scholarly journals Association of Interaction Between Smoking and CYP 2C19*3 Polymorphism With Coronary Artery Disease in a Uighur Population

2010 ◽  
Vol 16 (5) ◽  
pp. 579-583 ◽  
Author(s):  
Yi-Ning Yang ◽  
Xin-Lei Wang ◽  
Yi-Tong Ma ◽  
Xiang Xie ◽  
Zhen-Yan Fu ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Vascular Inflammation ◽  
Multiple Logistic Regression Analysis ◽  
Rflp Analysis ◽  
Biologically Active ◽  
Pcr Rflp ◽  
Cyp2c19 Gene ◽  
Independent Risk Factors ◽  
Artery Disease

Objectives: Cytochrome P450 (CYP) 2C19 is expressed in vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs), which are potent endogenous vasodilators and inhibitors of vascular inflammation. The purpose of this study is to explore the relationship between the interaction of CYP2C19*3 polymorphism and smoking and coronary artery disease (CAD) in a Uighur population. Methods: In a Chinese Uighur case-control study of patients with CAD (n = 336) and healthy controls (n = 370), we investigated the roles of polymorphism in the CYP2C19 gene by the use of polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) analysis. Results: The CYP2C19*3 AG + AA genotype was significantly more prevalent in patients with CAD (6.25.0% vs 2.96%; P = .03). Multiple logistic regression analysis showed 4 independent risk factors: the interaction of CYP2C19*3 and smoking (OR 7.22, 95% confidence interval [CI] 2.32-10.23; P = .009), smoking (OR 3.23, 95% CI 1.72-5.44; P = .003), blood sugar (OR 2.12, 95% CI 1.03-4.21; P < .01), and hypertension (OR 1.74, 95% CI 0.98-2.34; P = .013). Conclusions: The CYP2C19*3 polymorphism and CAD were synergistically and significantly associated in Chinese Uighur patients.

scholarly journals Studying of cyp2c19*2, *3 and *17 polymorphism in Vietnamese patients with coronary artery disease

2020 ◽  
Vol 18 (1) ◽  
pp. 41-48
Author(s):  
Nguyen Hai Ha ◽  
Le Thi Bich Thao ◽  
Nguyen Thi Thanh Hoa ◽  
Le Thi Thu Hien
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Restriction Enzymes ◽  
Metabolic Phenotype ◽  
Single Nucleotide ◽  
Pcr Rflp ◽  
Cyp2c19 Gene ◽  
Ultrarapid Metabolizers ◽  
Coronary Syndromes ◽  
Artery Disease

Coronary artery disease is the most common type of cardiovascular disease, due to the accumulation of atherosclerotic plaque inside the arterial wall which leads to block blood supply to the heart muscle. A number of clinical trials have demonstrated that Clopidogrel is able to inhibit platelet aggregation in patients with acute coronary syndromes, reduce mortality and cardiovascular events. However, the antiplatelet effectiveness of Clopidogrel significantly depends on CYP2C19 genotypes. Therefore, the aim of this study was to identify the CYP2C19*2, *3 and allele frequencies in Vietnamese coronary artery patients by using PCR-RFLP method. Total genomic DNA were extracted from peripheral blood of 96 patients diagnosed with coronary artery disease. Thereafter, single nucleotide polymorphism sites in the CYP2C19 gene were identified by PCR with specific primers. The amplified products were then digested by restriction enzymes SmaI, BamHI, and MnlI, respectively. The results showed that the proportion of heterozygous individuals for CYP2C19*2 (c. 681G>A, rs4244285), CYP2C19*3 (c. 636G>A, rs4986893), and CYP2C19*17 (g. -3402C>T, rs11188072) accounted for 39.58%, 6.25%, and 2.08%, respectively. Among 96 subjects, 41.67% of patients were predicted for intermediate metabolic phenotype CYP2C19*1/*2 (37.50%) and CYP2C19*1/*3 (4.17%). Approximately 10.42% of total patients represented poor metabolizers in which 8.34% had two copies of the same allele *2/*2 and 2.08% had *2/*3 genotype. Particularly, two individuals (2.08%) detected with CYP2C19*1/*17 genotype were able to increase CYP2C19 activity (ultrarapid metabolizers). The results of this study generate a foundation for introducing individualized antiplatelet therapy in Vietnam based on genetic testing.

scholarly journals Expression of adipocytokine genes and their content in various adipose tissue sites in patients with heart diseases

2020 ◽  
Author(s):  
Olga Gruzdeva ◽  
Yulia Dyleva ◽  
Ekaterina Belik ◽  
Daria Borodkina ◽  
Maxim Sinitsky ◽  
...  
Keyword(s):  
Gene Expression ◽  
Coronary Artery Disease ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Mitral Valve ◽  
Valve Replacement ◽  
Mitral Valve Replacement ◽  
Biologically Active ◽  
Fat Depots ◽  
Artery Disease

Abstract Background Adipose tissue (AT) is an endocrine and paracrine organ that synthesizes biologically active adipocytokines, which affect inflammation, fibrosis, and atherogenesis. Epicardial and perivascular fat depots are of great interest owing to potential effects on the myocardium and blood vessels. Objective To assess expression and secretion of adipocytokine genes in adipose tissue in patients coronary artery disease (CAD) and patients with aortic or mitral valve replacement. Methods The study included 84 patients with CAD and 50 patients with aortic or mitral valve replacement. Adipocytes were isolated from subcutaneous (SAT), epicardial (EAT), and perivascular AT (PVAT) samples. Isolated adipocytes were cultured for 24 h after which, gene expression and secretion levels of selected adipokines and cytokines in the culture medium were determined. Results The study parameters differed depending on the adipose tissue location. EAT adipocytes in CAD patients were characterized by a pronounced imbalance in the adipokine system. EAT had the lowest adiponectin gene expression and secretion, regardless of nosology and high expression levels of the leptin gene, its receptor, and interleukin-6 (IL-6) were detected. High leptin and IL-6 levels resulted in increased pro-inflammatory activity, as observed in both EAT and PVAT adipocytes, especially in individuals with coronary artery disease. Conclusion The "protective" potential of adipose tissue depends on its location.

scholarly journals Association of C1q/TNF-related protein-1 (CTRP1) serum levels with coronary artery disease

2019 ◽  
Vol 47 (6) ◽  
pp. 2571-2579 ◽  
Author(s):  
Linhui Shen ◽  
Shuhong Wang ◽  
Yuan Ling ◽  
Wei Liang
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Multiple Logistic Regression Analysis ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Artery Disease ◽  
Necrosis Factor

Objective Complement C1q tumor necrosis factor-related proteins (CTRPs), belonging to the CTRP superfamily, are extensively involved in regulating metabolism and the immune-inflammatory response. The inflammatory process is linked to the pathogenesis of coronary artery disease (CAD). Here, we investigated the association of serum levels of CTRP1 with CAD. Methods Study participants were divided into two groups according to the results of coronary angiography: a control group (n = 63) and a CAD group (n = 76). The concentrations of serum CTRP1 and inflammatory cytokines were determined by enzyme-linked immunosorbent assay. Further analysis of CTRP1 levels in individuals with different severities of CAD was conducted. The CAD severity was assessed by Gensini score. Results Serum levels of CTRP1 were significantly higher in CAD patients than in controls (17.24 ± 1.07 versus 9.31 ± 0.56 ng/mL), and CTRP1 levels increased with increasing severity of CAD. CTRP1 levels were positively correlated with concentrations of tumor necrosis factor-α and interleukin-6. Multiple logistic regression analysis showed that CTRP1 was significantly associated with CAD. Conclusions Our data showed close associations of serum CTRP1 levels with the prevalence and severity of CAD, indicating that CTRP1 can be regarded as a novel and valuable biomarker for CAD.

scholarly journals Association of Fibrinogen and Plasmin Inhibitor, but not Coagulation Factor XIII Gene Polymorphisms with Coronary Artery Disease

2020 ◽  
Author(s):  
Ana Bronic ◽  
Goran Ferencak ◽  
Robert Bernat ◽  
Jasna Lenicek Krleza ◽  
Jerka Dumic ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Factor Xiii ◽  
Active Form ◽  
Coagulation Factor ◽  
Rflp Analysis ◽  
Chain Gene ◽  
Nucleotide Polymorphisms ◽  
Artery Disease ◽  
Plasmin Inhibitor

Background: In the final phase of cloth formation, fibri(noge)n constitutes frame whereas factor XIII (FXIII) active form is responsible for the covalent cross-linking of fibrin fibers and plasmin inhibitor (PI), thus contributing to clot stability. It could be expected that any change of coagulation factors’ structure affects the clot formation and modulate the atherothrombotic risk. The aim was to determine the frequency of four single nucleotide polymorphisms: (i) A>G in codon 312 of the fibrinogen α-chain gene (rs6050, Thr312Ala FGA), (ii) C>T at position 10034 of the 3´untranslated region in the fibrinogen γ-chain gene (rs2066865, 10034C>T FGG), (iii) C>T in codon 564 of the FXIII-A subunit gene (rs5982, Pro564Leu FXIII-A), and (iv) C>T in codon 6 of the plasmin inhibitor gene (rs2070863, Arg6Trp PI) in Croatian patients and their association with coronary artery disease (CAD). Methods: We performed the unrelated case-control association study on the consecutive sample of patients ≥18 years old, who had undergone coronary angiography for investigation of chest pain and suspected CAD. Cases were patients with confirmed CAD (N=201) and controls were the subjects with no CAD (N=119). Samples were genotyped using PCR-RFLP analysis. Results: Observed frequencies of the rare alleles of Thr312Ala FGA, 10034C>T FGG, Leu564Pro FXIII-A and Arg6Trp PI polymorphisms were 21%, 17%, 14%, 20%, respectively. Patients with 10034C> T FGG CC genotype had 3.5 times (95% CI 1.02-12.03) higher adjusted odds for CAD than patients with 10034C> T FGG TT genotype. Patients with Arg6Trp PI CC genotype had 3.86 times (95% CI 1.23-12.12) higher odds for CAD than patients with Arg6Trp PI TT genotype. No difference was observed regarding any other investigated polymorphism, Conclusion: Our finding suggests that 10034C>T FGG and Arg6Trp PI are associated with CAD.

scholarly journals Leptin G-2548A promoter polymorphism is associated with increased plasma leptin and BMI in Brazilian women

2008 ◽  
Vol 52 (4) ◽  
pp. 611-616 ◽  
Author(s):  
Hamilton M. Hinuy ◽  
Mario H. Hirata ◽  
Neusa Forti ◽  
Jayme Diament ◽  
Marcelo F. Sampaio ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Body Mass Index ◽  
Coronary Artery ◽  
Body Mass ◽  
Serum Lipids ◽  
Promoter Polymorphism ◽  
Pcr Rflp ◽  
Artery Disease ◽  
Plasma Leptin ◽  
The Relationship

Variants in leptin gene (LEP) have been implicated in the pathogenesis of obesity. The relationship between LEP G-2548A polymorphism and obesity-related traits was evaluated in a sample of Brazilian women (n = 228) who were randomly selected from two clinical centers in Sao Paulo city. Blood samples were collected for DNA extraction, plasma leptin and serum lipids measurements. LEP G-2548A genotypes were identified by a PCR- RFLP strategy using the endonuclease Alw44I. LEP G-2548A was associated with obesity after adjustment for covariates (age, hypertension, coronary artery disease, smoking and physical activity). Women carrying G allele had a four times higher risk of obesity than the A allele carriers (OR: 4.11, CI95%: 1.06-15.90, p = 0.041). G allele was also related to increased plasma leptin (p = 0.024) and body mass index (p = 0.027). Hypertension, hyperglycemia, dyslipidemia and coronary artery disease were associated with obesity. However LEP G-2548A polymorphism was not related to these variables. All together these data suggest that LEP G-2548A polymorphism has an important role in regulating plasma leptin levels and body mass index in women.

Vascular Inflammation and Angiographic Severity of Coronary Artery Disease in Young Asian Indians

2014 ◽  
Vol 5 (1) ◽  
pp. 15-21
Author(s):  
Imran Ahmed ◽  
Achyut Sarkar ◽  
Arindam Pande ◽  
Naveen Chandra GS ◽  
Shailesh Patil ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Asian Indians ◽  
Vascular Inflammation ◽  
Artery Disease

scholarly journals Functional investigation of the coronary artery disease gene SVEP1

2020 ◽  
Vol 115 (6) ◽  
Author(s):  
Michael J. Winkler ◽  
Philipp Müller ◽  
Amin M. Sharifi ◽  
Jana Wobst ◽  
Hanna Winter ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Vascular Inflammation ◽  
Missense Variant ◽  
Leukocyte Recruitment ◽  
Wild Type ◽  
Cellular Source ◽  
Elevated Expression ◽  
Artery Disease

AbstractA missense variant of the sushi, von Willebrand factor type A, EGF and pentraxin domain containing protein 1 (SVEP1) is genome-wide significantly associated with coronary artery disease. The mechanisms how SVEP1 impacts atherosclerosis are not known. We found endothelial cells (EC) and vascular smooth muscle cells to represent the major cellular source of SVEP1 in plaques. Plaques were larger in atherosclerosis-prone Svep1 haploinsufficient (ApoE−/−Svep1+/−) compared to Svep1 wild-type mice (ApoE−/−Svep1+/+) and ApoE−/−Svep1+/− mice displayed elevated plaque neutrophil, Ly6Chigh monocyte, and macrophage numbers. We assessed how leukocytes accumulated more inside plaques in ApoE−/−Svep1+/− mice and found enhanced leukocyte recruitment from blood into plaques. In vitro, we examined how SVEP1 deficiency promotes leukocyte recruitment and found elevated expression of the leukocyte attractant chemokine (C-X-C motif) ligand 1 (CXCL1) in EC after incubation with missense compared to wild-type SVEP1. Increasing wild-type SVEP1 levels silenced endothelial CXCL1 release. In line, plasma Cxcl1 levels were elevated in ApoE−/−Svep1+/− mice. Our studies reveal an atheroprotective role of SVEP1. Deficiency of wild-type Svep1 increased endothelial CXCL1 expression leading to enhanced recruitment of proinflammatory leukocytes from blood to plaque. Consequently, elevated vascular inflammation resulted in enhanced plaque progression in Svep1 deficiency.

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