The E-selectin SER128ARG gene polymorphism and restenosis after successful coronary angioplasty

The E-selectin SER128ARG gene polymorphism and restenosis after successful coronary angioplasty
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DOI:
10.1016/s0167-5273(02)00073-6
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发表时间:
2002-06-01
影响因子:
3.5
通讯作者:
Gl채ser, C
Gl채ser, C
中科院分区:
医学2区
文献类型:
--
作者:
Rauchhaus, M;Gross, M;Gl채ser, C

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目的:冠状动脉血管成形术仍然受到再狭窄问题的困扰。遗传多态性可能通过介导内皮对血管成形术引起的损伤的过度炎症反应而导致再狭窄的发生。背景:E-选择素的丝氨酸(Ser)-128-精氨酸(Arg)基因多态性与冠状动脉疾病(CAD)的发病机制有关。我们试图探讨等位基因变异是否与血管成形术后再狭窄有关。方法:通过 PCR 对 101 名(衍生研究,年龄 54±1 岁,所有平均值+/-S.E.M.)和 92 名(验证研究,年龄 62±1 岁)接受成功血管成形术的 CAD 患者进行 128Arg 等位基因分析。结果:在随访期间,54/101 (53%) 和 43/92 (47%) 的患者发现再狭窄,定义为随访血管造影时目标病变处管腔直径减少 >50%。 128Arg等位基因频率在衍生研究中为10.39%,在验证研究中为11.96%。 128Arg 等位基因在再狭窄组中(分别为 14.81% 和 17.44%)比在无再狭窄组中更常见(分别为 5.32% 和 7.14%,p=0.027 和 p=0.031)。在多变量 Logistic 回归中,128Arg 等位基因在两项研究中均成为再狭窄的预测因子 (p0.20),并且在有再狭窄的患者与无再狭窄的患者之间也是如此 (43.8+/-3.2 vs. 47.4+/-3.1 ng/ml,p>0.20)。结论:E-选择素的128Arg等位基因可能与内皮细胞对损伤的反应增强有关,从而可能成为CAD患者血管成形术后再狭窄的危险因素。再狭窄的发生仍然是CAD患者的一个问题。在 101 名(衍生)和 92 名(验证)CAD 患者中分析了 E-选择素的 Ser128Arg 多态性。再狭窄患者(54/101 和 43/92)的 128Arg 等位基因频率(14.81 和 17.44%)高于没有再狭窄患者(5.32%,p=0.027 和 7.14%,p=0.031)。在逻辑回归中,128Arg 等位基因在两项研究中都成为再狭窄的预测因子 (p
Objectives: Coronary angioplasty remains plagued by the problem of restenosis. Genetic polymorphisms may contribute to the development of restenosis by mediating exaggerated inflammatory responses of the endothelium to angioplasty-induced injury. Background: The serine (Ser)-128-arginine (Arg) gene polymorphism of E-selectin has been implicated in the pathogenesis of coronary artery disease (CAD). We sought to explore whether allelic variants relate to post-angioplasty restenosis. Methods: The 128Arg allele was analyzed by PCR in 101 (derivation study, age 54+/-1 years, all mean+/-S.E.M.) and 92 (validation study, age 62 1 years) patients with CAD who underwent successful angioplasty. Results: Restenosis, defined as >50% luminal diameter reduction at the target lesion at follow-up angiography, was found in 54/101 (53%) and 43/92 (47%) patients during follow-up. The 128Arg allele frequency in the derivation study was 10.39% and was 11.96% in the validation study. The 128Arg allele was more prevalent in the restenosis groups (14.81% and 17.44%, respectively) than in the restenosis-free groups (5.32% and 7.14%, respectively, p=0.027 and p=0.031). In multivariate logistic regression, the 128Arg allele emerged as a predictor of restenosis in both studies (p0.20), and between patients with restenosis and those without (43.8+/-3.2 vs. 47.4+/-3.1 ng/ml, p>0.20). Conclusions: The 128Arg allele of E-selectin may be related to increased endothelial responses to injury, thereby potentially serving as a risk factor for post-angioplasty restenosis in patients with CAD.The development of restenosis remains a problem in patients with CAD. The Ser128Arg polymorphism of E-selectin was analyzed in 101 (derivation) and 92 (validation) CAD patients. Patients with restenosis (54/101 and 43/92) had a higher frequency of the 128Arg allele (14.81 and 17,44%) than those without (5.32%, p=0.027 and 7.14%, p=0.031). In logistic regression, the 128Arg allele emerged as a predictor of restenosis in both studies (p