The electrophysiological effects of RF ablation upon the areas in prox
imity to the lesioned zones have not yet been well characterized. An e
xperimental model is used to investigate atrial conduction in the boun
daries of RF damaged zones. In 11 isolated and perfused rabbit hearts,
endocardial atrial electrograms were recorded using an 80-lead multip
le electrode positioned in the left atrium. Both before and after the
RF application (5 W, 8 s, 1-mm diameter unipolar epicardial electrode)
in the mid-portion of the free left atrial wall, measurements were ma
de of conduction time from the pacing zone (posterior wall of the left
atrium) to three points between 7.5 and 7.9 mm distal to the damaged
zone. Conduction velocity and the direction of the activation propagat
ion vector were determined in ten groups of four electrodes positioned
around the damaged zone, and at the left a trial appendage. The mean
diameter (+/- SEM) of the transmural lesions produced by RF ablation a
nd defined by macroscopic examination was 4.2 +/- 0.2 mm. The conducti
on times to the three points distal to the lesion site were significan
tly prolonged as a result of RF ablation: 7.6 +/- 0.4, 7.4 +/- 0.5, an
d 6.9 +/- 1.0 ms (control); and 11.3 +/- 1.0 (P less than or equal to
0.01), 11.1 +/- 1.3 (P < 0.01), 10.6 +/- 1.4 ms (P < 0.05) (post-RF).
The differences between the conduction velocities determined in the ar
eas surrounding the lesion, before and offer RF application, failed to
reach statistical significance: 86.2 +/- 6.5 cm/s (control) versus 75
.5 +/- 5.7 cm/s (post-RF) (NS). After RF, significant variations were
only observed in the direction of impulse propagation in the proximal-
inferior quadrant adjacent to the lesion site, the difference being -6
1'' +/- 18'' (P < 0.02). In 2 of 4 experiments in which the lesion siz
e was increased by a second RF application (5 W, 16 s), tachycardias w
ith activation sequence around the lesion could be induced, with cycle
lengths of 56 and 50 ms, respectively. In the atrial wall, the conduc
tion times to the regions distal to the RF lesion are significantly pr
olonged. No significant changes are observed in conduction velocity in
the areas in proximity to the lesion. Prolonged conduction to the are
as distal to the ablation site is due to the lengthened pathway travel
ed by the impulses in reaching these areas. Tachycardias with activati
on patterns that suggest reentry around the RF damaged zone may be ind
uced.