Genetic factors in primary hypertension and coronary artery disease a reappraisal

1962 ◽  
Vol 15 (12) ◽  
pp. 1093-1108 ◽  
Author(s):  
Morton D. Schweitzer ◽  
E.Gurney Clark ◽  
Frances R. Gearing ◽  
George A. Perera
MicroRNA ◽  
2020 ◽  
Vol 09 ◽  
Author(s):  
Rashid Mir ◽  
Imadeldin Elfaki ◽  
Chandan k Jha ◽  
Jamsheed Javid ◽  
Suriya Rehman ◽  
...  

Aim: Apart from the modifiable risk factors, genetic factors are believed to also influence the outcome of the coronary artery diseases (CAD). Under the genetic factors, miRNA polymorphisms, namely Hsa-miR-146a-5p (rs2910164) have become an important tool to study the mechanism that underlies the pathogenesis of this disease. Therefore, we investigated the association of miR-146a gene variations with susceptibility of coronary artery diseases. Methodology: This study was conducted on 100 CAD patients and 117 matched healthy individuals. Genotyping of the Hsa-miR-146a-5p C>G gene variation was performed by using amplification refractory mutation system PCR method (ARMS-PCR). Results: The distribution of Hsa-miR-146a-5p rs2910164 C>G genotypes observed between patients and controls was significantly different (P=0.048). Moreover, the frequency of G allele (fG) was found to be significantly higher among patients than in controls (0.36 vs. 0.25). Our findings showed that the Hsa-miR-146a-5p C>G variant was associated with an increased risk of CAD in codominant inheritance model CC vs. CG genotype (OR = 1.84, 95 % CI, 1.02-3.31; p=0.040) and (OR = 3.18, 95 % CI, 1.02-9.9; p=0.045) for CC vs. GG genotype in dominant inheritance model. Whereas the G allele significantly increased the risk of coronary artery disease (OR =1,81, 95 % CI, 1.18-2.78; p=0.006) compared to C allele. Taken together, these results demonstrated that miR-146a/rs2910164 is associated with susceptibility to coronary artery disease, providing novel insights into the genetic etiology and underlying biology of coronary artery disease. Conclusion: Our findings indicated that Hsa-miR-146a-5p rs2910164 GG genotype and G allele are associated with an increased susceptibility to Coronary Artery Disease. A larger sample size can be the key to progress in establishing the genetic co-relation of miRNA gene polymorphisms and cardiovascular diseases.


2012 ◽  
Vol 58 (1) ◽  
pp. 104-112 ◽  
Author(s):  
Robert Roberts ◽  
Alexandre F R Stewart

Abstract BACKGROUND It has long been recognized that 50% of the susceptibility for coronary artery disease (CAD) is due to predisposing genetic factors. Comprehensive prevention is likely to require knowledge of these genetic factors. CONTENT Using a genomewide association study (GWAS), the Ottawa Heart Genomic Study and the deCODE group simultaneously identified the first genetic risk variant, at chromosome 9p21. The 9p21 variant became the first risk factor to be identified since 1964. 9p21 occurs in 75% of the population except for African Americans and is associated with a 25% increased risk for CAD with 1 copy and a 50% increased risk with 2 copies. Perhaps the most remarkable finding is that 9p21 is independent of all known risk factors, indicating there are factors contributing to the pathogenesis of CAD that are yet unknown. 9p21 in individuals with premature CAD is associated with a 2-fold increase in risk, similar to that of smoking and cholesterol. Routine genetic testing will probably remain controversial until a specific treatment is developed. Over a period of 5 years, however, GWASs have identified 30 genetic variants for CAD risk, of which only 6 act through the known risk factors. SUMMARY The 9p21 variant has now been established as an independent risk factor for CAD and, along with the additional 29 risk genetic variants recently identified, is likely to provide the thrust for genetic testing and personalized medicine in the near future.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
E Kozlova ◽  
I Starostin ◽  
A Balatskyi ◽  
O Bulkina ◽  
V Lopukhova ◽  
...  

Abstract Background The coronary collateral circulation (CCC) varies in patients with coronary artery disease (CAD). Although many studies were provided to detect factors associated with collateral development, genetic factors are still studied insufficiently. The goal of this study was to assess the association of single nucleotide polymorphisms (SNP) in genes involved in vascular growth with CCC in patients with stable CAD. Purpose To assess if genetic variations in hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), urokinase-type plasminogen activator (gene PLAU) are associated with the presence of coronary collaterals in patients with stable CAD. Methods A single-centered study was performed between March 2012 and December 2017. In 579 patients with stable CAD who underwent coronary angiography and had at least 50% stenosis in at least one major coronary artery collaterals were assessed by the use of the Rentrop score (0–3) during coronary angiography. SNPs PLAU rs4065, VEGF rs1570360, rs2010963 and rs699947, HGF rs5745752 were genotyped, multivariate logistic regression was carried out to determine the association of genotypes with CCC. Results 337 patients had visible coronary collaterals (Rentrop grade 1, 2 and 3) and 236 patients didn't have visible collaterals (Rentrop grade 0). Beside traditional risk factors of poor CCC - diabetes, smoking and arterial hypertension – patients without visible coronary collaterals (Rentrop 0) showed a higher frequency of the HGF rs5745752 CC genotype than those with visible coronary collaterals (Rentrop 1–3; p=0.001). (Fig. 1) The odds ratio of having CCC Rentrop 0 in patients with genotype CC was statistically significant (odds ratio = 1.94 [95% confidence interval: 1.38–2.76]; p=0.001). Statistical analysis showed that the PLAU rs4065 and VEGF rs1570360, rs2010963 and rs699947 polymorphisms were not associated with CCC (p<0.05). Conclusion An association was found between the HGF rs5745752 polymorphism and the CCC in patients with stable CAD. Patients with the CC genotype are at greater risk of developing poor coronary collaterals. Figure 1 Funding Acknowledgement Type of funding source: None


2017 ◽  
Vol 158 ◽  
pp. 22-24 ◽  
Author(s):  
Arwa M. Amin ◽  
Lim Sheau Chin ◽  
Dzul Azri Mohamed Noor ◽  
Hamza Mostafa ◽  
Muhamad Ali S.K. Abdul Kader ◽  
...  

2000 ◽  
Vol 151 (1) ◽  
pp. 130
Author(s):  
R. Hirano ◽  
Y. Momiyama ◽  
K. Miyazaki ◽  
N. Isomura ◽  
N. Katayama ◽  
...  

2001 ◽  
Vol 6 (2) ◽  
pp. 103-108 ◽  
Author(s):  
Won-Ha Lee ◽  
Tae-Hong Hwang ◽  
Goo Taeg Oh ◽  
Sung Uk Kwon ◽  
Yoon-Ho Choi ◽  
...  

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