ACUTE MODIFICATIONS IN THE WAVELENGTH OF THE ATRIAL EXCITATION PROCESS-INDUCED BY STRETCHING - AN EXPERIMENTAL-STUDY

Objective. An evaluation is made of the acute modifications in the wav elength of the atrial excitation process induced by atrial stretching. Material and methods. In 10 isolated Langendorff-perfused rabbit hear ts and using a multiple electrode the wavelength of the atrial activat ion process (functional refractory period x conduction velocity) was d etermined In the right atrium. An analysis was also made of the induci bility of rapid repetitive atrial responses after 20 episodes of atria l burst pacing. Measurements were made under control conditions, after inducing two degrees of atrial wall stretch (D1 and D2), and followin g the suppression of atrial dilatation. Results. Under control conditi ons the wavelength was 72.6 +/- 7.7 mm (250 ms cycle) and 54.0 +/- 5.1 mm (100 ms cycle). In D1 (mean longitudinal increase in atrial wall l ength = 24 +/- 3%) the wavelength shortened, with values of 59.8 +/- 6 .6 mm (250 ms cycle; p < 0.01) and 44.9 +/- 5.1 mm (100 ms cycle; p < 0.01). In D2 (mean longitudinal increase in atrial wall length = 41 +/ - 4%) the wavelength also shortened significantly, with values of 41.6 +/- 2.8 mm (250 ms cycle; p < 0.01 vs control) and 29.6 +/- 2.1 mm (1 00 ms cycle; p < 0.01 vs control). After suppresing atrial dilatation the wavelength was 65.7 +/- 8.0 mm (250 ms cycle, NS vs control) and 4 7.9 +/- 5.5 mm (100 ms cycle; NS vs control). The inducibility of rapi d repetitive atrial responses increased during dilatation (22 episodes with over 30 consecutive repetitive responses in D1 [p < 0.01], 50 ep isodes in D2 [p < 0.001] vs 5 episodes under control conditions), and diminished after suppresing atrial dilatation (0 episodes with over 30 consecutive repetitive responses; p < 0.05). Conclusions. In the expe rimental model used, acute atrial dilatation produced a shortening in refractoriness and a decrease in conduction velocity. Both effects sho rtened the wavelength of the atrial activation process, facilitating t he induction of atrial arrhythmias. The effects observed reverted upon suppresing atrial dilatation.