Abstract

Chronic atrial dilatation due to complete AV block creates a substrate of atrial fibrillation (AF) in the goat. The purpose of the present study was to characterize AF in dilated atria by high-resolution epicardial mapping. Methods: In 7 goats the His bundle was ablated and a slow idioventricular rhythm occurred (53.5 2.7 versus 113.7 4.5bpm in sinus rhythm, p 0.01). After 4 weeks, the animals were anesthetized, the chest was opened, AF was induced by burst pacing, and the free walls of both atria were mapped epicardially (240 electrodes, 2.4mm interelectrode distance). During 4 seconds, AF cycle length (AFCL) was determined for each electrode. Spatial heterogeneity in AFCL was defined as the largest difference in local median AFCL. Local conduction velocities (CV) were calculated for areas of 2.4x2.4mm. Then, the atria were fixed in formalin and stained (Azan, Sirius red) to determine myocyte dimensions and collagen content. In frozen tissue connexin40 and 43 was stained by antibodies. Six goats without AV block served as control. Results: Atrial myocytes were enlarged after 4 weeks of AV block (cell length 110 7 m versus 88 2 m, P 0.05; cell diameter 16.5 1.2 m versus 13.2 0.8 m, n.s.). The amount of collagen was not increased. Connexin40 and 43 expression was not different between the groups. The median AFCL was similar after 4 weeks of AV-block and in normal atria (RA: 127 15 vs. 123 13ms, LA: 137 5 vs.146 8ms, p 0.80). However, the spatial heterogeneity in median AFCL was higher in dilated atria (RA: 23 4ms vs. 13 3ms, LA: 38 10ms vs. 14 4ms, p 0.01). The incidence of conduction delay (CV 30cm/s) and block (CV 10cm/s) was higher in dilated versus normal atria (RA: 19.4 4.3 and 12.3 3.1% versus 12.0 4.2 and 7.0 2.7%; LA: 18.0 3.7 and 12.6 3.0% vs. 9.4 2.9% and 4.6 1.9%; p 0.05 and p 0.05). Overall, the incidence of local conduction block correlated with mean cell length (r 0.60, p 0.03). Conclusions: In atria dilated due to complete AV block, atrial fibrillation is more heterogeneous and local conduction delays occur. This is not related to atrial fibrosis or to changes in connexin expression. Interestingly, atrial cell size and impaired conduction are interrelated in this model.

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