scholarly journals Association of Platelet Membrane Glycoprotein HPA-2a/b, GP VI T13254C, and GP IbαVNTR Polymorphisms with Risk of Coronary Artery Disease: A Meta-Analysis

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Wei Ni ◽  
Jidong He ◽  
Haoyu Wang ◽  
Tao Liu

Background and Aims. Recently, controversial results have been reported regarding the association of the polymorphisms of platelet membrane glycoproteins (HPA-2a/b, GP VI T13254C, and GP IbαVNTR) with coronary artery disease (CAD). We performed this meta-analysis to further assess the polymorphisms of platelet membrane glycoproteins with a risk of CAD.Methods. A systematic electronic literature search was conducted in Embase, Cochrane Library, PubMed, and the Chinese Biomedical Literature Database (CBM). Analyses were performed using the Cochrane software package Review Manager 5.2 and Stata 12.0 software package.Results. Twenty-nine full-text articles were included in the meta-analysis. Based on random-effects meta-analysis, a significant association between the HPA-2a/b polymorphism and CAD was identified (allele model: odds ratio = 1.43, 95% confidence interval = 1.07–1.91; dominant genetic model: odds ratio = 1.57, 95% confidence interval = 1.08–2.28). Our study showed no association between the GP VI T13254C polymorphism and CAD in either a random-effects model or a fixed-effects model. Furthermore, there was no evidence to suggest that the GP IbαVNTR polymorphism was associated with CAD in any of the genetic analysis models.Conclusions. The HPA-2a/b polymorphism correlated significantly with a risk of CAD, and the HPA-2b allele and the HPA-2ab + HPA-2bb genotype may increase the risk of CAD. There was no evidence to suggest that polymorphisms of GP VI T13254C and GP IbαVNTR were associated with CAD.

2018 ◽  
Vol 8 (3) ◽  
pp. 192-198
Author(s):  
Haroon Kamran ◽  
Eric Kupferstein ◽  
Navneet Sharma ◽  
Gagandeep Singh ◽  
James R. Sowers ◽  
...  

Introduction: End-stage renal disease requiring renal transplantation comprises a growing patient population at risk for cardiovascular disease (CVD) morbidity and mortality in large part due to accelerated atherosclerosis. Consequently, these patients are at even higher risk of major surgical CVD mortality. A paucity of research has addressed the posttransplantation CVD outcomes related to different treatment strategies in this patient population and therefore, there are no specific preoperative guidelines regarding management of coronary artery disease in this high-risk population undergoing renal transplantation. Objective: Through meta-analysis we compare coronary revascularization to medical management prior to renal transplantation in patients who are found to have significant obstructive coronary artery disease. Results: A total of 6 studies were deemed suitable out of 777 articles reviewed. This included 260 patients who received medical management and 338 who received coronary revascularization. There were 36 events in the revascularization and 57 events in the medical management group. One study only reported hazard ratios but no CVD outcomes. Comprehensive Meta-Analysis software was used to calculate pooled odds ratio with 95% confidence intervals (CI) for the fixed effects. The data is presented as forest plots. The pooled odds ratio with 95% CI for the fixed effects was 1.415 (95% CI 0.885–2.263), p = 0.147, indicating that there is no difference in CVD outcomes between pretransplant treatment strategy. This observation suggests that the CVD outcomes posttransplantation are not affected when optimal medical therapy is used instead of coronary revascularization.


2021 ◽  
Author(s):  
Xinyi Zhang ◽  
Sicong Li ◽  
Yuxuan Zhao ◽  
Ningjia Tang ◽  
Tong Jia ◽  
...  

Aim: The aim of this study was to assess the association between PEAR1 polymorphisms and ischemic clinical outcomes. Materials & methods: We searched the electronic database for articles on the relationship of PEAR1 SNPs and ischemic events in patients with coronary artery disease (CAD) up to October 2020. Results: A total of 9914 patients with CAD from six studies focusing on 12 SNPs of PEAR1 were included in this study. The A allele of rs12041331 were associated with ischemic events (odds ratio: 1.40; 95% CI: 1.04–1.88; p = 0.03). The AA homozygotes of rs2768759 was related to a higher risk of ischemic events than carriers of the C allele (odds ratio: 2.08; 95% CI: 1.09–3.97; p = 0.03). Conclusion: PEAR1 rs12041331 and rs2768759 are significantly associated with ischemic events in patients with CAD.


2021 ◽  
Vol 53 (08) ◽  
pp. 541-561
Author(s):  
Mi Su ◽  
Aimei Jia ◽  
Yilan He ◽  
Yongyan Song

AbstractThe relationships between the rs266729, rs1501299, and rs2241766 polymorphisms in adiponectin gene (ADIPOQ) and circulating levels of adiponectin and lipids remain to be clarified. Databases including PubMed and Embase were searched for eligible studies. The random-effects model was used, and standardized mean difference (SMD) with 95% confidence interval (CI) was calculated to estimate the differences in circulating levels of adiponectin and lipids between the subjects with different genotypes. A total of 12 810, 17 319, and 21 361 subjects were identified in the analyses for the rs266729, rs1501299, and rs2241766 polymorphisms, respectively. G allele carriers of the rs266729 polymorphism had lower levels of adiponectin (SMD=–0.28, 95% CI=–0.43 to–0.12) and high-density lipoprotein cholesterol (HDL-C) (SMD=–0.10, 95% CI=–0.17 to–0.02) than CC homozygotes; T allele carriers of the rs1501299 polymorphism had higher levels of adiponectin (SMD=0.21, 95% CI=0.05 to 0.36) and HDL-C (SMD=0.09, 95% CI=0.04 to 0.15) and lower levels of triglycerides (SMD=–0.06, 95% CI=–0.12 to–0.01) than GG homozygotes; G allele carriers of the rs2241766 polymorphism had lower levels of adiponectin (SMD=–0.18, 95% CI=–0.31 to–0.05) and HDL-C (SMD=–0.12, 95% CI=–0.20 to–0.04) than TT homozygotes. This meta-analysis suggests that the rs266729, rs1501299, and rs2241766 polymorphisms of ADIPOQ are significantly associated with circulating levels of adiponectin and lipids, which may partly explain the associations between these polymorphisms and coronary artery disease.


2021 ◽  
Vol 43 (1) ◽  
Author(s):  
Nader Salari ◽  
Kamran Mansouri ◽  
Amin Hosseinian-Far ◽  
Hooman Ghasemi ◽  
Masoud Mohammadi ◽  
...  

Abstract Background Coronary Artery Disease (CAD) is caused by the blockage of the coronary arteries. it is argued that there has an association between the Interleukin-6 gene and the occurrence of atherosclerosis, coronary artery disease, Due to the short half-life and high variability of Interleukin-6 (IL-6), limited studies have been performed on the association of serum levels of interleukin-6 with coronary artery disease. The aim of this study is to investigate the relationship between IL-6 gene polymorphisms and coronary artery disease. Methods This study was conducted as a meta-analysis of selected articles with no lower time limit and upto March 2020. Articles related to the subject were obtained by searching several data sources,such as the SID, IranDoc, Scopus, Embase, Web of Science (ISI), PubMed, Science Direct, and Google Scholar databases. The heterogeneity of the studies was assessed using the I2 index in the Comprehensive Meta-Analysis software. Results The GG genotype of the IL-6174 G> C polymorphism with a 0.8 odds ratio tended to reduce the risk of CAD by 20%. The odds ratio of CAD in CG and GG genotypes were found to be 1.16 and 1.48 times respectively, indicating the increasing effect of these two genotypes. In the IL-6-572 C>G polymorphism, CG and GG genotypes increased the risk of CAD by 1.21 and 1.27 times respectively, and the CC genotype tended to reduce the risk of CAD by 15%, considering the odds ratio of 0.85. Conclusion This study showed a relationship between IL-6174G> C and Interleukin-6 (IL-6) 572 C>G genes and coronary artery disease. Moreover, the protective effects of GG genotype in IL-6 gene 174 G> C and CC genotype in IL-6 gene 572 C>G gene were reported. The study also confirmed that the CG and CC genotypes of the G>C IL-6174 gene have an increasing effect on coronary artery disease. Moreover, CG and GG genotypes in the IL-6 gene 572 C>G increased the risk of developing CAD. It should be noted that the increased risk of developing CAD was limited to meta-analytic studies in reported literatures.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Sana Ashiq ◽  
Kanwal Ashiq

Abstract Background Numerous studies have investigated the role of apolipoprotein E (APOE) polymorphisms in coronary artery disease (CAD), but some controversies exist regarding the outcomes as the results were not consistent and remain uncertain. Therefore, the present meta-analysis was conducted to evaluate the association of APOE polymorphisms with coronary artery disease. Methods All the relevant studies published in English language till August 2020 were identified by searching through various electronic databases. The complete data was independently extracted by the two researchers. The data were analyzed by using the Comprehensive Meta-Analysis program and MetaGenyo program. The pooled odds ratio was used to check the associations between CAD and APOE polymorphisms. The following genetic models were used to calculate the odds ratio: ε2 vs. ε3 and ε4 vs. ε3. Results In the final analysis, we include 12 studies regarding the role of APOE polymorphism in CAD. The pooled odds ratio for ε4 allele was higher (OR 2.00; 95% and CI, 1.48–2.71). There is no statistical significant association for ε2 allele with CAD (OR 1.38; 95% CI, 1.18–1.62). This analysis showed no publication bias exists in the current meta-analysis. Conclusions Our findings suggest that the apolipoprotein ε4 allele appears as a significant genetic risk factor for coronary artery disease while the ε2 allele is beneficial to alleviate the CAD risk. Trial registration Registered with PROSPERO International Prospective Register of Systematic Reviews. PROSPERO registration number CRD42020190464


2001 ◽  
Vol 47 (7) ◽  
pp. 1234-1240 ◽  
Author(s):  
Mehran Haidari ◽  
Ebrahim Javadi ◽  
Mehry Kadkhodaee ◽  
Arashmidos Sanati

Abstract Background: Convincing evidence points to oxidative modification of LDL as an important trigger in a complex chain of events leading to atherosclerosis. We investigated the occurrence of enhanced susceptibility of LDL to oxidation and decreased vitamin E concentration in LDL as additional risk factors promoting atherosclerosis among patients with established coronary artery disease (CAD). Methods: We examined 132 patients with angiographically confirmed CAD and compared them with 111 healthy control individuals. We measured conjugated diene production to assess susceptibility of LDL to copper-mediated oxidation. Vitamin E content of LDL was measured by HPLC. Results: The mean lag time of LDL oxidation and LDL α-tocopherol/LDL-cholesterol ratio were lower in the patients with CAD (55 ± 14 min and 2.4 ± 1.0 mmol/mmol) than in the controls (63 ± 13 min and 2.9 ± 1.1 mmol/mmol; P <0.0001 and <0.001, respectively). Multiple stepwise regression analysis demonstrated the lag time (odds ratio, 1.96; 95% confidence interval, 1.34–2.87; P <0.0001) and concentration of vitamin E in LDL (odds ratio, 1.65; 95% confidence interval, 1.16–2.33; P <0.005) as independent determinants of CAD. Significant inverse Spearman rank correlations were found between lag time (r = −0.285; P <0.001) or concentration of vitamin E in LDL (r = −0.197; P <0.002) and severity of CAD. Lag times were not significantly correlated with serum C-reactive protein or ferritin. Conclusions: Our data suggest that a short LDL oxidation lag time and a low concentration of vitamin E in LDL might be independent coronary risk factors for stable CAD in Iranian people.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Hengying Chen ◽  
Jiaying Zhang ◽  
Jiayu Lai ◽  
Yingyu Zhou ◽  
Xiaoping Lin ◽  
...  

Abstract Background Retinol binding protein 4 (RBP4) has been proposed to play a role in the pathophysiology of coronary artery disease (CAD), but previous findings on the association of RBP4 levels with CAD are inconsistent. Methods A meta-analysis based on observational studies was conducted to evaluate the association between circulating RBP4 levels and CAD. Databases including PubMed, Web of Science, Embase, Google Scholar and ClinicalTrials.gov database were searched for eligible studies published up to 12 July 2021. Standard mean differences (SMDs) with 95% confidence intervals (CIs) were calculated using the inverse variance heterogeneity (IVhet) and random-effects model for data with moderate and high heterogeneity (I2 > 30%) and data with low heterogeneity were analysed using a fixed-effects model (I2 ≤ 30%). Moreover, a bias-adjusted quality-effects model was generated, and the prediction interval was also calculated under the random-effects model. Results Two nested case-control studies, one cohort study and twelve case–control studies with a total of 7111 participants were included. Circulating RBP4 levels in patients with CAD were comparable to those in the controls under the IVhet model (SMD: 0.25, 95% CI: − 0.29-0.79, I2: 96.00%). The quality-effects model produced consistent results. However, the association turned to be significant under the random-effect model (SMD: 0.46, 95% CI: 0.17–0.75, I2: 96.00%), whereas the 95% predictive interval (PI) included null values (95% PI: − 0.82-1.74). Subgroup analyses illustrated a positive relationship between CAD and RBP4 levels in patients with complications (SMD: 1.34, 95% CI: 0.38–2.29, I2: 96.00%). The meta-regression analysis revealed that the mean BMI of patients (P = 0.03) and complication status (P = 0.01) influenced the variation in SMD. Conclusions There was low-quality evidence that patients with CAD exhibited similar circulating RBP4 levels compared with controls, and high inter-study heterogeneity was also observed. Thus, RBP4 might not be a potential risk factor for CAD. Comparisons among different subtypes of RBP4 with larger sample size are needed in the future.


Circulation ◽  
2018 ◽  
Vol 138 (6) ◽  
pp. 590-599 ◽  
Author(s):  
Johan Ljungberg ◽  
Mikael Janiec ◽  
Ingvar A. Bergdahl ◽  
Anders Holmgren ◽  
Johan Hultdin ◽  
...  

Background: Aortic valve stenosis (AS) is the most common indication for cardiac valve surgery; untreated AS is linked to high mortality. The etiological background of AS is unknown. Previous human studies were typically based on case-control studies. Biomarkers identified in prospective studies could lead to novel mechanistic insights. Methods: Within a large population survey with blood samples obtained at baseline, 334 patients were identified who later underwent surgery for AS (median age [interquartile range], 59.9 [10.4] years at survey and 68.3 [12.7] at surgery; 48% female). For each case, 2 matched referents were allocated. Plasma was analyzed with the multiplex proximity extension assay for screening of 92 cardiovascular candidate proteins. Conditional logistic regression models were used to assess associations between each protein and AS, with correction for multiple testing. A separate set of 106 additional cases with 212 matched referents was used in a validation study. Results: Six proteins (growth differentiation factor 15, galectin-4, von Willebrand factor, interleukin 17 receptor A, transferrin receptor protein 1, and proprotein convertase subtilisin/kexin type 9) were associated with case status in the discovery cohort; odds ratios ranged from 1.25 to 1.37 per SD increase in the protein signal. Adjusting the multivariable models for classical cardiovascular risk factors at baseline yielded similar results. Subanalyses of case-referent triplets (n=133) who showed no visible coronary artery disease at the time of surgery in the index person supported associations between AS and growth differentiation factor 15 (odds ratio, 1.40; 95% confidence interval, 1.10-1.78) and galectin-4 (odds ratio, 1.27; 95% confidence interval, 1.02-1.59), but these associations were attenuated after excluding individuals who donated blood samples within 5 years before surgery. In triplets (n=201), which included index individuals with concurrent coronary artery disease at the time of surgery, all 6 proteins were robustly associated with case status in all sensitivity analyses. In the validation study, the association of all but 1 (interleukin 17 receptor A) of these proteins were replicated in patients with AS with concurrent coronary artery disease but not in patients with AS without coronary artery disease. Conclusions: We provide evidence that 5 proteins were altered years before AS surgery and that the associations seem to be driven by concurrent atherosclerotic disease.


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