In remodeled canine atria, sympathetic stimulation significantly increased the inducibility of sustained atrial fibrillation from 7% to 60% (P=0.005), whereas vagal stimulation was the primary trigger in normal atria.
Does autonomic stimulation differentially affect the genesis of atrial fibrillation in remodeled canine atria compared to normal atria?
In remodeled atria (AV block model), sympathetic stimulation is crucial for the genesis of AF, contrasting with normal atria where vagal stimulation is the primary trigger.
Absolute Event Rate: 60% vs 7%
p-value: p=0.005
BACKGROUND: The role of autonomic effects in the occurrence and maintenance of atrial fibrillation (AF) has undergone little investigation in the remodeling heart. METHODS AND RESULTS: In the present study, 2 groups were studied: those with complete atrioventricular block (AVB) produced by radiofrequency current application (AVB dogs, n=17) and those not undergoing AVB (sham dogs, n=5). Eight weeks after creation of AVB, electrophysiologic study, including pulmonary vein (PV) pacing for AF induction, was performed under vagal nerve stimulation (VNS) and sympathetic stimulation (SS) in both groups. After 8 weeks, atrial dimensions and the percentage of fibrosis in the atria were significantly greater in the AVB dogs. In AVB dogs, atrial and PV effective refractory periods were shorter (P<0.01), and atrial conduction velocity increased (P=0.01) during SS, but not during VNS. Inducibility of AF increased only during SS in the AVB dogs (sustained AF: control 7%, SS 60%; P=0.005), whereas it increased only during VNS in the sham dogs. CONCLUSIONS: In the remodeled atria, sympathetic stimulation was crucial for the genesis of AF, which is completely different from the condition in normal atria.
Furukawa et al. (Thu,) conducted a other in Atrial fibrillation (n=22). Sympathetic stimulation (isoproterenol) vs. Control (no stimulation) was evaluated on Inducibility of sustained atrial fibrillation (s-AF) (p=0.005). In remodeled canine atria, sympathetic stimulation significantly increased the inducibility of sustained atrial fibrillation from 7% to 60% (P=0.005), whereas vagal stimulation was the primary trigger in normal atria.
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