International journal of cardiology · 2009
Atrial electrical remodeling in a canine model of sinus node dysfunction.
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Li Guangping, Liu Enzhao, Liu Tong, Wang Jing'an, Dai Jianjun, Xu Gang, Korantzopoulos Panagiotis, Yang Wansong
Аннотация
AIMS: To study atrial tachycardia-induced electrical remodeling in a canine model of sinus node dysfunction (SND).
MATERIALS AND METHODS: A canine model of SND was established by contacting a cotton patch with 20% formaldehyde on the sinus node. Atrial effective refractory period (ERP), ERP dispersion, and inducibility of atrial fibrillation (AF) were recorded at multiple sites in the atrium, before and after SND induction as well as after rapid atrial pacing. The recovery of atrial ERP in the left and right atrium (LA and RA) after cessation of atrial pacing was also recorded.
RESULTS: Compared with baseline, the atrial ERPs were shortened after SND (P<0.05). After rapid atrial stimulation, the atrial ERPs were further decreased significantly (P<0.05), and the dispersion of atrial ERPs measured at different pacing cycle lengths (PCLs) showed significant variation. Seven sites were used to induce AF in each dog (56 sites in 8 dogs). The average duration and inducibility of AF after SND was increased compared with baseline (16.5±4.7 vs 2.3±1.2 s and 12/56 vs 4/56 sites, P<0.05). After rapid atrial stimulation, the average duration and inducibility of AF were further increased (16.5±4.7 vs 33.6±16.1 s and 12/56 vs 25/56 sites, P<0.05). The recovery of atrial ERP in LA was significantly delayed compared to the RA.
CONCLUSION: SND induces atrial electrical remodeling which is further aggravated by atrial tachycardia. Therefore, SND creates an electrophysiological substrate that facilitates AF initiation and perpetuation.
MATERIALS AND METHODS: A canine model of SND was established by contacting a cotton patch with 20% formaldehyde on the sinus node. Atrial effective refractory period (ERP), ERP dispersion, and inducibility of atrial fibrillation (AF) were recorded at multiple sites in the atrium, before and after SND induction as well as after rapid atrial pacing. The recovery of atrial ERP in the left and right atrium (LA and RA) after cessation of atrial pacing was also recorded.
RESULTS: Compared with baseline, the atrial ERPs were shortened after SND (P<0.05). After rapid atrial stimulation, the atrial ERPs were further decreased significantly (P<0.05), and the dispersion of atrial ERPs measured at different pacing cycle lengths (PCLs) showed significant variation. Seven sites were used to induce AF in each dog (56 sites in 8 dogs). The average duration and inducibility of AF after SND was increased compared with baseline (16.5±4.7 vs 2.3±1.2 s and 12/56 vs 4/56 sites, P<0.05). After rapid atrial stimulation, the average duration and inducibility of AF were further increased (16.5±4.7 vs 33.6±16.1 s and 12/56 vs 25/56 sites, P<0.05). The recovery of atrial ERP in LA was significantly delayed compared to the RA.
CONCLUSION: SND induces atrial electrical remodeling which is further aggravated by atrial tachycardia. Therefore, SND creates an electrophysiological substrate that facilitates AF initiation and perpetuation.