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首页> 外文期刊>American Journal of Physiology >Electromechanical analysis of infarct border zone in chronic myocardial infarction.
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Electromechanical analysis of infarct border zone in chronic myocardial infarction.

机译:慢性心肌梗塞梗死边界区的机电分析。

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摘要

To test the hypothesis that alterations in electrical activation sequence contribute to depressed systolic function in the infarct border zone, we examined the anatomic correlation of abnormal electromechanics and infarct geometry in the canine post-myocardial infarction (MI) heart, using a high-resolution MR-based cardiac electromechanical mapping technique. Three to eight weeks after an MI was created in six dogs, a 247-electrode epicardial sock was placed over the ventricular epicardium under thoracotomy. MI location and geometry were evaluated with delayed hyperenhancement MRI. Three-dimensional systolic strains in epicardial and endocardial layers were measured in five short-axis slices with motion-tracking MRI (displacement encoding with stimulated echoes). Epicardial electrical activation was determined from sock recordings immediately before and after the MR scans. The electrodes and MR images were spatially registered to create a total of 160 nodes per heart that contained mechanical, transmural infarct extent, and electrical data. The average depth of the infarct was 55% (SD 11), and the infarct covered 28% (SD 6) of the left ventricular mass. Significantly delayed activation (>mean + 2SD) was observed within the infarct zone. The strain map showed abnormal mechanics, including abnormal stretch and loss of the transmural gradient of radial, circumferential, and longitudinal strains, in the region extending far beyond the infarct zone. We conclude that the border zone is characterized by abnormal mechanics directly coupled with normal electrical depolarization. This indicates that impaired function in the border zone is not contributed by electrical factors but results from mechanical interaction between ischemic and normal myocardium.
机译:为了检验电激活序列的改变有助于梗塞边界区收缩功能降低的假说,我们使用高分辨率MR检查了犬心肌梗死后心肌的异常机电和梗死几何结构的解剖相关性基于心脏的机电映射技术。在六只狗中出现心梗后三到八周,在开胸手术中将247电极心外膜袜子放在心室心外膜上方。 MI的位置和几何形状通过延迟超增强MRI进行评估。使用运动追踪MRI(受激回波的位移编码)在五个短轴切片中测量心外膜和心内膜层的三维收缩应变。根据MR扫描前后的袜子记录确定心外膜电激活。对电极和MR图像进行空间配准,以创建每个心脏总共160个结点,其中包含机械,透壁梗死范围和电数据。梗塞的平均深度为55%(SD 11),梗塞面积占左心室肿块的28%(SD 6)。在梗塞区内观察到明显延迟的激活(>平均值+ 2SD)。应变图显示了异常的力学,包括异常拉伸,以及在远远超出梗塞区的区域中径向,周向和纵向应变的透壁梯度丢失。我们得出结论,边界区域的特征是机械异常直接与正常的电去极化耦合。这表明边界区功能受损不是由电因素引起的,而是由缺血性心肌与正常心肌之间的机械相互作用导致的。

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