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梗死的、Langendorff灌注的人体心脏中的室性心动过速:存活心肌纤维排列的作用

Ventricular tachycardia in the infarcted, Langendorff-perfused human heart: role of the arrangement of surviving cardiac fibers.

作者信息

de Bakker J M, Coronel R, Tasseron S, Wilde A A, Opthof T, Janse M J, van Capelle F J, Becker A E, Jambroes G

机构信息

Department of Experimental Cardiology, Academic Medical Center, Amsterdam, The Netherlands.

出版信息

J Am Coll Cardiol. 1990 Jun;15(7):1594-607. doi: 10.1016/0735-1097(90)92832-m.

DOI:10.1016/0735-1097(90)92832-m
PMID:2345240
Abstract

Electrophysiologic and histologic studies were performed on Langendorff-perfused human hearts from patients who underwent heart transplantation because of extensive infarction. In nine hearts, 15 sustained ventricular tachycardias could be induced by programmed stimulation. In all hearts, mapping of epicardial and endocardial electrical activity during tachycardia was carried out. Histologic examination of the infarcted area between the site of latest activation of one cycle and the site of earliest activation of the next cycle revealed zones of viable myocardial tissue. In two hearts in which the time gap between latest and earliest activation was small, surviving myocardial tissue constituted a continuous tract that traversed the infarct. In three other hearts in which the time gap was large, surviving tissue consisted of parallel bundles that coursed separately over a few hundred micrometers, then merged into a single bundle and finally branched again. The direction of the fibers within the bundles was perpendicular to the direction of the activation front in that area. A similar type of inhomogeneous anisotrophy and activation delay was found in an infarcted papillary muscle removed from one of the explanted hearts and studied in a tissue bath during basic stimulation. Histologic examination of this preparation revealed that the delay was caused by a zigzag route of activation over branching and merging bundles of surviving myocytes separated by connective tissue.

摘要

对因广泛梗死而接受心脏移植患者的Langendorff灌注人心进行了电生理和组织学研究。在9颗心脏中,通过程序刺激可诱发15次持续性室性心动过速。在所有心脏中,均在心动过速期间进行了心外膜和心内膜电活动标测。对一个心动周期最晚激动部位与下一个心动周期最早激动部位之间梗死区域的组织学检查发现了存活心肌组织区域。在最晚和最早激动之间时间间隔较小的两颗心脏中,存活心肌组织构成了一条穿过梗死区的连续束带。在另外三颗时间间隔较大的心脏中,存活组织由平行束组成,这些束在几百微米的范围内分别走行,然后合并成一束,最后再次分支。束内纤维的方向与该区域激动波前的方向垂直。在从一颗移植心脏中取出并在组织浴中进行基础刺激研究的梗死乳头肌中,也发现了类似类型的不均匀各向异性和激动延迟。对该标本的组织学检查显示,延迟是由激动在被结缔组织分隔的存活心肌细胞分支和合并束上呈曲折路径所致。

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