Schoels W, Kuebler W, Yang H, Gough W B, el-Sherif N
Department of Medicine, University of Heidelberg, Germany.
J Am Coll Cardiol. 1993 Jan;21(1):73-84. doi: 10.1016/0735-1097(93)90719-h.
This study was designed to test the concept of a functional/anatomic interaction in a canine model of reentry based on right atrial enlargement and to elucidate the electrophysiologic basis for functional conduction block.
The monotonic feature of atrial flutter suggests a uniform substrate for the arrhythmia. Atrial flutter in the sterile pericarditis model is due to single-loop circus movement around a functional or a functional/anatomic obstacle near the atrioventricular (AV) ring. Sustained circus movement requires a critical interaction of a functional arc of block, a natural obstacle, the AV ring and a zone of slow conduction. The location of the inferior vena cava predisposes the lower right atrium to single-loop reentry.
In 11 dogs with right atrial enlargement, 127 bipolar epicardial electrograms were obtained during atrial flutter. For correlation of activation and refractory maps, the effective refractory period under each electrode was determined using the extrastimulus technique.
Atrial flutter was due to single-loop reentry around functional arcs of block near the AV ring (n = 2) or around functional/anatomic obstacles (n = 8) involving the inferior vena cava. A slow zone was located between the arc and the AV ring and between the inferior vena cava and AV ring, respectively. During initiation, the arc joined the AV ring, forcing activation to proceed around the free end of the arc before breaking through the arc near the AV ring. Arrhythmia termination required the arc of block to rejoin the AV ring. Inducibility of sustained atrial flutter was associated with a marked spatial dispersion of refractoriness. The configuration of the functional arc of block was critically dependent on the spatial pattern of refractoriness.
Atrial flutter requires a similar functional or functional/anatomic substrate independent of the underlying etiology. The spatial distribution of refractoriness in enlarged canine atria provides an adequate substrate for the development of functional conduction block.
本研究旨在基于右心房扩大的犬类折返模型测试功能/解剖相互作用的概念，并阐明功能性传导阻滞的电生理基础。
心房扑动的单调特征提示该心律失常存在统一的基质。无菌性心包炎模型中的心房扑动是由于围绕房室（AV）环附近的功能性或功能性/解剖性障碍物的单环折返运动。持续的折返运动需要功能性阻滞弧、天然障碍物、AV环和缓慢传导区之间的关键相互作用。下腔静脉的位置使右下心房易发生单环折返。
在11只右心房扩大的犬中，在心房扑动期间获取了127个双极心外膜电图。为了关联激活图和不应期图，使用额外刺激技术确定每个电极下的有效不应期。
心房扑动是由于围绕AV环附近的功能性阻滞弧（n = 2）或围绕涉及下腔静脉的功能性/解剖性障碍物（n = 8）的单环折返。一个缓慢区分别位于阻滞弧与AV环之间以及下腔静脉与AV环之间。在起始时，阻滞弧与AV环相连，迫使激动在阻滞弧的自由端周围进行，然后在AV环附近突破阻滞弧。心律失常的终止需要阻滞弧重新与AV环相连。持续性心房扑动的可诱导性与明显的不应期空间离散有关。功能性阻滞弧的形态严重依赖于不应期的空间模式。
心房扑动需要类似的功能性或功能性/解剖性基质，而与潜在病因无关。扩大的犬心房中不应期的空间分布为功能性传导阻滞的发生提供了合适的基质。
