Bromberg B I, Schuessler R B, Gandhi S K, Rodefeld M D, Boineau J P, Huddleston C B
Division of Pediatric Cardiology, Washington University School of Medicine, St. Louis, Missouri, USA.
J Electrocardiol. 1998;30 Suppl:85-93. doi: 10.1016/s0022-0736(98)80038-1.
Atrial flutter (AFL) is a common problem in children who have undergone a Fontan operation for single ventricle physiology. Although this has been attributed to the atrial stretch inherent in the earlier forms of this operation, AFL has persisted in spite of a modification that minimizes atrial distension. Therefore, it was hypothesized that AFL following the modified Fontan procedure may result from anatomic barriers related to suture lines rather than from atrial stretch or hypertension. In a series of experiments performed in dogs under general anesthesia, the modified Fontan repair was simulated by placing only the suture line of the intra-atrial repair. No baffle was placed, thus avoiding any hemodynamic alterations. After closure of the atriotomy, 253 point unipolar atrial endocardial form-fitting electrodes were inserted through the mitral and tricuspid valves via bilateral ventriculotomies. Induction of AFL was attempted with atrial burst pacing and programmed extrastimulation, and activation sequence maps of subsequent reentry were generated from the endocardial electrodes. Atrial flutter was induced in all of 17 dogs, with a median cycle length of 177 +/- 31 ms. Activation sequence maps demonstrated conduction block along the crista terminalis corresponding to the free wall portion of the suture line. This created an isthmus between the suture line and tricuspid annulus, which appeared critical for sustaining AFL, although the circuit used both the septal and free wall surfaces of the right atrium. In seven dogs, a cryolesion was placed from the tricuspid annulus to the free wall segment of the suture line, terminating the AFL, in all seven. When the free wall segment of the suture line was moved 5 mm medial to the crista terminalis, AFL was induced in four of five dogs, but only in the presence of isoproterenol and at a shorter cycle length (136 +/- 8 ms, P < .001). Atrial flutter was not inducible, even with the addition of isoproterenol, in any of five dogs in which the suture line was placed 10 mm anterior to the crista terminalis and incorporated into closure of the atriotomy. This acute canine model of the modified Fontan operation demonstrates that conduction block from the free wall portion of the suture line creates an isthmus of tissue between the suture line and the tricuspid annulus. This is a sufficient substrate to produce AFL; no hemodynamic alteration is required. Injury to the crista terminalis is a significant risk factor in this model, which suggests that a modification of the suture line might reduce the incidence of AFL in patients following this operation.
心房扑动（AFL）是接受过单心室生理Fontan手术的儿童中常见的问题。尽管这被归因于该手术早期形式中固有的心房拉伸，但尽管进行了使心房扩张最小化的改良，AFL仍持续存在。因此，有人提出假设，改良Fontan手术后的AFL可能是由与缝线相关的解剖学屏障引起的，而不是由心房拉伸或高血压引起的。在一系列对全麻下的犬进行的实验中，仅通过放置心房内修复的缝线来模拟改良Fontan修复。未放置挡板，从而避免任何血流动力学改变。心房切开术关闭后，通过双侧心室切开术经二尖瓣和三尖瓣插入253个点的单极心房心内膜贴合电极。尝试通过心房猝发起搏和程控期外刺激诱发AFL，并从心内膜电极生成后续折返的激动顺序图。17只犬均诱发了心房扑动，中位周期长度为177±31毫秒。激动顺序图显示沿对应于缝线游离壁部分的终末嵴存在传导阻滞。这在缝线和三尖瓣环之间形成了一个峡部，这似乎对维持AFL至关重要，尽管折返环使用了右心房的间隔和游离壁表面。在7只犬中，从三尖瓣环到缝线的游离壁段放置了冷冻损伤，7只犬的AFL均终止。当缝线的游离壁段向终末嵴内侧移动5毫米时，5只犬中有4只诱发了心房扑动，但仅在存在异丙肾上腺素的情况下且周期长度较短（136±8毫秒，P<.001）。在5只将缝线放置在终末嵴前方10毫米并纳入心房切开术关闭的犬中，即使添加异丙肾上腺素也未诱发心房扑动。这种改良Fontan手术的急性犬模型表明，缝线游离壁部分的传导阻滞在缝线和三尖瓣环之间形成了一个组织峡部。这是产生AFL的充分基质；不需要血流动力学改变。在该模型中，终末嵴损伤是一个重要的危险因素，这表明缝线的改良可能会降低该手术后患者心房扑动的发生率。
