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心肌梗死中间带折返环的形成。

Formation of reentrant circuits in the mid-myocardial infarct border zone.

作者信息

Ciaccio Edward J, Coromilas James, Wit Andrew L, Peters Nicholas S, Garan Hasan

机构信息

Division of Cardiology, Department of Medicine, Columbia University Medical Center, New York, United States.

Division of Cardiovascular Diseases & Hypertension, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, United States.

出版信息

Comput Biol Med. 2016 Apr 1;71:205-13. doi: 10.1016/j.compbiomed.2016.02.009. Epub 2016 Feb 22.

DOI:10.1016/j.compbiomed.2016.02.009
PMID:26945600
Abstract

INTRODUCTION

In this study, the mechanisms for onset and maintenance of mid-myocardial (intramural) reentrant circuits are considered, based upon anatomical structure.

METHOD

A model of electrical activation wavefront curvature in the mid-myocardial postinfarction border zone is developed. Two arrhythmogenic structures are considered: 1. a constrained slab of viable tissue, and 2. a strand of surviving myocardial fibers with distal expansion. Equations are formulated to estimate activation coupling intervals, and ranges in taper and circuit dimensions, that will support functional conduction block during premature stimulation and reentrant ventricular tachycardia.

RESULTS

For onset and maintenance of reentry, the arrhythmogenic regions forming both slab and strand circuits are in the range of 50-600µm at their thinnest dimension. For constrained slabs, unidirectional block leading to reentry forms in the thin-to-thick direction during premature stimulation, and functional block at lateral boundaries enable formation of a double-loop circuit. The activation wavefront proceeds around the impediment and then curves in the opposite direction through the slab, reentering the previously excited tissue. For strands, unidirectional block forms at a distal expansion in response to premature stimulation. The strand reentrant circuit is bounded by infarcted tissue causing anatomical block, and can be single-loop or coaxial. For all architectures, circuit dimensions ranging from 1.6×1.6mm to 3.5×3.5mm support functional block when premature stimulus coupling intervals are 117-150ms and ventricular tachycardia cycle lengths are 160-350ms.

CONCLUSIONS

For slab and strand mid-myocardial arrhythmogenic structures, taper and circuit dimensions govern ranges in premature excitation coupling intervals and tachycardia cycle lengths necessary to support functional block.

摘要

引言

在本研究中,基于解剖结构探讨了心肌中层(壁内)折返环路的起始和维持机制。

方法

建立了心肌梗死后边缘区电激活波前曲率模型。考虑了两种致心律失常结构:1. 一块受约束的存活组织平板;2. 一束有远端扩张的存活心肌纤维。制定了方程来估计激活耦合间期,以及在过早刺激和折返性室性心动过速期间支持功能性传导阻滞的锥度和环路尺寸范围。

结果

对于折返的起始和维持,形成平板和束状环路的致心律失常区域在其最薄维度上为50 - 600μm。对于受约束的平板,过早刺激期间在薄到厚的方向上形成导致折返的单向阻滞,并且侧向边界处的功能性阻滞使得能够形成双环回路。激活波前绕过障碍物,然后在相反方向穿过平板弯曲,重新进入先前兴奋的组织。对于束状结构,过早刺激时在远端扩张处形成单向阻滞。束状折返环路由导致解剖学阻滞的梗死组织界定,可以是单环或同轴的。对于所有结构,当过早刺激耦合间期为117 - 150ms且室性心动过速周期长度为160 - 350ms时,尺寸范围为1.6×1.6mm至3.5×3.5mm的环路支持功能性阻滞。

结论

对于平板和束状心肌中层致心律失常结构,锥度和环路尺寸决定了支持功能性阻滞所需的过早兴奋耦合间期和心动过速周期长度范围。

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