Mori Yoshiki, Shoji Makiko, Nakanishi Toshio, Fujii Takanari, Nakazawa Makoto
Department of Pediatric Cardiology, Tokyo Women's Medical University, Shinjuku-ku, Tokyo, Japan.
Am Heart J. 2007 Jun;153(6):987-94. doi: 10.1016/j.ahj.2007.03.009.
Aortopulmonary collaterals (APCs) are frequently observed before and after the Fontan procedure. However, the mechanism of the development of APCs is unknown. We hypothesized that one or several antiangiogenic and/or angiogenic growth factors might play a role in the development of APCs.
Eighty-five patients were enrolled and divided into 3 groups (Fontan group: 30 patients after the Fontan procedure, cyanotic group: 29 patients with cyanotic heart disease, and control group: 26 patients with cyanotic heart disease after biventricular repair). We measured basic fibroblast growth factor, vascular endothelial growth factor (VEGF), hepatocyte growth factor, and endostatin at catheterization. Angiographic evaluation for the presence of APCs using a 4-point scale (grade 1: absent APCs, > or = grade 2: significantly present APCs) was performed, and the relation of the serum levels of these factors to the presence of APCs was assessed.
The grade of APCs significantly increased in the Fontan group, but it decreased in the control group. The serum VEGF levels were higher in the Fontan group (280 +/- 174 pg/mL) and the cyanotic group (302 +/- 245 pg/mL) than in the control group (111 +/- 91 pg/mL) (P = .0004), and they were higher in patients with APCs (383 +/- 204 pg/mL) than in those without APCs (115 +/- 65 pg/mL) (P < .0001). There was no significant difference in the serum basic fibroblast growth factor, hepatocyte growth factor, and endostatin levels between the 3 groups.
Aortopulmonary collaterals increase after the Fontan procedure. Serum VEGF levels are associated with the presence of APCs. Vascular endothelial growth factor may play a role in the development of APCs in patients with cyanotic heart disease and after the Fontan procedure.
在Fontan手术前后常可观察到主肺动脉侧支血管（APCs）。然而，APCs形成的机制尚不清楚。我们推测一种或几种抗血管生成和/或血管生成生长因子可能在APCs的形成中起作用。
纳入85例患者并分为3组（Fontan组：30例Fontan手术后患者；青紫组：29例青紫型心脏病患者；对照组：26例双心室修复后的青紫型心脏病患者）。我们在导管插入术时测量碱性成纤维细胞生长因子、血管内皮生长因子（VEGF）、肝细胞生长因子和内皮抑素。使用4分制（1级：无APCs，≥2级：明显存在APCs）对APCs的存在进行血管造影评估，并评估这些因子的血清水平与APCs存在之间的关系。
Fontan组APCs分级显著增加，但对照组则降低。Fontan组（280±174 pg/mL）和青紫组（302±245 pg/mL）的血清VEGF水平高于对照组（111±91 pg/mL）（P = 0.0004），且有APCs的患者（383±204 pg/mL）高于无APCs的患者（115±65 pg/mL）（P < 0.0001）。3组之间血清碱性成纤维细胞生长因子、肝细胞生长因子和内皮抑素水平无显著差异。
Fontan手术后主肺动脉侧支血管增加。血清VEGF水平与APCs的存在相关。血管内皮生长因子可能在青紫型心脏病患者及Fontan手术后APCs的形成中起作用。
