Left ventricular systolic dysfunction induced by ventricular ectopy: a novel model for premature ventricular contraction-induced cardiomyopathy.
Left ventricular systolic dysfunction induced by ventricular ectopy: a novel model for premature ventricular contraction-induced cardiomyopathy.
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DOI：
10.1161/circep.111.962381
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发表时间：
2011-08
期刊：
影响因子：
--
通讯作者：
Wood MA
中科院分区：
文献类型：
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作者：
Huizar JF;Kaszala K;Potfay J;Minisi AJ;Lesnefsky EJ;Abbate A;Mezzaroma E;Chen Q;Kukreja RC;Hoke NN;Thacker LR 2nd;Ellenbogen KA;Wood MA
室性早搏通常与心肌病并存。最近，室性早搏已被确定为心肌病的可能原因。我们利用一种新颖的过早起搏算法建立了室性早搏诱导的心肌病动物模型，以评估这种心肌病的时间框架和可逆性，并检查相关的组织病理学异常。研究人员给13只杂种狗植入了一种能够模拟室性心动过速的特殊程序起搏器。动物被随机分配到12周的双性室性早搏组（n=7）和无室性早搏组（n= 6）。连续24小时动态心电图证实了PVC组的心室重分化（PVC 49.8% vs.对照组<0.01%,P < 0.0001）。12周后，只有PVC组出现心肌病，左室射血分数明显降低（PVC 39.7±5.4%，对照组60.7±3.8%，P<0.0001），左室收缩末期尺寸增加（LVESD, PVC 33.3±3.5mm，对照组23.7±3.6mm， P<0.001）。PVC组心室有效不应期有延长的趋势。室性早搏引起的心肌病在停用室性早搏后2-4周内消失。在室性早搏引起的心肌病中，未观察到炎症、纤维化、细胞凋亡和线粒体氧化磷酸化的变化。这种新颖的PVC动物模型表明，频繁的室性早搏可以在其他结构正常的心脏中诱发可逆形式的心肌病。pvc诱导的CM缺乏其他犬CM模型的大体组织病理学和线粒体异常。
Premature ventricular contractions (PVCs) commonly coexist with cardiomyopathy. Recently, PVCs have been identified as possible cause of cardiomyopathy. We developed a PVC-induced cardiomyopathy animal model using a novel premature pacing algorithm to assess timeframe and reversibility of this cardiomyopathy and examine the associated histopathological abnormalities. Thirteen mongrel dogs were implanted with a specially programmed pacemaker capable of simulating ventricular extrasystoles. Animals were randomly assigned to either 12 weeks of bigeminal PVCs (n=7) or no PVCs (control, n=6). Continuous 24-hr Holter corroborated ventricular bigeminy in the PVC group (PVC 49.8% vs. control <0.01%, P < 0.0001). After 12 weeks, only the PVC group developed cardiomyopathy with a significant reduction in left ventricular (LV) ejection fraction (PVC 39.7±5.4% vs. control 60.7±3.8%, P<0.0001) and an increase in LV end-systolic dimension (LVESD, PVC 33.3±3.5mm vs. control 23.7±3.6mm, P<0.001). Ventricular effective refractory period showed a trend to prolong in the PVC group. PVC-induced cardiomyopathy was resolved within 2-4 weeks after discontinuation of PVCs. No inflammation, fibrosis, or changes in apoptosis and mitochondrial oxidative phosphorylation were observed with PVC-induced cardiomyopathy. This novel PVC animal model demonstrates that frequent PVCs alone can induce a reversible form of cardiomyopathy in otherwise structurally normal hearts. PVC-induced CM lacks gross histopathological and mitochondrial abnormalities seen in other canine models of CM.