Abnormal Left Ventricular Mechanics of Ventricular Ectopic Beats: Insights Into Origin and Coupling Interval in Premature Ventricular Contraction-Induced Cardiomyopathy.
Abnormal Left Ventricular Mechanics of Ventricular Ectopic Beats: Insights Into Origin and Coupling Interval in Premature Ventricular Contraction-Induced Cardiomyopathy.
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DOI：
10.1161/circep.115.003047
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发表时间：
2015-10
期刊：
影响因子：
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通讯作者：
Huizar JF
中科院分区：
文献类型：
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作者：
Potfay J;Kaszala K;Tan AY;Sima AP;Gorcsan J 3rd;Ellenbogen KA;Huizar JF
室性早搏（PVCs）引起的左心室（LV）不同步被认为是PVC诱导的心肌病（CM）的机制。我们试图了解不同PVC位置和耦合间期（早产）对LV局部力学和PVC搏动本身的整体功能的影响。使用我们的过早起搏算法，在200- 375 ms的耦合间隔下，从心外膜右心室（RV）心尖、RV流出道（RVOT）和LV游离壁输送五联室性早搏（PVC），以及在200 ms的耦合间隔下，从左心房（LA）附件输送房性早搏（PAC）。在所有异位搏动和VP期间获得LV短轴超声心动图图像、LV每搏输出量（SV）和dP/dtmax。通过上述每次搏动期间6个不同LV节段之间的QRS-峰值应变（最早-最后QRS-峰值应变）的离散度评估LV不同步性（GE，EchoPac）。与400 ms时的快速VP相比，375 ms时的长耦合PVC和短耦合PVC的LV不同步性更大（P<0.0001），而PVC位置之间没有差异。PVC偶联间期越长，SV和dP/dtmax越大，尽管不同步性更明显（P<0.001）。具有较长耦合间期的PVC表现出更明显的LV不同步，而PVC位置的影响最小。左心室不同步不能单独归因于早产或异常心室激动，而是两者的组合。这项研究表明，如果不同步性是PVC诱导的CM的主要机制，则晚偶联PVC可能导致更严重的心肌病。
Left ventricular (LV) dyssynchrony caused by premature ventricular contractions (PVCs) has been proposed as a mechanism of PVC-induced cardiomyopathy (CM). We sought to understand the impact of different PVC locations and coupling intervals (prematurity) on LV regional mechanics and global function of the PVC beat itself. Using our premature pacing algorithm, pentageminal PVCs at coupling intervals of 200–375ms were delivered from the epicardial right ventricular (RV) apex, RV outflow tract (RVOT), and LV free wall, as well as premature atrial contractions (PACs) from the left atrial (LA) appendage at a coupling interval of 200ms in seven healthy canines. LV short axis echocardiographic images, LV stroke volume (SV) and dP/dtmax were obtained during all ectopic beats and VP. LV dyssynchrony was assessed by dispersion of QRS-to-peak strain (earliest – last QRS-to-peak strain) between 6 different LV segments during each of the aforementioned beats (GE, EchoPac). LV dyssynchrony was greater during long- rather than short-coupled PVCs and PVCs at 375ms compared with rapid VP at 400ms (P<0.0001), whereas, no difference was found between PVC locations. Longer PVC coupling intervals were associated with greater SV and dP/dtmax despite more pronounced dyssynchrony (P<0.001). PVCs with longer coupling intervals demonstrate more pronounced LV dyssynchrony, whereas PVC location has minimal impact. LV dyssynchrony cannot be attributed to prematurity or abnormal ventricular activation alone, but rather to a combination of both. This study suggests that late-coupled PVCs may cause a more severe cardiomyopathy if dyssynchrony is the leading mechanism responsible for PVC-induced CM.