Promotion of atrial fibrillation by heart failure in dogs - Atrial remodeling of a different sort

Background-Studies of atrial fibrillation (AF) due to atrial tachycardia ha ve provided insights into the remodeling mechanisms by which "AF begets AF" but have not elucidated the substrate that initially supports AF before re modeling occurs. We studied the effects of congestive heart failure (CHF), an entity strongly associated with clinical AF, on atrial electrophysiology in the dog and compared the results with those in dogs subjected to rapid atrial pacing (RAP; 400 bpm) with a controlled ventricular rate (AV block p lus Ventricular pacemaker at 80 bpm). Methods and Results-CHF induced by 5 weeks of rapid ventricular pacing (220 to 240 bpm) increased the duration of AF induced by burst pacing (from 8 /- 4 seconds in control dogs to 535 +/- 82 seconds; P < 0.01), similar to t he effect of 1 week of RAP (713 +/- 300 seconds). In contrast to RAP, CHF d id not alter atrial refractory period, refractoriness heterogeneity, or con duction velocity at a cycle length of 360 ms; however, CHF dogs had a subst antial increase in the heterogeneity of conduction during atrial pacing (he terogeneity index in CHF dogs, 2.76 +/- 0.16 versus 1.46 +/- 0.10 for contr ol and 1.51 +/- 0.06 for RAP dogs; P < 0.01) owing to discrete regions of s low conduction. Histological examination revealed extensive interstitial fi brosis (connective tissue occupying 12.8 +/- 1.9% of the cross-sectional ar ea) in CHF dogs compared with control (0.8 +/- 0.3%) and RAP (0.9 +/- 0.2%) dogs. Conclusions-Experimental CHF strongly promotes the induction of sustained A F by causing interstitial fibrosis that interferes with local conduction. T he substrates of AF in CHF are very different from those of atrial tachycar dia-related AF, with important potential implications for understanding, tr eating, and preventing AF related to CHF.