Schoels W, Gough W B, Restivo M, el-Sherif N
Department of Medicine, State University of New York, Brooklyn.
Circ Res. 1990 Jul;67(1):35-50. doi: 10.1161/01.res.67.1.35.
The mechanisms of single-loop reentry in a syncytium without anatomically predetermined pathways have not been shown. Using a "jacket electrode" with 111 bipolar electrodes in a nylon matrix, we mapped in situ the atrial epicardial surface during atrial flutter in dogs with sterile pericarditis. Of 21 episodes of reentrant atrial flutter, only four showed double-loop ("figure-eight") reentry, whereas in 17 episodes a single loop was present. During initiation of single-loop reentry, an arc of functional block extended to the atrioventricular (AV) ring. This forced activation to proceed as a single wave around the free end of the arc, before breaking through the arc close to the AV ring. Activation continued as one loop around an arc close to the AV ring (in eight episodes) or around a combined functional and anatomic obstacle (in nine episodes) when the arc joined an atrial vessel. A zone of slow conduction was consistently bordered by the arc of block and the AV ring or by the anatomic obstacle and the AV ring. Spontaneous termination occurred when conduction failed in this area and the arc rejoined the AV ring. High-density recordings (2 mm) along the arc of block showed double potentials separated by an isoelectric interval, interpreted as local activation and electrotonus due to activation on the opposite side of the arc. Histologically, a diffuse inflammatory reaction involved 50-80% of the atrial wall. A transitional layer of myocardial bundles with preserved cross striation, but separated by edema and inflammatory cells, was enclosed between an epicardial layer of fragmented myocytes and an endocardial layer of grossly intact myocardium. There were no distinctive features at sites of functional conduction block or slowed conduction. In conclusion, single-loop reentry is the common pattern during atrial flutter in this model. Its induction depends on an interaction of the AV ring, a functional arc of block, and a zone of slow conduction. The location of the inferior vena cava predisposes the lower right atrium to this type of reentry.
在没有解剖学上预先确定路径的心肌纤维网中,单环折返机制尚未得到证实。我们使用一种带有111个双极电极的尼龙基质“套状电极”,在无菌性心包炎犬心房扑动期间原位绘制心房心外膜表面图。在21次折返性心房扑动发作中,只有4次显示双环(“8字形”)折返,而17次发作中存在单环。在单环折返起始时,功能性阻滞弧延伸至房室(AV)环。这迫使激动作为单个波围绕弧的自由端进行,然后在靠近AV环处突破该弧。当弧与心房血管相连时,激动继续围绕靠近AV环的弧形成一个环(8次发作)或围绕功能性和解剖性联合障碍物形成一个环(9次发作)。一个缓慢传导区始终由阻滞弧和AV环或由解剖性障碍物和AV环界定。当该区域传导失败且弧重新与AV环连接时,自发终止发生。沿着阻滞弧的高密度记录(2毫米)显示双电位被等电位间隔分开,解释为由于弧另一侧的激动引起的局部激动和电紧张。组织学上,弥漫性炎症反应累及心房壁的50-80%。心肌束的过渡层保留了横纹,但被水肿和炎症细胞分隔,包绕在破碎心肌细胞的心外膜层和大体完整心肌的心内膜层之间。在功能性传导阻滞或传导减慢部位没有明显特征。总之,单环折返是该模型中心房扑动期间的常见模式。其诱发取决于AV环、功能性阻滞弧和缓慢传导区之间的相互作用。下腔静脉的位置使右心房下部易发生这种类型的折返。