Korrelation von genetischen Polymorphismen mit dem Schweregrad der Intimahyperplasie nach Stentimplantation
type: CreativeWork
description: The instent-restenosis after coronary implantation is today the predominant problem in the cardiology. Many variables have been put in connection with instent-retenosis. After a pilot study on 100 patients this job investigated the influence of the PAI-1 promoter polymorphism on the "late loss" (a quantitative surrogate of the instent-restenosis) on 300 patients, smokers as well as non-smokers. The 4G/5G promoter polymorphism determines up to 40% of the PAI-1 plasma mirror. Whereas both alleles bind one transcription factor, the 5G allele also binds one repressor protein. The late loss has been identified through QCA. With the non-smoking patients the late loss was so much bigger the more 4G alleles the gene bearers had. With the smokers the late loss was identically relative to the gene bearers which were heterozygotic respectively homozygotic for the 4G allele. Smokers who were homozygotic for the 5G allele showed, however, the biggest late loss. We came to the conclusion that the promoter polymorphism of the PAI-1 gene had a statistically conspicuous Influence on the instent-restenosis rate after coronary stent implantation. Furthermore we could show an interaction between smoker habits and genotype on the extend of the restenonis. Summarizing we found out that the PAI-1 promoter polymorphism has a significant influence on the patho-morphologically process of the instent restenosis. Smoking habits affect the neo intima hyperplasia at specific 4G/5G gene bearers. The result of this study shows an important example for an environmentally-genetically reciprocal action in the development of instent- restenosis. Further studies must investigate the complex reciprocal action between PAI-1 genotype (and probably other genes of the coagulating system), smoking, gene products and neo intima hyperplasia.
abstract: The instent-restenosis after coronary implantation is today the predominant problem in the cardiology. Many variables have been put in connection with instent-retenosis. After a pilot study on 100 patients this job investigated the influence of the PAI-1 promoter polymorphism on the "late loss" (a quantitative surrogate of the instent-restenosis) on 300 patients, smokers as well as non-smokers. The 4G/5G promoter polymorphism determines up to 40% of the PAI-1 plasma mirror. Whereas both alleles bind one transcription factor, the 5G allele also binds one repressor protein. The late loss has been identified through QCA. With the non-smoking patients the late loss was so much bigger the more 4G alleles the gene bearers had. With the smokers the late loss was identically relative to the gene bearers which were heterozygotic respectively homozygotic for the 4G allele. Smokers who were homozygotic for the 5G allele showed, however, the biggest late loss. We came to the conclusion that the promoter polymorphism of the PAI-1 gene had a statistically conspicuous Influence on the instent-restenosis rate after coronary stent implantation. Furthermore we could show an interaction between smoker habits and genotype on the extend of the restenonis. Summarizing we found out that the PAI-1 promoter polymorphism has a significant influence on the patho-morphologically process of the instent restenosis. Smoking habits affect the neo intima hyperplasia at specific 4G/5G gene bearers. The result of this study shows an important example for an environmentally-genetically reciprocal action in the development of instent- restenosis. Further studies must investigate the complex reciprocal action between PAI-1 genotype (and probably other genes of the coagulating system), smoking, gene products and neo intima hyperplasia.
author: Pisters, Astrid
language: ger
keywords: info:eu-repo/classification/ddc/610, Medizin, KHK, PTCA, Instentrestenose, genetische Polymorphismen
date published: 2003
date modified: 2026-07-30T19:42:39Z
provider: RWTH Aachen University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Publikationsserver der RWTH Aachen University