Atrial remodeling after the Fontan operation.

Atrial remodeling after the Fontan operation.
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DOI:
10.1016/j.amjcard.2009.07.061
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发表时间:
2009-12-15
影响因子:
2.8
通讯作者:
Walsh, Edward P.
Walsh, Edward P.
中科院分区:
医学3区
文献类型:
--
作者:
Wolf, Cordula M.;Seslar, Stephen P.;den Boer, Karen;Juraszek, Amy L.;McGowan, Francis X.;Cowan, Douglas B.;Del Nido, Pedro;Triedman, John K.;Berul, Charles I.;Walsh, Edward P.

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Fontan手术后的血流动力学明显表现为右心房(RA)高血压和扩张。这种应激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Fontan心脏(n = 47)尸检标本的RA和左心房(LA)组织进行形态学和组织病理学分析,并与心房血流动力学正常的年轻患者(n = 15)的对照样本进行比较。大多数Fontan标本来自年轻患者,他们在Fontan生理学相对较短的时间后死亡。分析组织的壁厚度、纤维化含量和纤维化模式。Fontan心脏中RA(3.0±1.0 mm)和LA(2.3±0.6 mm)的平均壁厚显著大于对照心脏(分别为RA = 1.8±0.4 mm和LA = 1.8±0.5 mm,p<0.001和p=0.024)。RA增厚的预测因素包括:a)Fontan手术时年龄较大,B)死亡时年龄较大,c)Fontan循环持续时间较长。Fontan心脏和对照组表现出几乎相同的RA和LA纤维化模式。壁厚和纤维化均不随潜在心脏缺损或Fontan连接方式而变化。总之,单心室心脏生理学Fontan手术后的心房重构涉及RA和LA的壁厚增加。在Fontan心房中也观察到间质纤维化,但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Fontan血流动力学的特异性反应。Fontan房壁增厚程度不足以在导管或外科消融折返性心律失常时排除透壁损伤。
Hemodynamics following Fontan surgery are notable for right atrial (RA) hypertension and dilation. The effect of this stress on atrial cytoarchitecture has not been studied systematically, and may be relevant to arrhythmias and their treatment. Morphologic and histopathologic analysis was performed on RA and left atrial (LA) tissue from post-mortem specimens of Fontan hearts (n = 47) and compared to control samples from young patients with normal atrial hemodynamics (n = 15). Most Fontan specimens were from young patients who expired after a relatively short duration of Fontan physiology. Tissues were analyzed for wall thickness, fibrosis content, and fibrosis pattern. Mean wall thickness for both RA (3.0±1.0 mm) and LA (2.3±0.6 mm) in Fontan hearts was significantly greater than in control hearts (RA = 1.8±0.4 mm and LA = 1.8±0.5 mm, p<0.001 and p=0.024, respectively). Predictors for RA thickening included: a) older age at Fontan surgery, b) older age at death, and c) longer duration of Fontan circulation. Fontan hearts and controls exhibited nearly identical RA and LA fibrosis patterns. Neither wall thickness nor fibrosis varied with 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 Fontan atria, but because a similar pattern was present in control tissue, this likely represents normal fibroelastic atrial structure rather than a specific response to Fontan hemodynamics. The degree of wall thickening observed in Fontan atria was not so excessive as to preclude transmural lesions during catheter or surgical ablation of reentrant arrhythmias.
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