High rate of in-stent restenosis after coronary intervention in carriers of the mutant mannose-binding lectin allele

Zsolt Bagyura, Loretta Kiss, Balázs Berta, Ágnes Szilágyi, Kristóf Hirschberg, Gábor Széplaki, Árpád Lux, Zsolt Szelid, Pál Soós, B. Merkely

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Background: 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. Methods: 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. Results: 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. Conclusions: 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.

Original languageEnglish
Article number4
JournalBMC Cardiovascular Disorders
Volume17
Issue number1
DOIs
Publication statusPublished - Jan 5 2017

Fingerprint

Coronary Restenosis
Mannose-Binding Lectin
Stents
Alleles
Genotype
Metals
Control Groups
Age Distribution
Codon
Introns
Biological Availability
Genes
Single Nucleotide Polymorphism
Real-Time Polymerase Chain Reaction
Atherosclerosis
Coronary Vessels
Proteins
Multivariate Analysis
Logistic Models
Prospective Studies

Keywords

  • Bare metal stent
  • Cardiology
  • Gene association
  • In-stent restenosis
  • MBL genetic variant

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

High rate of in-stent restenosis after coronary intervention in carriers of the mutant mannose-binding lectin allele. / Bagyura, Zsolt; Kiss, Loretta; Berta, Balázs; Szilágyi, Ágnes; Hirschberg, Kristóf; Széplaki, Gábor; Lux, Árpád; Szelid, Zsolt; Soós, Pál; Merkely, B.

In: BMC Cardiovascular Disorders, Vol. 17, No. 1, 4, 05.01.2017.

Research output: Contribution to journalArticle

Bagyura, Z, Kiss, L, Berta, B, Szilágyi, Á, Hirschberg, K, Széplaki, G, Lux, Á, Szelid, Z, Soós, P & Merkely, B 2017, 'High rate of in-stent restenosis after coronary intervention in carriers of the mutant mannose-binding lectin allele', BMC Cardiovascular Disorders, vol. 17, no. 1, 4. https://doi.org/10.1186/s12872-016-0440-y
Bagyura, Zsolt ; Kiss, Loretta ; Berta, Balázs ; Szilágyi, Ágnes ; Hirschberg, Kristóf ; Széplaki, Gábor ; Lux, Árpád ; Szelid, Zsolt ; Soós, Pál ; Merkely, B. / High rate of in-stent restenosis after coronary intervention in carriers of the mutant mannose-binding lectin allele. In: BMC Cardiovascular Disorders. 2017 ; Vol. 17, No. 1.
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abstract = "Background: 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. Methods: 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. Results: 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. Conclusions: 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.",
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AU - Bagyura, Zsolt

AU - Kiss, Loretta

AU - Berta, Balázs

AU - Szilágyi, Ágnes

AU - Hirschberg, Kristóf

AU - Széplaki, Gábor

AU - Lux, Árpád

AU - Szelid, Zsolt

AU - Soós, Pál

AU - Merkely, B.

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N2 - Background: 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. Methods: 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. Results: 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. Conclusions: 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.

AB - Background: 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. Methods: 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. Results: 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. Conclusions: 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.

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KW - Cardiology

KW - Gene association

KW - In-stent restenosis

KW - MBL genetic variant

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