Bagyura Zsolt, Kiss Loretta, Berta Balázs, Szilágyi Ágnes, Hirschberg Kristóf, Széplaki Gábor, Lux Árpád, Szelid Zsolt, Soós Pál, Merkely Béla
Heart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
3rd Department of Internal Medicine, Research Laboratory, Semmelweis University, Budapest, Hungary.
BMC Cardiovasc Disord. 2017 Jan 5;17(1):4. doi: 10.1186/s12872-016-0440-y.
In-stent restenosis occurs in 10-30% of patients following bare metal stent (BMS) implantation and has various risk factors. Mannose-binding lectin (MBL) is known to have effect on the progression of atherosclerosis. Single nucleotide polymorphisms (SNP) of the MBL2 gene intron 1 (codon 52, 54, 57) are known to modulate the bioavailability of the MBL protein. Our aim was to identify the association of these polymorphisms of the MBL gene in the occurrence of in-stent restenosis after coronary artery bare metal stent implantation.
In a non-randomized prospective study venous blood samples were collected after recoronarography from 225 patients with prior BMS implantation. Patients were assigned to diffuse restenosis group and control group based on the result of the coronarography. MBL genotypes were determined using quantitative real-time PCR. Proportion of different genotypes was compared and adjusted with traditional risk factors using multivariate logistic regression.
Average follow-up time was 1.0 (+ - 1.4) year in the diffuse restenosis group (N = 117) and 2.7 (+ - 2.5) years in the control group (N = 108). The age, gender distribution and risk status was not different between study groups. Proportion of the MBL variant genotype was 26.8% (29 vs. 79 normal homozygous) in the control group and 39.3% (46 vs. 71 normal homozygous) in the restenosis group (p = 0.04). In multivariate analysis the mutant allele was an independent risk factor (OR = 1.96, p = 0.03) of in-stent restenosis.
MBL polymorphisms are associated with higher incidence of development of coronary in-stent restenosis. The attenuated protein function in the mutant allelic genotype may represent the underlying mechanism.
裸金属支架（BMS）植入术后，10%-30%的患者会发生支架内再狭窄，且存在多种风险因素。已知甘露糖结合凝集素（MBL）对动脉粥样硬化的进展有影响。MBL2基因内含子1（密码子52、54、57）的单核苷酸多态性（SNP）可调节MBL蛋白的生物利用度。我们的目的是确定这些MBL基因多态性与冠状动脉裸金属支架植入术后支架内再狭窄发生之间的关联。
在一项非随机前瞻性研究中，对225例曾植入BMS的患者进行再次冠状动脉造影后采集静脉血样本。根据冠状动脉造影结果将患者分为弥漫性再狭窄组和对照组。采用定量实时PCR法测定MBL基因型。比较不同基因型的比例，并使用多因素逻辑回归对传统风险因素进行校正。
弥漫性再狭窄组（N = 117）的平均随访时间为1.0（±1.4）年，对照组（N = 108）为2.7（±2.5）年。研究组之间的年龄、性别分布和风险状况无差异。对照组中MBL变异基因型的比例为26.8%（29例变异型对79例正常纯合子），再狭窄组为39.3%（46例变异型对71例正常纯合子）（p = 0.04）。多因素分析显示，突变等位基因是支架内再狭窄的独立危险因素（OR = 1.96，p = 0.03）。
MBL多态性与冠状动脉支架内再狭窄的较高发生率相关。突变等位基因基因型中蛋白功能减弱可能是其潜在机制。
