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采用开胸右室起搏方法建立犬心动过速心肌病模型的初步尝试
庄晓华1,徐涛2,王昊2,廖德宁2
0
(1.上海市浦东医院心内科,上海 201399
2.第二军医大学长征医院心内科,上海 200003)
摘要:
目的 初步尝试建立室性早搏诱发心动过速性心肌病犬模型,并探讨频发室早对左心功能的影响。方法 健康杂种犬随机分为假手术组、起搏组(n=8)。起搏组犬在开胸直视条件下,分别于右室心尖和右室流出道缝制起搏电极,连接脉冲发放器,调节起搏参数,建立室性早搏二联律模型。假手术组同样行开胸手术,但不给予起搏。术前及术后4周,所有犬行超声心动图检查。结果 4周后,起搏组1只犬死于感染;起搏组犬左室舒张末期内径(cm)较术前增大(3.35±0.27 vs 2.86±0.10, P<0.05),左室收缩末期内径(cm)也较术前增大(2.72±0.21 vs 2.07±0.20, P<0.05),左室射血分数较术前减小\[(43.66±3.88)% vs (67.57±4.49)%,P<0.05\]。假手术组手术前后无明显改变。结论 采用开胸右室程序起搏可初步建立室性早搏二联律犬模型,频发室性早搏可导致左心室扩大和左心功能减退。
关键词:  室性早搏复合征  二联律  扩张型心肌病  动物模型
DOI:
投稿时间:2013-03-25修订日期:2013-07-07
基金项目:
Implanting dual-chamber pacemaker through right thoracotomy to establish a canine tachycardia-mediated cardiomyopathy model
ZHUANG Xiao-hua1,XU Tao2,WANG Hao2,LIAO De-ning2
(1. Department of Cardiology, Shanghai Pudong Hospital, Shanghai 201399, China
2. Department of Cardiology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China
*Corresponding author.)
Abstract:
Objective To create a canine model of premature ventricular contraction-induced tachycardia-mediated cardiomyopathy, and to explore the effect of frequent premature ventricular contraction on the function of the left ventricular function. Methods Sixteen mongrel dogs were randomly divided into sham operation group and paced group. Animals in the paced group underwent the implantation of a dual-chamber pacemaker through right thoracotomy, and the pacemaker was connected to two epicardial right ventricular leads, with one creviced in the cardiac apex and the other one in the outflow tract of the right ventricle, with an atrioventricular delay adjusted to ensure the presence of coupled pacing to simulate ventricular bigeminy. Dogs in the control group were not connected to the leads. Echocardiographic measurements were obtained before and 4 weeks after operation. Results One dog in the paced group died of infection after 4 weeks. In the paced group (n=7), LV end-diastolic diameter (LV-EDD) increased from (2.86±0.10) cm before operation to (3.35±0.27) cm after operation (P<0.05) and LV end-systolic diameter (LV-ESD) increased from (2.07±0.20) cm before operation to (2.72±0.21) cm after operation (P<0.05). In addition, the left ventricular ejection fraction (LVEF) decreased from (67.57±4.49)% before operation to (43.66±3.88) % after operation (P<0.05). No significant changes in LV dimensions or function were noted before and after operation in the control group. Conclusion It is feasible to simulate ventricular bigeminy with coupled pacing in canines. Premature ventricular contraction-induced cardiomyopathy can lead to increased LV dimensions and decreased LV function.
Key words:  ventricular premature complexes  bigeminy  dilated cardiomyopathy  animal models