Study On The Acute Atrial Fibrillation And Electrical Remodeling Induced By Rapid Pacing In The Atrium Of Dogs With Sinus Node Dysfunction

Objectives: The study is to establish the sinus node dysfunction (SND) and atrial fibrillation (AF) of canine model induced by rapid pacing in the atrium for observing changes of electrophysiological characteristics: atrail effective refractory period (AERP), AERP discrete, atrial activity sequence, atrial activity time and the incidence of secondary AF, the restoration process of AERP, exploring the relationship between the reoccurrence and maintenance of AF and atrial electrical remodeling. To investigate the electrophysiological mechanisms of atrial electrical remodeling in canine atrium with short-time rapid pacing under slowing cardiac arrhythmia, we hope our experiment could provide some way to the therapy of AF.Methods: The model of SND was established in 12 dogs with Formaldehyde method (wet compress the sinus node region of the dogs). 7 bipolar recording electrode were sutured to the 7 sites on the epicedium. Acute atrial fibrillation was induced by rapid atrial pacing (S₁S₁) with a cycle length of 150 ms in 8 dogs after successful SND. AERP, AERP dispersion, AERP rate adaptating feature, and the inter-atrium conduction time were measured with S₁S₁ stimulation before and after SND and AF 2 hours in multiple sites under different pacing cycle length ( 350 ms, 250ms, 200 ms ) respectively. In the other 4 dogs, AF were induced by rapid atrial pacing (400 bpm) and the AERP was measured at the sites of left and right atrial appendage for every 20 min after secession of AF to observe the recovery course of the shortened AERP.Results : After SND, for any pacing cycle length (PCL), AERP at 7 sites weresignificantly shortened, the inter-atrium conduction time were slowing (41.75± 1.48ms VS 44.58±2.27ms, P<0.05) and the atrial activity sequence was disorder. Acute 2 hour" AF was induced by rapid atrial pacing under any pacing cycle length in 8 dogs after SND, the inter-atrium conduction time was more slow(46.92 ±2.71ms VS 44.58±2.27ms, P<0.05) and the atrial activity sequence was disturbance. AERP at 7 sites were more shortened than the pre-AF's, the percentage of maladapation of AERP increased significantly and AERP dispersion was increased (Chart 9 ). Meanwhile, the percentage of secondary AF increased significantly (36.6+7.58% Vs 20.2±2.41%, P<0.01), the indelibility and duration of secondary AF also increased significantly. (33.6±16.1 second VS 16.5±4. 7 second, P<0.05 ) . Additional, the recovery course of AERP was slower at left a trial appendage than that at the right atrial appendage (140 min vs 80 min). The AERP at some sites which was induced AF was more shorten than the sites which cannot (PCL350: 91±13 ms VS 102±14ms; PCL250: 90±llms VS 101±12ms; PCL200: 88+llms VS 95+llms, P<0.05) . The shortness of AERP had significant negative correlation with indelibility and duration of secondary AF. AERP dispersion was increased at the sites which was induced AF (31±10ms VS 23±7 ms, P=0.002), but hadn't significant correlation with indelibility and duration of secondary AF. At PCL350 and PCL250, the percentage of secondary AF at sites of maladapation of AERP increased more significantly than the sites of AERP adaptation20/63 VS 6/105, P<0.001; 11/63 VS 5/105, P=0.041). However, it was indifferent at PCL200 (10/63 VS 11/105, P=0.551). Comparing the sites of the premature beats released from, we found premature beats form lower right atrium and left atrial appendage obtained higher indelibility and duration of secondary AF, which were more significant [LRA: (6/56) 10.71%, HLA: (8/56) 14.29%].