高频起搏犬房颤模型心房重塑及窦房结和房室结功能的变化

 目的:持续高频起搏犬左心房，观察房颤(AF)发生率、心房重塑以及窦房结、房室结传导功能。方法: 健康比格犬15只随机分为起搏组(P组，n=9)和对照组(N组，n=6)。2组均在左心房心外膜缝合固定一起搏电极，P组以400 min-1的频率起搏，N组不起搏。采用程序起搏技术测定电生理参数。结果: (1) 4周后P组阵发性AF和持续性AF的诱发率与N组比较差异均有统计学意义（分别P<0.05,P<0.01），P组第2周2只犬自发AF，第4周AF诱发率达100%，且持续性AF的发生率高。 (2) P组4周后心房有效不应期(AERP)在不同基本起搏周期(250 ms、300 ms和350 ms)时均较N组缩短 (P<0.05)；房室结文氏点(AVN-Wen) 较N组有意义延长［(294.44±26.03)min-1 vs (328.33±24.01)min-1, P<0.05］；房室结有效不应期(AVERP)在不同起搏周期均明显延长 (P<0.01)。(3) 与N组比较，P组4周后窦房结恢复时间（SNRT）和校正恢复时间（cSNRT）均延长（P<0.01）；P波时限2组比较差异没有统计学意义(P>0.05)。(4) P组2周后心脏超声与N组比较显示左心房前后、上下、左右径都有明显增大(P<0.01)，右心房上下增大(P<0.05)。结论: 持续４周心房高频起搏后房颤发生率高，心房肌、窦房结和房室结电生理发生特征性的相应改变，左、右心房不同程度扩大，提示电重塑、结构重塑与房颤的发生关系密切。

Effect of high-rate left atrial pacing on atrial remodeling and functions of sinoatrial node and atrioventricular node in dogs

AIM: To determine whether sinoatrial node (SAN) and atrioventricular node (AVN) undergo functional remodeling during atrial fibrillation (AF). METHODS: The Beagle dogs were randomized into pacing group (n=9) and control group (n=6). In open-chest dogs, the electrode catheters were sutured at left atria for pacing and data recording. SAN and AVN conductive properties were studied. The dogs in pacing group underwent 4 weeks of high-rate left atrial pacing (400 min-1). The dogs in control group were not subject to pacing. RESULTS: The animal model of chronic AF was successfully established by pacing the left atrium at 400 min-1 in the dogs. Two of those animals were recorded with spontaneous AF at the end of 2 weeks, and the induction rate of AF reached 100% following 4 weeks of pacing. The incidences of paroxysmal AF and permanent AF were significantly increased by pacing compared to control group. After 4 weeks of  pacing, atrial effective refractory periods (AERP) at various at pacing cycle lengths (PCL; 250 ms, 300 ms and 350 ms) were all statistically shorter than those in control group. Compared with control group, a longer AVN Wenckebach point ［(294.44±26.06)min-1 vs (328.33±24.01)min-1,P<0.05］ and longer atrioventricular node effective refractory period (AVERP) (P<0.01) in pacing group were observed. The sinus node recovery time (SNRT) and corrected SNRT both showed significant increases. No significant change of P-wave and PA interval between the two groups was found. The left atrial dimensions (anteroposterior, superoinferior and left-right diameters) and the right atrial superoinferior diameter were measured to be significantly increased after 2 weeks of pacing. CONCLUSION: The animal model of left atrium pacing can induce AF occurrence with a higher incidence. The characteristic electrophysiological indexes about atria, AVN and SAN were observed during AF in the canine model, indicating that electrical and structural remodeling accompanies with AVN and SAN remodeling during AF.