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犬心肌梗死晚期的折返性室性心律失常。13. 激动图与不应期图的相关性。

Reentrant ventricular arrhythmias in the late myocardial infarction period in the dog. 13. Correlation of activation and refractory maps.

作者信息

Gough W B, Mehra R, Restivo M, Zeiler R H, el-Sherif N

出版信息

Circ Res. 1985 Sep;57(3):432-42. doi: 10.1161/01.res.57.3.432.

DOI:10.1161/01.res.57.3.432
PMID:4028346
Abstract

Isochronal maps of ventricular activation were analyzed in dogs 3-5 days after ligation of the left anterior descending coronary artery utilizing a 64-channel multiplexer. Isochronal maps of the effective refractory period were determined from 62 epicardial sites and correlated with the activation maps. The ischemia occurring in the surviving epicardial layer prolonged refractoriness in a spatially nonuniform manner. The resulting pattern of refractoriness on the epicardial surface resembled concentric rings of isorefractoriness which increased in duration from the normal zone to the center of the ischemic zone. The formation of an arc of functional unidirectional conduction block occurred along the gradient of refractoriness and the exact location of the arc depended on the S1-S2 interval. When a short S1-S2 failed to induce reentry, fewer adjacent sites with sufficiently disparate refractoriness formed a smaller arc of block. A subsequent S3 encountered further nonuniformly shortened refractoriness (normal areas had shortened refractoriness greater than ischemic areas) and the arc of block was lengthened. This required a longer time for the wavefront to circulate around the arc. When it then reached the distal side of the arc, refractoriness had expired proximal to the arc and reentry occurred. Similarly, nonuniform shortening of refractoriness explained why one reentrant beat may or may not produce successive reentrant beats. Therefore, the spatial pattern of refractoriness forms the substrate for the arc of unidirectional conduction block that is fundamental to the development of ventricular reentry in this experimental model.

摘要

利用64通道多路复用器,分析了左冠状动脉前降支结扎3至5天后犬的心室激活等时图。从62个心外膜部位确定有效不应期的等时图,并与激活图相关联。存活的心外膜层发生的缺血以空间不均匀的方式延长了不应期。心外膜表面产生的不应期模式类似于等不应期的同心环,从正常区域到缺血区域中心,其持续时间增加。功能性单向传导阻滞弧沿着不应期梯度形成,弧的确切位置取决于S1-S2间期。当短的S1-S2未能诱发折返时,较少的相邻部位具有足够不同的不应期,形成较小的阻滞弧。随后的S3遇到进一步非均匀缩短的不应期(正常区域的不应期缩短大于缺血区域),阻滞弧延长。这需要更长的时间让波前围绕弧循环。当它随后到达弧的远端时,弧近端的不应期已经过期,折返发生。同样,不应期的非均匀缩短解释了为什么一个折返搏动可能产生也可能不产生连续的折返搏动。因此,不应期的空间模式形成了单向传导阻滞弧的基础,这在该实验模型中是心室折返发生的根本。

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