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Circulating retinol binding protein 4 levels in coronary artery disease: a systematic review and meta-analysis.
Chen, H, Zhang, J, Lai, J, Zhou, Y, Lin, X, Deng, G, Zhang, Z, Li, L
Lipids in health and disease. 2021;(1):89
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.
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The Relationship of Coronary Artery Calcium and Clinical Coronary Artery Disease with Cognitive Function: A Systematic Review and Meta-Analysis.
Xia, C, Vonder, M, Sidorenkov, G, Oudkerk, M, de Groot, JC, van der Harst, P, de Bock, GH, De Deyn, PP, Vliegenthart, R
Journal of atherosclerosis and thrombosis. 2020;(9):934-958
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AIM: Coronary artery disease (CAD) and cognitive impairment are common in the elderly, with evidence for shared risk factors and pathophysiological processes. The coronary artery calcium (CAC) score is a marker of subclinical CAD, which may allow early detection of individuals prone to cognitive decline. Prior studies on associations of CAC and clinical CAD with cognitive impairment had discrepant results. This systematic review aims to evaluate the association of (sub)clinical CAD with cognitive function, cognitive decline, and diagnosis of mild cognitive impairment (MCI) or dementia. METHODS A systematic search was conducted in MEDLINE, Embase, and Web of Science until February 2019, supplemented with citations tracking. Two reviewers independently screened studies and extracted information including odds ratios (ORs) and hazard ratios (HRs). RESULTS Forty-six studies, 10 on CAC and 36 on clinical CAD, comprising 1,248,908 participants were included in the systematic review. Studies about associations of (sub)clinical CAD with cognitive function and cognitive decline had heterogeneous methodology and inconsistent findings. Two population-based studies investigated the association between CAC and risk of dementia over 6-12.2 years using different CAC scoring methods. Both found a tendency toward higher risk of dementia as CAC severity increased. Meta-analysis in 15 studies (663,250 individuals) showed an association between CAD and MCI/dementia (pooled OR 1.32, 95%CI 1.17-1.48) with substantial heterogeneity (I2=87.0%, p<0.001). Pooled HR of CAD for incident MCI/dementia over 3.2-25.5 years in six longitudinal studies (70,060 individuals) was 1.51 (95%CI 1.24-1.85), with low heterogeneity (I2=14.1%, p=0.32). Sensitivity analysis did not detect any study that was of particular influence on the pooled OR or HR. CONCLUSIONS Limited evidence suggests the CAC score is associated with risk of dementia. In clinical CAD, risk of MCI and dementia is increased by 50%, as supported by stronger evidence.
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Predictive value of coronary artery calcium score in cardiovascular disease.
Liu, S, Zheng, X, Xu, J, Wang, X, Zhang, Y, Lv, B, Zheng, L, Sun, K
Frontiers in bioscience (Elite edition). 2020;(1):113-125
Abstract
We investigated coronary heart disease (CHD) and cardiovascular disease (CVD) event rates in a diverse population with a coronary artery calcium score (CACS) of 0 and the role of CACS in the detection of subclinical noncalcified atherosclerotic plaque. A total of 15,884 participants in five studies were included in this meta-analysis. Hazard ratios (HRs) with 95% confidence intervals (95% CIs) were calculated. The results showed that CHD incidence significantly increased with increased CACS (HR=0.05, 95% CI 0.03-0.06, Z=5.82, P=0.002). The CHD rate was low and further increased with CACS of 101-300. With CACS >300, the CHD rate was highest. Similarly, CVD rate was low with CACS of 0, increased with CACS of 1-100 (HR=0.03, 95% CI 0.01-0.06, Z=1.66, P=0.096), and further increased with CACS of 101-300. With CACS >300, the CVD rate was highest. Clinical evidence indicated that the higher the CACS, the higher the CHD and CVD rates, while the CVD rate does not always decreased compared with CHD rate with the same CACS, especially with CACS of 0.
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Genome-wide association meta-analysis of coronary artery disease and periodontitis reveals a novel shared risk locus.
Munz, M, Richter, GM, Loos, BG, Jepsen, S, Divaris, K, Offenbacher, S, Teumer, A, Holtfreter, B, Kocher, T, Bruckmann, C, et al
Scientific reports. 2018;(1):13678
Abstract
Evidence for a shared genetic basis of association between coronary artery disease (CAD) and periodontitis (PD) exists. To explore the joint genetic basis, we performed a GWAS meta-analysis. In the discovery stage, we used a German aggressive periodontitis sample (AgP-Ger; 680 cases vs 3,973 controls) and the CARDIoGRAMplusC4D CAD meta-analysis dataset (60,801 cases vs 123,504 controls). Two SNPs at the known CAD risk loci ADAMTS7 (rs11634042) and VAMP8 (rs1561198) passed the pre-assigned selection criteria (PAgP-Ger < 0.05; PCAD < 5 × 10-8; concordant effect direction) and were replicated in an independent GWAS meta-analysis dataset of PD (4,415 cases vs 5,935 controls). SNP rs1561198 showed significant association (PD[Replication]: P = 0.008 OR = 1.09, 95% CI = [1.02-1.16]; PD [Discovery + Replication]: P = 0.0002, OR = 1.11, 95% CI = [1.05-1.17]). For the associated haplotype block, allele specific cis-effects on VAMP8 expression were reported. Our data adds to the shared genetic basis of CAD and PD and indicate that the observed association of the two disease conditions cannot be solely explained by shared environmental risk factors. We conclude that the molecular pathway shared by CAD and PD involves VAMP8 function, which has a role in membrane vesicular trafficking, and is manipulated by pathogens to corrupt host immune defense.
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Common Variants of Vitamin D Receptor Gene Polymorphisms and Susceptibility to Coronary Artery Disease: A Systematic Review and Meta-Analysis.
Alizadeh, S, Djafarian, K, Alizadeh, H, Mohseni, R, Shab-Bidar, S
Journal of nutrigenetics and nutrigenomics. 2017;(1-2):9-18
Abstract
BACKGROUND AND AIMS ApaI, FokI, TaqI, and BsmI polymorphisms in the vitamin D receptor (VDR) gene have been reported to be associated with the risk of coronary artery disease (CAD), although the results of previous studies have been inconsistent. The aim of this study was to explore whether these polymorphisms play a role in the genetic susceptibility to CAD. METHODS A comprehensive search of Medline and Embase databases was conducted for studies evaluating the association between the VDR polymorphisms and CAD risk. Odds ratios with 95% confidence intervals were calculated to assess the strength of association in the dominant model, recessive model, allelic model, and genotypes contrast. RESULTS Nine studies involving a total of 5,259 cases and 1,981 controls were finally included in this meta-analysis. Overall, no significant associations were found between ApaI, FokI, TaqI, and BsmI polymorphisms and the risk of CAD in any of the genetic models (all p ˃ 0.05). Moreover, a subgroup analysis by ethnicity did not reveal a significant relationship between any of the examined polymorphisms and CAD risk in Caucasians and East-Asians for any model (all p ˃ 0.05). CONCLUSION Current evidence suggests that the ApaI, FokI, TaqI, and BsmI polymorphisms of the VDR gene might not be associated with genetic susceptibility to CAD. Further well-designed studies with large sample sizes are needed to confirm our results.
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Associations between XRCC1 Gene Polymorphisms and Coronary Artery Disease: A Meta-Analysis.
Ma, WQ, Han, XQ, Wang, X, Wang, Y, Zhu, Y, Liu, NF
PloS one. 2016;(11):e0166961
Abstract
Genetic variations that influence DNA repair efficiency may contribute to coronary artery disease (CAD) susceptibility. Previous studies have investigated whether there was evidence of an association between polymorphisms at the X-ray repair cross complementing 1 (XRCC1) gene and susceptibility to CAD, but findings have been inconclusive. We identified eligible studies through a comprehensive literature search to determine whether an association exists between XRCC1 gene polymorphisms and CAD susceptibility. Findings were assessed using the odds ratio (OR) and corresponding 95% confidence interval (CI), which were calculated using a fixed- or random-effects model, based on the heterogeneity of the studies. Ten eligible studies were finally included in this meta-analysis. Our pooled analysis found that XRCC1 polymorphisms were significantly associated with CAD susceptibility under recessive (Arg194Trp: OR = 1.47, 95% CI = 1.13-1.93; Arg399Gln: OR = 1.45, 95% CI = 1.12-1.89), homozygous (Arg194Trp: OR = 1.37, 95% CI = 1.03-1.81; Arg399Gln: OR = 1.56, 95% CI = 1.19-2.05), and allele (Arg399Gln: OR = 1.18, 95% CI = 1.06-1.32) genetic models. Following subgroup analysis by ethnicity, in Asian populations, we found evidence of associations between the XRCC1 Arg194Trp polymorphism and CAD under recessive and homozygous genetic models, and between the XRCC1 Arg399Gln polymorphism and CAD under recessive, homozygous, and allele genetic models. Subgroup analysis stratified by control source revealed associations between the Arg194Trp and Arg399Gln polymorphisms and susceptibility to CAD under recessive and homozygous modes of inheritance, respectively. In addition, subgroup analysis stratified by sample size found that findings of the Arg194Trp polymorphism in large sample sizes were comparable to those found using pooled eligible studies. Based on our meta-analysis, we concluded that the XRCC1 gene polymorphisms, Arg194Trp and Arg399Gln, are associated with CAD susceptibility, specifically in Asian populations. However, additional, comprehensive and well-designed studies are warranted to confirm these findings.
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Association Between Low-Density Lipoprotein Cholesterol-Lowering Genetic Variants and Risk of Type 2 Diabetes: A Meta-analysis.
Lotta, LA, Sharp, SJ, Burgess, S, Perry, JRB, Stewart, ID, Willems, SM, Luan, J, Ardanaz, E, Arriola, L, Balkau, B, et al
JAMA. 2016;(13):1383-1391
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Abstract
IMPORTANCE Low-density lipoprotein cholesterol (LDL-C)-lowering alleles in or near NPC1L1 or HMGCR, encoding the respective molecular targets of ezetimibe and statins, have previously been used as proxies to study the efficacy of these lipid-lowering drugs. Alleles near HMGCR are associated with a higher risk of type 2 diabetes, similar to the increased incidence of new-onset diabetes associated with statin treatment in randomized clinical trials. It is unknown whether alleles near NPC1L1 are associated with the risk of type 2 diabetes. OBJECTIVE To investigate whether LDL-C-lowering alleles in or near NPC1L1 and other genes encoding current or prospective molecular targets of lipid-lowering therapy (ie, HMGCR, PCSK9, ABCG5/G8, LDLR) are associated with the risk of type 2 diabetes. DESIGN, SETTING, AND PARTICIPANTS The associations with type 2 diabetes and coronary artery disease of LDL-C-lowering genetic variants were investigated in meta-analyses of genetic association studies. Meta-analyses included 50 775 individuals with type 2 diabetes and 270 269 controls and 60 801 individuals with coronary artery disease and 123 504 controls. Data collection took place in Europe and the United States between 1991 and 2016. EXPOSURES Low-density lipoprotein cholesterol-lowering alleles in or near NPC1L1, HMGCR, PCSK9, ABCG5/G8, and LDLR. MAIN OUTCOMES AND MEASURES Odds ratios (ORs) for type 2 diabetes and coronary artery disease. RESULTS Low-density lipoprotein cholesterol-lowering genetic variants at NPC1L1 were inversely associated with coronary artery disease (OR for a genetically predicted 1-mmol/L [38.7-mg/dL] reduction in LDL-C of 0.61 [95% CI, 0.42-0.88]; P = .008) and directly associated with type 2 diabetes (OR for a genetically predicted 1-mmol/L reduction in LDL-C of 2.42 [95% CI, 1.70-3.43]; P < .001). For PCSK9 genetic variants, the OR for type 2 diabetes per 1-mmol/L genetically predicted reduction in LDL-C was 1.19 (95% CI, 1.02-1.38; P = .03). For a given reduction in LDL-C, genetic variants were associated with a similar reduction in coronary artery disease risk (I2 = 0% for heterogeneity in genetic associations; P = .93). However, associations with type 2 diabetes were heterogeneous (I2 = 77.2%; P = .002), indicating gene-specific associations with metabolic risk of LDL-C-lowering alleles. CONCLUSIONS AND RELEVANCE In this meta-analysis, exposure to LDL-C-lowering genetic variants in or near NPC1L1 and other genes was associated with a higher risk of type 2 diabetes. These data provide insights into potential adverse effects of LDL-C-lowering therapy.
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Magnesium Levels in Drinking Water and Coronary Heart Disease Mortality Risk: A Meta-Analysis.
Jiang, L, He, P, Chen, J, Liu, Y, Liu, D, Qin, G, Tan, N
Nutrients. 2016;(1)
Abstract
Epidemiological studies have demonstrated inconsistent associations between drinking water magnesium levels and risk of mortality from coronary heart disease (CHD); thus, a meta-analysis was performed to assess the association between them. Relevant studies were searched by the databases of Cochrane, EMBASE, PubMed and Web of Knowledge. Pooled relative risks (RR) with their 95% CI were calculated to assess this association using a random-effects model. Finally, nine articles with 10 studies involving 77,821 CHD cases were used in this study. Our results revealed an inverse association between drinking water magnesium level and CHD mortality (RR = 0.89, 95% CI = 0.79-0.99, I² = 70.6). Nine of the 10 studies came from Europe, and the association was significant between drinking water magnesium level and the risk of CHD mortality (RR = 0.83, 95% CI = 0.69-0.98). In conclusion, drinking water magnesium level was significantly inversely associated with CHD mortality.
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The Associations Between the Polymorphisms of Vitamin D Receptor and Coronary Artery Disease: A Systematic Review and Meta-Analysis.
Lu, S, Guo, S, Hu, F, Guo, Y, Yan, L, Ma, W, Wang, Y, Wei, Y, Zhang, Z, Wang, Z
Medicine. 2016;(21):e3467
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Vitamin D receptor (VDR) polymorphisms were indicated to be associated with coronary artery disease (CAD); however, published studies reported inconsistent results.The aim of this meta-analysis is to reach a more accurate estimation of the relationship between VDR genetic polymorphisms and CAD risk.Eligible studies were retrieved by searching PubMed, Embase, VIP, Wanfang and China National Knowledge Infrastructure databases. Included and excluded criteria were formulated. The case group was patients with CAD, and the control group was healthy subjects. Summary odds ratios (ORs) and 95% confidence intervals (CIs) were used to evaluate VDR polymorphisms associations with CAD risk. Heterogeneity was evaluated by Q statistic and I statistic.Seven studies of a total of 2306 CAD patients and 4151 control subjects met the inclusion criteria. The pooled results from Taq1 showed increased risk in allelic model (OR = 1.14, 95% CI = 1.02-1.28), dominant model (OR = 1.21, 95% CI = 1.02-1.43), heterozygote model (OR = 1.19, 95% CI = 1.00-1.1.42), and homozygote model (OR = 1.27, 95% CI = 1.01-1.61). Besides, Fok1 T > C showed decreased risk in allelic model (OR = 0.81, 95% CI = 0.65-1.00) and Fok1 A > G also showed decreased risk in allelic model (OR = 0.67, 95% CI = 0.45-1.00) and recessive model (OR = 0.55, 95% CI = 0.31-0.97). In Caucasian subgroup, Bsm1showed increased risk in allelic model (OR = 1.23, 95% CI = 1.02-1.47), heterozygote model (OR = 1.20, 95% CI = 1.00-1.44), and homozygote model (OR = 1.22, 95% CI = 1.02-1.45). In CAD patients with type 2 diabetes mellitus (T2DM), Apa1showed a decreased risk in heterozygote model (OR = 0.80, 95% CI = 0.66-0.98); however, increased risk in recessive model (OR = 5.00, 95% CI = 2.74-9.13) was discovered in CAD patients without T2DM.The Fok1 polymorphism may play a protective role in CAD, and the possible protective role in Apa1 CA genotype in CAD patients with T2DM needs further studies. The Taq1 polymorphism is found to be associated with a significant increase in CAD risk based on our analysis; moreover, increased risk in Apa1 polymorphism in CAD patients without T2DM and Bsm1 polymorphism in Caucasian group is also detected.
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Biomarkers of Coronary Artery Disease Differ Between Asians and Caucasians in the General Population.
Gijsberts, CM, den Ruijter, HM, Asselbergs, FW, Chan, MY, de Kleijn, DP, Hoefer, IE
Global heart. 2015;(4):301-311.e11
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Coronary artery disease (CAD) markers have not been thoroughly investigated among Asians. The incidence of CAD, however, is rising rapidly in Asia. In this review, we systematically discuss publications that compare CAD biomarkers between Asians and Caucasians in the general population. A PubMed search yielded 5,570 hits, containing 59 articles describing 47 unique cohorts that directly compare Asians with Caucasians. Ten biomarkers were taken into account for this review: total cholesterol; triglycerides; high-density lipoprotein cholesterol; low-density lipoprotein cholesterol; C-reactive protein; glucose; insulin; glycated hemoglobin; fibrinogen; and plasminogen activator inhibitor-1. Triglycerides were 1.13-fold higher in South Asians than in Caucasians, and insulin levels were 1.33-fold higher. In Japanese and Chinese subjects, lower C-reactive protein levels were reported: 0.52 and 0.36-fold, respectively. Ethnicity-specific prognostic measures of CAD biomarkers were rarely reported. CAD biomarker levels differ between Asians and Caucasians and among Asian ethnic groups in population-based cohorts. The ethnicity-specific prognostic value of CAD biomarkers is yet to be determined.