Association between VEGF Gene Polymorphisms and In-Stent Restenosis after Coronary Intervention Treated with Bare Metal Stent

Bagyura, Zsolt; Kiss, Loretta; Hirschberg, Kristóf; Berta, Balázs; Lux, Árpád; Szelid, Zsolt; Soós, Pál; Merkely, Béla

doi:10.1155/2017/9548612

Cited by 13 publications

(7 citation statements)

References 40 publications

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“…In human studies, it was found that, following a decrease in NF-kB/p65 translocation, the expression of VCAM-1, E-selectin, and endothelial cell activation also diminished dramatically. Therefore, a reduced NF-kB/p65 pathway can be one of the valuable therapeutic targets to prevent the progression of ISR [104]. Studies show that among the various risk factors contributing to ISR, the role of genetics is very prominent.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory Growth Factors and In-Stent Restenosis: Effect of Cytokines and Growth Factors

Maleknia

Ansari

Haybar

et al. 2020

SN Compr. Clin. Med.

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Highlights•PDGF is considered as prime culprit among growth factors in the pathogenesis of restenosis.•Inflammatory cytokines can stimulate VSMC migration by recruiting monocytes and releasing growth factors.•VEGF can be used to inhibit restenosis because of its revascularization and re-endothelialization properties. AbstractFollowing stent implantation and vascular injury, restenosis is one of the prominent clinical problems due to the synergism effects of inflammatory cytokines and growth factors. Restenosis development is accompanied by increased proliferation and migration of vascular smooth muscle cells (VSMCs) into the intimal region. The content has been obtained from PubMed database and the Google Scholar search engine through searching English-language articles (1989-2019) using keywords "Vascular injury," "Restenosis," "Growth factors," "Cytokines," and "Smooth muscle cells." After the vascular injury, the secretion of inflammatory factors can stimulate inflammatory cells, which lead to the release of growth factors. This can stimulate the migration of VSMCs and neointimal hyperplasia, and, as a result, lead to restenosis. Inflammatory cytokines, such as transforming growth factor-beta (TGFβ), often stimulate growth factors such as platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF), which can accelerate the restenosis process. Other cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) in the initial inflammation inhibit restenosis by affecting insulin-like growth factor binding proteins (IGFBPs). Considering the synergism effects of inflammatory cytokines and growth factors in the pathogenesis of restenosis, it is expected that these factors can be used as prognostic markers with therapeutic purposes.

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Section: Discussionmentioning

confidence: 99%

Inflammatory Growth Factors and In-Stent Restenosis: Effect of Cytokines and Growth Factors

Maleknia

Ansari

Haybar

et al. 2020

SN Compr. Clin. Med.

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“…On the other hand, we did not find any relationship between VEGFA rs699947 and the risk of binary ISR [ 10 ]. Moreover, Bagyura et al who analyzed the relationship between VEGFA polymorphisms and the risk of ISR in patients who underwent PCI with BMS implantation reported that rs699947 polymorphism is associated with neither the risk of diffuse nor focal ISR [ 50 ]. Our current analysis shows for the first time that the rs699947 A/A genotype is associated with a higher TLR risk.…”

Section: Discussionmentioning

confidence: 99%

The Relationship between VEGFA and TGFB1 Polymorphisms and Target Lesion Revascularization after Elective Percutaneous Coronary Intervention

et al. 2017

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Background and Aim The specific association between genetic variation and in-stent restenosis is still only partly understood. The aim of this study is to analyze the relationship between functional polymorphisms in the genes encoding vascular endothelial growth factor A (VEGF-A; rs699947) and transforming growth factor beta 1 (TGF-β1; rs1800470) and target lesion revascularization (TLR) risk. Methods A total of 676 patients (805 lesions) with stable coronary artery disease (SCAD) who received elective percutaneous coronary intervention (PCI) with at least one bare-metal stent implantation were included. The primary study endpoint was TLR at a 4-year follow-up. Results The TLR rate was higher in patients with the VEGFA A/A genotype (15.4%) than in patients with the VEGFA A/C (7.9%) and C/C (8.9%) genotypes (p = 0.009). The VEGFA A/A genotype, after adjustment for clinical and procedural covariates, remained significantly and independently associated with the TLR (hazard ratio—2.09 [95% confidence interval 1.32–3.33, p = 0.0017]). However, we found no association between TLR and the TGFB1 genotype. Conclusion The VEGFA A/A genotype is significantly and independently associated with TLR risk in Polish SCAD patients who received elective PCI with bare-metal stent implantation.

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“…Вони показали, що втрата просвіту була значно вищою в пацієнтів з генотипом A/А поліморфізму rs699947 гена ВЭФР-A порівняно з генотипами A/C і C/C (p < 0,05) [37]. Z. Bagyura та співавтори аналізували асоціацію двох поліморфізмів rs699947 і rs2010963 гена ВЕФР-А та розвиток рестенозу після імплантації металевого стента [4]. У цьому дослідженні поліморфізм rs699947 не був пов'язаний з ризиком розвитку рестенозу стента, та навпаки, наявність варіацій у локусі rs2010963 мала прогностичне значення.…”

Section: роль внутрішньосудинних зображеньunclassified

Causes and risk factors for stent restenosis in patients after percutaneous coronary interventions

Kopytsya¹,

Kutya²,

Rodionova³

et al. 2023

CSIC

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Percutaneous coronary intervention (PCI) is one of the main components in the treatment of the coronary artery disease (CAD) and especially its acute forms. Nevertheless, restenosis of stented coronary arteries, which significantly worsens the course of CAD, remains a significant clinical problem of this technology. Prevention of this complication requires a modern understanding of the complex pathogenetic mechanisms of restenosis. Based on the literature data, the frequency of restenosis development in stents with medical coatings is in the range from 3 to 20 %. The mechanism of restenosis is multifactorial and includes biological, mechanical, and genetic factors. The main mechanical causes are insufficient expansion of the stent or its destruction, and biological factors include local inflammation, leading to aggressive neointimal proliferation and late neoatherosclerosis. The search for genetic factors and possibilities of influence on the development of this complication is still ongoing. Intracoronary imaging is crucial for identifying mechanisms of restenosis and selecting individual therapy.

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Association between VEGF Gene Polymorphisms and In-Stent Restenosis after Coronary Intervention Treated with Bare Metal Stent

Cited by 13 publications

References 40 publications

Inflammatory Growth Factors and In-Stent Restenosis: Effect of Cytokines and Growth Factors

Inflammatory Growth Factors and In-Stent Restenosis: Effect of Cytokines and Growth Factors

The Relationship between VEGFA and TGFB1 Polymorphisms and Target Lesion Revascularization after Elective Percutaneous Coronary Intervention

Causes and risk factors for stent restenosis in patients after percutaneous coronary interventions

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