Department of Pediatrics, Harvard Medical School, Boston, MA, USA.
Am J Cardiol. 2009 Dec 15;104(12):1737-42. doi: 10.1016/j.amjcard.2009.07.061.
The hemodynamics after Fontan surgery are notable for hypertension and dilation of the right atrium (RA). The effect of this stress on atrial cytoarchitecture has not been systematically studied and might be relevant to arrhythmias and their treatment. Morphologic and histopathologic analyses were performed on tissue from the RA and left atrium (LA) from autopsy specimens of Fontan hearts (n = 47). The findings were compared to those from control samples from young patients with normal atrial hemodynamics (n = 15). Most Fontan specimens were from young patients who died after a relatively short duration of Fontan physiology. The tissues were analyzed for wall thickness, fibrosis content, and fibrosis pattern. The mean wall thickness for the RA (3.0 +/- 1.0 mm) and LA (2.3 +/- 0.6 mm) in the Fontan hearts was significantly greater than that in the control hearts (RA, 1.8 +/- 0.4 mm; LA, 1.8 +/- 0.5 mm; p <0.001 and p = 0.024, respectively). The predictors for thickening of the RA included (1) older age at Fontan surgery, (2) older age at death, and (3) longer duration of Fontan circulation. The Fontan hearts and control hearts exhibited nearly identical fibrosis patterns in the RA and LA. Neither wall thickness nor fibrosis varied with the underlying heart defect or style of Fontan connection. In conclusion, atrial remodeling after Fontan surgery for univentricular heart physiology involves increased wall thickness in both the RA and LA. Interstitial fibrosis was also observed in the Fontan atria; however, because a similar pattern was present in the control tissue, this likely represented normal fibroelastic atrial structure, rather than a specific response to Fontan hemodynamics. The degree of wall thickening observed in the Fontan atria was not so excessive as to preclude transmural lesions during catheter or surgical ablation of reentrant arrhythmias.
法乐四联症术后的血液动力学表现为高血压和右心房(RA)扩张。这种压力对心房细胞结构的影响尚未得到系统研究,可能与心律失常及其治疗有关。对法乐四联症心脏的尸检标本的右心房(RA)和左心房(LA)组织进行了形态学和组织病理学分析(n = 47)。将这些发现与来自具有正常心房血液动力学的年轻患者的对照样本(n = 15)进行了比较。大多数法乐四联症标本来自在经历相对较短的法乐四联症生理过程后死亡的年轻患者。对这些组织进行了壁厚度、纤维化含量和纤维化模式的分析。法乐四联症心脏的 RA(3.0 +/- 1.0 mm)和 LA(2.3 +/- 0.6 mm)的平均壁厚度明显大于对照组的心脏(RA,1.8 +/- 0.4 mm;LA,1.8 +/- 0.5 mm;p <0.001 和 p = 0.024)。RA 增厚的预测因素包括(1)法乐四联症手术时年龄较大,(2)死亡时年龄较大,以及(3)法乐四联症循环时间较长。法乐四联症心脏和对照组心脏的 RA 和 LA 均表现出几乎相同的纤维化模式。壁厚度和纤维化均不受基础心脏缺陷或法乐四联症连接方式的影响。总之,单心室心脏生理的法乐四联症术后心房重构涉及 RA 和 LA 壁厚度增加。在法乐四联症心房中也观察到间质纤维化;然而,由于对照组织中存在类似的模式,这可能代表正常的纤维弹性心房结构,而不是对法乐四联症血液动力学的特定反应。在法乐四联症心房中观察到的壁增厚程度并不足以在导管或手术消融折返性心律失常时导致穿透性病变。