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首页> 外文期刊>PACE: Pacing and clinical electrophysiology >Transmural mapping of myocardial refractoriness and endocardial dispersion of repolarization in an ovine model of chronic myocardial infarction.
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Transmural mapping of myocardial refractoriness and endocardial dispersion of repolarization in an ovine model of chronic myocardial infarction.

机译:在慢性心肌梗死绵羊模型中,心肌不应性的透壁映射和心内膜复极分布。

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BACKGROUND: Myocardial refractoriness and repolarization is an important electrophysiological property that, when altered, increases the risk of arrhythmogenesis. These electrophysiological changes associated with chronic myocardial infarction (MI) have not been studied in detail. We assessed the influence of left ventricular (LV) scarring on local refractoriness, repolarization, and electrogram characteristics. METHODS: MI was induced in five sheep by percutaneous left anterior descending artery occlusion for 3 hours. Mapping was performed at 19 +/- 6 weeks post-MI. A total of 20 quadripolar transmural needles were deployed at thoracotomy in the LV within and surrounding scar. Bipolar pacing was performed from each needle to assess the effective refractory period (ERP) of the subendocardium and subepicardium. The activation (AT) and repolarization (RT) times, and modified activation recovery interval (ARI(m)) were determined from endocardial unipolar electrograms recorded in sinus rhythm simultaneously from all needles. Scarring was quantified histologically and compared with electrophysiological characteristics. RESULTS: Increased scarring corresponded with increased ERP (P < 0.01), decreased subendocardial electrogram amplitude (P < 0.001), and slope (P < 0.001). ERP did not differ between endocardium and epicardium (P > 0.05). The ARI(m) and RT were prolonged during early myocardial activation (P < 0.001). After adjusting for AT, the RT and ARI(m) were prolonged in areas of scarring (P < 0.001). After adjusting for electrogram amplitude, the ARI(m) was prolonged in dense scar (P < 0.05). CONCLUSIONS: We confirmed histologically that scarring contributes to prolongation of repolarization, increased refractoriness, and reductions in conduction and voltage post-MI. Prolongation of repolarization may be further augmented when local activation is earliest or electrogram voltage is decreased within scar.
机译:背景:心肌的难治性和复极化是一种重要的电生理特性,当改变时,会增加心律失常的风险。尚未详细研究与慢性心肌梗死(MI)相关的这些电生理变化。我们评估了左心室(LV)疤痕对局部耐火性,复极和电描记图特征的影响。方法:5只绵羊经皮左前降支经皮阻塞3小时诱发心肌梗死。测绘在心梗后19 +/- 6周进行。共有20根四极经壁穿刺针在疤痕内及其周围的左室开胸术中展开。从每个针头进行双极起搏,以评估心内膜下和心外膜下的有效不应期(ERP)。从所有针头同时记录窦性心律的心内膜单极心电图确定激活(AT)和复极化(RT)时间以及修改的激活恢复间隔(ARI(m))。通过组织学定量瘢痕形成,并与电生理特征进行比较。结果:疤痕增加与ERP增加(P <0.01),心内膜下心电图幅度减少(P <0.001)和斜率(P <0.001)相对应。心内膜和心外膜之间的ERP没有差异(P> 0.05)。早期心肌激活期间ARI(m)和RT延长(P <0.001)。调整AT后,疤痕区域的RT和ARI(m)延长(P <0.001)。调整电描记图振幅后,致密疤痕中的ARI(m)延长(P <0.05)。结论:我们在组织学上证实瘢痕形成有助于延长复极时间,增加耐火度,并降低心梗后的传导和电压。当最早的局部激活或疤痕内的电描记图电压降低时,重新极化的时间可能会进一步增加。

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