts with different activation cycle lengths.