title: High rate of in-stent restenosis after coronary intervention in carriers of the mutant mannose-binding lectin allele.
abstract: 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.
authors.affiliation: Heart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary. bagyura@gmail.com.
authors.forename: Zsolt
authors.identifier: 0000-0001-8120-2322
authors.initials: Z
authors.lastname: Bagyura
authors.affiliation: Heart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
authors.forename: Loretta
authors.initials: L
authors.lastname: Kiss
authors.affiliation: Heart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
authors.forename: Balázs
authors.initials: B
authors.lastname: Berta
authors.affiliation: 3rd Department of Internal Medicine, Research Laboratory, Semmelweis University, Budapest, Hungary.
authors.forename: Ágnes
authors.initials: Á
authors.lastname: Szilágyi
authors.affiliation: Heart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.|Department of Cardiology, University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
authors.forename: Kristóf
authors.initials: K
authors.lastname: Hirschberg
authors.affiliation: Heart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
authors.forename: Gábor
authors.initials: G
authors.lastname: Széplaki
authors.affiliation: Heart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
authors.forename: Árpád
authors.initials: Á
authors.lastname: Lux
authors.affiliation: Heart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Szelid
authors.affiliation: Heart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
authors.forename: Pál
authors.initials: P
authors.lastname: Soós
authors.affiliation: Heart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
authors.forename: Béla
authors.initials: B
authors.lastname: Merkely
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000628:therapy*; D023903:Coronary Restenosis / Q000000981:diagnostic imaging / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D016015:Logistic Models; D008297:Male; D037601:Mannose-Binding Lectin / Q000235:genetics*; D008670:Metals; D008875:Middle Aged; D015999:Multivariate Analysis; D016017:Odds Ratio; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects* / Q000295:instrumentation*; D010641:Phenotype; D020641:Polymorphism, Single Nucleotide; D011446:Prospective Studies; D011474:Prosthesis Design; D060888:Real-Time Polymerase Chain Reaction; D018570:Risk Assessment; D012307:Risk Factors; D015607:Stents; D013997:Time Factors
chemical_list: C445619:MBL2 protein, human; D037601:Mannose-Binding Lectin; D008670:Metals
keywords: Bare metal stent; Cardiology; Gene association; In-stent restenosis; MBL genetic variant