Akoum Nazem W, Daccarett Marcos, Wasmund Stephen L, Hamdan Mohamed H
Nora Eccles Harrison Cardiovascular Research and Training Institute, Salt Lake City, Utah, USA.
Pacing Clin Electrophysiol. 2011 Mar;34(3):291-5. doi: 10.1111/j.1540-8159.2010.02947.x. Epub 2010 Nov 11.
Ectopy-induced cardiomyopathy is an increasingly recognized cause of reversible left ventricular (LV) dysfunction. The underlying mechanisms remain unknown. Our goal was to create an animal model for ectopy-induced cardiomyopathy.
Eleven mongrel dogs underwent the implantation of a dual-chamber pacemaker. Four dogs served as the control group and seven as the paced group. In the paced group, the pacemaker was connected to two endocardial right ventricular leads, one inserted into the atrial port and the other one into the ventricular port with an atrioventricular delay adjusted to ensure the presence of coupled pacing simulating ventricular bigeminy. Echocardiographic measurements of LV size (LV end-diastolic diameter [LV-EDD], LV end-systolic diameter [LV-ESD]), LV ejection fraction (LVEF), and mitral regurgitation (MR) were obtained at baseline and after 4 weeks of monitoring or pacing in all dogs except one who had lead dislodgement.
In the control group (n = 4), no significant changes in LV dimensions or function were noted. In the paced group (n = 6), LV-EDD and LV-ESD increased from 3.58 ± 0.65 cm and 2.47 ± 0.55 cm to 4.15 ± 0.59 cm and 3.21 ± 0.47 cm, respectively (P < 0.01). In addition, LVEF decreased from 60 ± 7% to 46 ± 9% (P < 0.05). No changes in MR were noted.
We have shown that coupled pacing simulating ventricular bigeminy was feasible and resulted in increased LV dimensions and decreased LV function. By controlling the percentage of pacing, the coupling interval and the location of the pacing lead, this new model will allow the assessment of the relative roles of these variables in the development of ectopy-induced cardiomyopathy.
异位心律诱发的心肌病是导致可逆性左心室（LV）功能障碍的一个日益被认识到的原因。其潜在机制尚不清楚。我们的目标是创建一个异位心律诱发的心肌病动物模型。
11只杂种犬接受了双腔起搏器植入。4只犬作为对照组，7只作为起搏组。在起搏组中，起搏器连接到两根心内膜右心室导线，一根插入心房端口，另一根插入心室端口，并调整房室延迟以确保存在模拟室性二联律的耦合起搏。除一只导线脱位的犬外，对所有犬在基线时以及监测或起搏4周后进行超声心动图测量左心室大小（左心室舒张末期直径[LV-EDD]、左心室收缩末期直径[LV-ESD]）、左心室射血分数（LVEF）和二尖瓣反流（MR）。
对照组（n = 4）左心室尺寸或功能无显著变化。起搏组（n = 6）中，LV-EDD和LV-ESD分别从3.58±０.65 cm和2.47±０.55 cm增加到4.15±０.59 cm和3.21±０.47 cm（P < 0.01）。此外，LVEF从60±7%降至46±9%（P < 0.05）。MR无变化。
我们已经证明模拟室性二联律的耦合起搏是可行的，并导致左心室尺寸增加和左心室功能降低。通过控制起搏百分比、耦合间期和起搏导线位置，这个新模型将有助于评估这些变量在异位心律诱发的心肌病发展中的相对作用。
