Single nucleotide polymorphism of P2RY12 and CYP3A5 genes in clopidogrel resistant and nonresistant ischemic heart disease patients

2017 ◽  
Vol 08 (02) ◽  
Author(s):  
Ghulam Mustafa
Medicine ◽  
2019 ◽  
Vol 98 (24) ◽  
pp. e15846 ◽  
Author(s):  
Franca R. Guerini ◽  
Enrico Ripamonti ◽  
Andrea S. Costa ◽  
Milena Zanzottera ◽  
Cristina Agliardi ◽  
...  

2009 ◽  
Vol 2009 ◽  
pp. 1-6 ◽  
Author(s):  
Maria Bucova ◽  
Jan Lietava ◽  
Peter Penz ◽  
Frantisek Mrazek ◽  
Jana Petrkova ◽  
...  

The aim of our work was to find if MCP-1 -2518 (A/G) single nucleotide polymorphism (SNP) influences somehow the serum concentrations of high-sensitive CRP (hsCRP) both in patients suffering from ischemic heart disease (IHD), myocardial infarction (MI), angina pectoris (AP), and hypertension (HT) and in control group of healthy subjects. Totally, 263 patients with the diagnosis of IHD, out of them 89 with MI, 145 with AP, 205 with HT, and also 67 healthy subjects were included in the study. First, we estimated the serum levels of hsCRP. We found that patients with AP had significantly higher serum level of hsCRP than both control group of healthy subjects (P=.043) and IHD patients without AP (P=.026). The presence of the mutant G allele statistically significantly correlated with the higher serum levels of hsCRP in patients with IHD (P=.016), AP (P=.004), and HT (P=.013). Higher correlations were found in men (AP:P=.019; HT:P=.047). In all cases the highest levels of hsCRP were found both in patients and healthy controls with homozygous GG genotype.


Kardiologiia ◽  
2015 ◽  
Vol 11_2015 ◽  
pp. 12-15 ◽  
Author(s):  
A.V. Balatsky Balatsky ◽  
D.Yu. Konovalov Konovalov ◽  
L.M. Samokhodskaya Samokhodskaya ◽  
T.N. Kochegura Kochegura ◽  
K.A. Rubina Rubina ◽  
...  

2021 ◽  
Author(s):  
Huan Chen ◽  
Tianjiao Li ◽  
Yuqing Wu ◽  
Xi Wang ◽  
Mingyuan Wang ◽  
...  

Abstract Background: NKX2.5 is a transcription factor that plays a key role in cardiovascular growth and development. Many independent studies have been conducted to investigate the association between the single nucleotide polymorphism 606G>C (rs3729753) in the coding region of NKX2.5 and congenital heart disease (CHD), although the results were inconsistent. This study aimed to reveal as much as possible the relationship between NKX2.5 single nucleotide polymorphism 606G>C and the risk of congenital heart disease in the Chinese population through meta-analysis.Methods and Results: After retrieving related articles in PubMed, MEDLINE, EMBASE, Web of science, Coherane, China National Knowledge Infrastructure (CNKI), Wanfang DATA, VIP database until Aug 2021, a total of 8 studies were finally included. Then, we merged the qualified research data into allele model, dominant model, recessive model, heterozygous model, homozygous model, additive model respectively. Overall meta-analysis results showed that 606G>C was not associated with congenital heart disease of the Chinese population in any model. Also, subgroup analysis based on congenital heart disease type gave the same negative result. Sensitivity analysis showed that there was no significant correlation after the deletion of each study. The results were negative and the heterogeneity was not significant.Conclusion: Our results show that NKX2-5 single nucleotide polymorphism 606G> C may not lead to the risk of congenital heart disease in Chinese.


Author(s):  
Jie V. Zhao ◽  
C. Mary Schooling

Background: Coagulation plays a role in ischemic heart disease (IHD). However, which coagulation factors are targets of intervention is unclear. We assessed how genetically predicted vWF (von Willebrand factor), ETP (endogenous thrombin potential), FVIII (factor VIII), d -dimer, tPA (tissue-type plasminogen activator), and PAI (plasminogen activator inhibitor)-1 affected IHD. We similarly estimated effects on lipids to determine whether any associations were independent of lipids. Methods and Results: Separate sample instrumental variable analysis with genetic instruments, that is, Mendelian randomization, was used to obtain unconfounded estimates of effects on IHD using extensively genotyped studies of coronary artery disease/myocardial infarction, CARDIoGRAMplusC4D Metabochip (64 374 cases, 130 681 controls) and CARDIoGRAMplusC4D 1000 Genomes (60 801 cases, 123 504 controls), and on lipids using the Global Lipids Genetics Consortium Results (n=196 475). Genetically predicted ETP was positively associated with IHD (odds ratio, 1.05 per log-transformed SD; 95% confidence interval, 1.03–1.07) based on 15 single-nucleotide polymorphisms, as were vWF (odds ratio, 1.05 per SD; 95% confidence interval, 1.02–1.08) and FVIII (odds ratio, 1.06 per SD; 95% confidence interval, 1.03–1.09) based on 16 and 6 single-nucleotide polymorphisms, respectively, but the latter associations were null after considering pleiotropy. vWF and FVIII were associated with higher LDL (low-density lipoprotein) cholesterol, but not after considering pleiotropy. Genetically predicted d -dimer, tPA, and PAI-1 were not clearly associated with IHD or lipids based on 3, 3, and 5 single-nucleotide polymorphisms, respectively. Conclusions: ETP may affect IHD. Assessing the role of its drivers in more precisely phenotyped studies of IHD could be worthwhile.


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