Reduction of atrial fibrillation inducibility by radiofrequency ablation: An experimental study

A study is made of the antifibrillatory effects of radiofrequency (RF)-indu ced atrial lesions using nine Langendorff-perfused rabbit hearts in which t he atrial electrophysiological properties and atrial fibrillation (AF) indu cibility were modified by atrial stretching. Using a multiple electrode con sisting of 121 unipolar electrodes, determinations were made of the atrial refractory periods, conduction velocity, wavelength of the atrial activatio n process, and the inducibility of sustained AF episodes (duration over 30 s) by atrial burst pacing in four situations: (a) control; (b) following di latation of the right atrium; (c) after adding an RF linear lesion at the c ava-tricuspid annulus isthmus; and (d) after adding two RF linear lesions r ounding the base of the right atrial appendage and extending from the infer ior zone of the sulcus terminalis to the anterior wall of the appendage. Un der control conditions, AF was not induced in any of the experiments. The w avelengths were 10.5 +/- 1.2 cm for basic cycles of 250 ms and 6.6 +/- 0.5 cm for cycles of 100 ms. Following dilatation, a significant decrease was r ecorded in the atrial refractory periods, conduction velocity, and waveleng th, which reached values of 6.1 +/- 0.7 cm (250-ms cycle, P < 0.01), and 3. 9 +/- 0.3 cm (100-ms cycle, P < 0.01); AF was induced in five cases (P < 0. 05). After producing the lesion at the cava-tricuspid isthmus, the electrop hysiological modifications induced by atrial dilatation persisted (waveleng th = 6.2 +/- 0.6 cm (250-ms cycle) and 4.3 +/- 0.3 cm (100-ms cycle); P < 0 .01 vs the control) and AF was triggered in eight cases (P < 0.0001). In tu rn, on adding the two lesions at the right atrial free wall and appendage, AF was induced only in one experiment IP = NS vs control), and the dilatati on-induced decrease in refractoriness and wavelength was attenuated. Nevert heless, differences remained significant with respect to the controls, with the exception of the functional refractory periods determined at cycles of 100 ms. In this phase, the wavelength was 6.6 0.7 cm (250-ms cycle, P < 0. 01 vs control) and 4.9 +/- 0.5 cm (100-ms cycle; P < 0.05). Atrial conducti on between the zones separated by the lesions was blocked at any frequency, or selectively at rapid atrial activation frequencies. In conclusion: (al the production of three linear lesions in the right atrium (cava-tricuspid isthmus, atrial appendage, and inferior free wall) reduces AF inducibility in the experimental model used; Ib) conduction block (either absolute or fr equency dependent) through the lesions, reduction in tissue mass caused by lesion creation, and possibly the attenuation of the shortening of atrial r efractoriness and wavelength in the zones not separated by the lesions are implicated in the reduction of AF inducibility; and Icl the single lesion i n the cava-tricuspid isthmus does not impede AF inducibility.