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慢性心肌梗死绵羊模型中心肌不应期的透壁标测及复极的心内膜离散度

Transmural mapping of myocardial refractoriness and endocardial dispersion of repolarization in an ovine model of chronic myocardial infarction.

作者信息

Pouliopoulos Jim, Thiagalingam Aravinda, Eipper Vicki E, Campbell Craig, Ross David L, Kovoor Pramesh

机构信息

Department of Cardiology, Westmead Hospital, Sydney, Australia.

出版信息

Pacing Clin Electrophysiol. 2009 Jul;32(7):851-61. doi: 10.1111/j.1540-8159.2009.02399.x.

Abstract

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.

摘要

背景

心肌不应期和复极化是一项重要的电生理特性,一旦发生改变,会增加心律失常的风险。与慢性心肌梗死(MI)相关的这些电生理变化尚未得到详细研究。我们评估了左心室(LV)瘢痕形成对局部不应期、复极化及心电图特征的影响。

方法

通过经皮闭塞左前降支动脉3小时,在5只绵羊中诱导MI。在MI后19±6周进行标测。开胸手术时,在LV内瘢痕及其周围共置入20根四极透壁针。从每根针进行双极起搏,以评估心内膜下和心外膜下的有效不应期(ERP)。从所有针同步记录的窦性心律的心内膜单极心电图中确定激动(AT)和复极化(RT)时间,以及改良激动恢复间期(ARI(m))。对瘢痕进行组织学定量分析,并与电生理特征进行比较。

结果

瘢痕形成增加与ERP增加(P<0.01)、心内膜下心电图振幅降低(P<0.)、斜率降低(P<0.001)相关。心内膜和心外膜之间的ERP无差异(P>0.05)。在心肌早期激动期间,ARI(m)和RT延长(P<0.001)。校正AT后,瘢痕形成区域的RT和ARI(m)延长(P<0.001)。校正心电图振幅后,致密瘢痕中的ARI(m)延长(P<0.05)。

结论

我们通过组织学证实,瘢痕形成导致MI后复极化延长、不应期增加以及传导和电压降低。当瘢痕内局部激动最早或心电图电压降低时,复极化延长可能会进一步加剧。

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