Toll Like Receptor 2 Genotypes and Intra-Coronary Stent Restenosis
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- Category: Vol. 87, September 2019
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Toll Like Receptor 2 Genotypes and Intra-Coronary Stent Restenosis, TAREK ABDELAZIZ, RANDA HUSSINY, MARWA GAD and MOHAMED GAMEL
Abstract
Background: Intra-coronary Stent Restenosis (ISR) is a common complication after Percutaneous Coronary Interven-tion (PCI). There is an association between many genes such as Toll Like Receptor 2 (TLR2), Adrenergic B2 Receptor (ADRB2), platelet glycoprotein IIIa, Nitric Oxide Synthase3 (NOS3), P2Y12 receptor (P2Y12), cyclin-dependent kinase inhibitor (p27kip1) and the process of intra-coronary stent restenosis. Study of the genetic polymorphisms of these genes is very important to detect which is protective against intra-coronary stent restenosis, and which is risky for development of this problem. Our study selected TLR2 gene to detect its different genotypes involved in the problem of ISR.
Aim of Study: To find the association between TLR2 genotypes, polymorphisms and Intra-coronary Stent Restenosis (ISR) complication after PCI procedures.
Patients and Methods: The study included 200 patients with previous coronary revascularization by stent implantation. All patients were re-admitted to coronary angiography because of objective evidence of myocardial ischemia. The patients were classified into two groups: Group (A) included 100 patients who developed ISR and Group (B) included 100 patients who did not develop ISR. The two groups were compared regarding distribution of TLR2 genotypes and alleles.
Results: 78% of patients with (GG) genotype, 14% of patients with (GA) genotype and 7% of patients with (AA) genotype developed ISR. There was no association between TLR2 (GA), (AA) genotypes and risk of ISR when compared by (GG) wild homozygous genotype (p>0.05, OR=1.2). We also did not find any association between TLR2 gene alleles and risk of ISR complication (p>0.05, OR=0.9).
Conclusion: There was no association between different TLR2 genotypes, alleles and risk of ISR development.