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Genetic markers of restenosis after coronary angioplasty and after stent implantation

机译：冠状动脉成形术后和支架植入后再狭窄的遗传标志

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Apart from coronary artery bypass grafting, percutaneous transluminal coronary angioplasty (PTCA) and intracoronary stent placement are well established treatment strategies for CAD. Substantial differences exist in the mechanisms of restenosis between conventional PTCA and stenting. Arterial remodeling is the main contributor to lumen re-narrowing after PTCA, whereas neointimal hyperplasia is almost the sole mechanism of restenosis after stenting. Several reports have demonstrated that genetic factors may be involved in the pathogenesis of restenosis after PTCA and in-stent restenosis. In this review the candidate genes involved in the pathogenesis of restenosis are analyzed as potential genetic markers of restenosis after PTCA and in-stent restenosis. The I/D angiotensin-I converting enzyme gene polymorphism, gene polymorphisms of the endothelial nitric oxide synthase (Glu298Asp, –786T>C), the glycoprotein IIIa PlA1/A2 gene polymorphism, gene polymorphism of the estrogen (PvuII), allele 2 of the interleukin-1ra gene, and the GT repeats in heme oxygenase-1 gene promoter may be used as genetic markers for in-stent-restenosis. On the other hand, only the stromelysin-1 5A/6A gene polymorphism and allele 2 of the interleukin -1ra gene may be used as a genetic marker for restenosis after PTCA.
机译：除冠状动脉搭桥术外，经皮腔内冠状动脉成形术（PTCA）和冠状动脉内支架置入术也是公认的CAD治疗策略。常规PTCA和支架置入术之间的再狭窄机制存在很大差异。 PTCA后，动脉重构是导致管腔重新狭窄的主要因素，而内膜增生几乎是支架置入后再狭窄的唯一机制。几篇报道表明，遗传因素可能与PTCA和支架内再狭窄后再狭窄的发病机理有关。在这篇综述中，参与再狭窄发病机制的候选基因被分析为PTCA和支架内再狭窄后再狭窄的潜在遗传标志。 I / D血管紧张素-I转换酶基因多态性，内皮型一氧化氮合酶的基因多态性（Glu298Asp，–786T> C），糖蛋白IIIa PlA1 / A2基因多态性，雌激素的基因多态性（PvuII），等位基因2白介素-1ra基因和血红素加氧酶-1基因启动子中的GT重复序列可以用作支架内再狭窄的遗传标记。另一方面，只有stromelysin-1 5A / 6A基因多态性和白介素-1ra基因的等位基因2可以用作PTCA后再狭窄的遗传标记。

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