No abstract available.
Coronary Disease/*genetics ; Female ; Humans ; Male ; Myocardial Infarction/*genetics

OBJECTIVETo evaluate relationship between ApoE gene polymorphism and coronary heart disease (CHD).

METHODSMeta-analysis was applied with a random-effect model for the collected data.

RESULTSDifference in pooled frequencies, d, of apoE genotypes E3/2, E4/2, E3/3, E4/3 and E4/4 between case and control groups were 2.3%, -0.8%, -8.5%, 10.5% and 0.9%, respectively. Difference in pooled frequencies, d, of apoE alleles epsilon2, epsilon3 and epsilon4 were -1.5%, -4.2% and 5.8%, respectively, with a statistical significance between four groups.

CONCLUSIONSapoE gene polymorphism was involved in coronary heart disease. Persons with apoE E3/3 genotype or epsilon3 allele were not susceptible to CHD, but those with apoE E4/4 genotype or epsilon4 allele had higher risk suffering from CHD than others.

Apolipoproteins E ; genetics ; Coronary Disease ; genetics ; Humans ; Polymorphism, Genetic

To explore the relation of angiotensin-converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) gene polymorphism with coronary heart disease (CHD) and the severity of coronary artery stenosis, 130 CHD patients who underwent coronary angiography were examined for the number of affected coronary vessels (> or = 75% stenosis) and coronary Jeopardy score. The insertion/deletion of ACE gene polymorphism and AT1R gene polymorphism (an A-->C transversion at nucleotide position 1166) were detected by using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) in CHD patients and 90 healthy serving as controls. The results showed that DD genotype and of ACE were more frequent in CHD patients than that in control group (38.5% vs 14.4%, P<0.001). The frequency of the AT1R A/C genotypes did not differ between the patients and the controls (10% vs 13.1%, P>0.05). The relative risk associated with the ACE-DD was increased by AT1R-AC genotype. Neither the number of affected coronary vessels nor the coronary score differed among the ACE I/D genotypes (P>0.05). But the number of affected coronary vessels and the coronary score were significantly greater in the patients with the AT1R-AC genotype than in those with the AA genotype (P<0.05). In conclusion, DD genotype may be risk factor for CHD and MI in Chinese people, and is not responsible for the development of the coronary artery stenosis. The AT1R-C allele may increase the relative risk associated with the ACE-DD genotype, and may be involved in the development of the stenosis of coronary artery.
Coronary Disease/genetics ; Coronary Disease/pathology ; Coronary Stenosis/*genetics ; Coronary Stenosis/*pathology ; Peptidyl-Dipeptidase A/*genetics ; Polymorphism, Genetic ; Receptor, Angiotensin, Type 1/*genetics

BACKGROUNDC-reactive protein (CRP) gene +1059 G/C polymorphism has been reported to be associated with coronary heart disease (CHD) risk, but the results remain inconclusive. This meta-analysis was therefore conducted to clarify these controversies.

METHODSA comprehensive search was conducted to identify all case control studies on the association between CRP gene +1059 G/C polymorphism and CHD risk. All the related studies were further strictly selected according to the inclusion criteria. Meta-analysis was performed with STATA 10.1 (StataCorp, USA). The association was assessed by odds ratio (OR) and 95% confidence interval (CI); both Begg's funnel plot and Egger's regression test were used to assess the publication bias.

RESULTSThis meta-analysis on a total of 13 studies comprising 6316 CHD cases and 4467 controls showed no significant association between CRP gene +1059 G/C polymorphism and CHD risk in the overall study (for C/C+C/G vs. G/G: OR = 1.01, 95% CI = 0.81-1.25, P = 0.96; for C/C vs. C/G+G/G: OR = 1.17, 95% CI = 0.77-1.77, P = 0.47; for C/C vs. G/G: OR = 1.17, 95% CI = 0.77-1.77, P = 0.47; for C allele vs. G allele: OR = 1.01, 95% CI = 0.81-1.24, P = 0.96). However, in the subgroup analysis by ethnicity, the results showed significant association between CRP gene +1059 G/C polymorphism and CHD risk among Caucasians (for C/C vs. G/G: OR = 2.54, 95% CI = 1.13-5.72, P = 0.02; C/C vs. C/G+G/G: OR = 2.45, 95% CI = 1.09-5.51, P = 0.03), but not among Asians and Africans (P > 0.05).

CONCLUSIONCRP gene +1059 G/C polymorphism may be associated with increased CHD risk among Caucasians and more evidences need to validate the conclusion.

C-Reactive Protein ; genetics ; Coronary Disease ; genetics ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Polymorphism, Genetic ; genetics

BACKGROUND AND OBJECTIVES: Genetic predisposition is an important risk factor for coronary artery disease (CAD). In this study, we aimed to evaluate the impact of rs10757274 and rs2383206 polymorphisms in chromosome 9p21 on presence and severity of CAD in a Turkish population. SUBJECTS AND METHODS: A total of 646 patients who underwent coronary angiography were included in this study. Coronary vessel score and Gensini score were calculated to assess the angiographic severity of CAD. Alleles of AA, AG, and GG were determined for rs10757274 (polymorphism-1) and rs2383206 (polymorphism-2) polymorphisms located in chromosome 9p21 from the blood samples. RESULTS: There was a significant difference between the alleles in polymorphism-1 in the presence of coronary artery disease (38.9% in AA, 48.0% in GG and 56.4% in AG, p=0.017). However, there was no difference between the alleles in polymorphism-2. According to vessel scores, there was a significant difference between the alleles in polymorphism-1 (AA 0.71±1.04, GG 0.88±1.07, AG 1.06±1.12, p=0.018). In polymorphism-2, vessel scores did not show a difference between the alleles. In polymorphism-1, there was a significant difference in Gensini score (p=0.041). Gensini scores did not differ between the alleles in polymorphism-2 (p>0.05 for all). In multivariate analyses, none of the alleles was an independent factor for presence of CAD. CONCLUSION: The presence of rs10757274 polymorphism including AG allele in chromosome 9p21 was related to CAD. However, this relationship was not independent of other cardiovascular risk factors.
Alleles ; Atherosclerosis ; Coronary Angiography ; Coronary Artery Disease* ; Coronary Vessels* ; Genetic Predisposition to Disease ; Genetics ; Humans ; Multivariate Analysis ; Risk Factors

OBJECTIVETo review the functional mechanism of apolipoprotein J (apoJ) in the process of atherosclerosis and the feasibility of apoJ as a therapeutic endpoint.

DATA SOURCESRelevant articles published in English from 1983 to present were selected from PubMed. The terms of "atherosclerosis, apolipoprotein J, clusterin (CLU), oxidative stress, and inflammation" were used for searching.

STUDY SELECTIONArticles studying the role of apoJ with atherosclerosis and restenosis after injury were reviewed. Articles focusing on the intrinsic determinants of atherosclerosis were selected. The exclusion criteria of articles were that the studies on immunologic vasculitis.

RESULTSApoJ, involved in numerous physiological process important for lipid transportation and vascular smooth muscle cell differentiation, including apoptotic cell death, cell-cycle regulation, cell adhesion, tissue remodeling, immune system regulation, and oxidative stress, plays a role in the development of clinical atherosclerosis. In the process of relieving atherosclerosis, apoJ can promote cholesterol and phospholipid export from macrophage-foam cells, and exhibit cytoprotective and anti-inflammatory actions by interacting with lots of known inflammatory proteins which may predict the onset of clinical cardiovascular events and may actually play a causal role in mediating atherosclerotic disease such as C-reactive protein, paraoxonase, and leptin. As known as CLU, apoJ has been identified to play central roles in the process of vascular smooth cells migration, adhesion, and proliferation, which can contribute significantly to restenosis after vascular injury.

CONCLUSIONSIntense effort and substantial progress have been made to identify the apoJ that relieves atherosclerosis and vascular restenosis after percutaneous coronary intervention. More work is needed to elucidate the exact mechanisms of and the interrelationship between the actions of apoJ and to successfully achieve regression of atherosclerosis by regarding it as a therapeutic endpoint.

Cardiovascular Diseases ; genetics ; mortality ; Clusterin ; genetics ; metabolism ; Coronary Artery Disease ; genetics ; metabolism ; Coronary Restenosis ; genetics ; metabolism ; Humans

Since a decade ago, apolipoprotein (apo) E polymorphism has been focussed as a risk factor for cardiovascular disease. ApoE plays a central role as a receptor ligand for the uptake of lipoproteins from the circulation. There was an agreement on apoE polymorphism being one of the major risk factors for coronary artery disease (CAD) by its effects on lipid profiles. However, the effects of apoE have not been noted in all populations and conflicting results in the risk of CAD have been noted. Recently, in situ expression of apoE on the atherosclerotic plaque has been studied. We, therefore, investigated the effects of apoE genotype on patients with acute coronary syndrome, including unstable angina and acute myocardial infarction, in non-diabetic patients. While we could not find significant risk effects of apoE on coronary artery disease and lipid profiles on simple comparison with the normal control group, we could find significantly decreased frequencies of apo epsilon 3 allele in patients with acute coronary syndrome compared with stable angina patients (77.8% vs 88.8%). We suggest that the apoE genotype could be associated with acute coronary events in CAD and further study with in situ biochemical methods will be needed on the effects of apoE polymorphism on plaque stability.
Apolipoproteins E/genetics* ; Coronary Disease/genetics* ; Genotype ; Human ; Polymorphism (Genetics)/genetics* ; Syndrome

OBJECTIVE: To investigate the association of CXCL12 and CXCR4 polymorphisms with the genetic risk and severity of coronary stenosis in patients with coronary artery disease (CAD). METHODS: Competitive allele specific PCR(KASP) was performed to identify the genotypes of rs2297630 and rs2322864 polymorphisms in 302 CAD patients and 302 age-and gender-matched healthy controls. The severity of CAD patients was assessed by the Gensini scoring system according to the results of coronary arteriography. The association of rs2297630 and rs2322864 polymorphisms with genetic risk of CAD and Gensini scores were analyzed by unconditional logistic regression and multivariate linear regression respectively. RESULTS: There were significant differences in the genotype and allele frequencies of both rs2297630 and rs2322864 between the CAD group and healthy control (all <0.01). Regression analysis showed that rs2297630 polymorphism was associated with genetic risk of CAD and Gensini scores (all <0.01). People who carried the AA genotype suffered higher risk of CAD susceptibility and more serious coronary stenosis (all <0.01), compared with GG genotype carriers. There was also significant association between rs2322864 polymorphism and genetic risk of CAD (<0.01); those who carried the CT genotype had higher risk of CAD (<0.01), compared with TT genotype carriers. However, rs2322864 polymorphism was not associated with the severity of coronary stenosis (>0.05). CONCLUSIONS Gene polymorphism of CXCL12 rs2297630 is associated with the genetic risk of CAD and the severity of coronary stenosis. Moreover, the gene polymorphism of CXCR4 rs2322864 is associated with genetic risk of CAD, but not with the severity of coronary stenosis.
Chemokine CXCL12 ; genetics ; Coronary Angiography ; Coronary Artery Disease ; complications ; Coronary Stenosis ; complications ; genetics ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Polymorphism, Genetic ; Receptors, CXCR4 ; genetics ; Risk Factors

BACKGROUNDCoronary heart disease (CHD) is a multifactorial disease and is thought to have a polygenic basis. Apolipoprotein E (APOE) gene is one such candidate with its common ε2/ε3/ε4 polymorphism in CHD. In recent years, numerous case-control studies have investigated the relationship of APOE polymorphism with CHD risk. However, the results are confusing.

METHODSTo clarify this point, we undertook a meta-analysis based on 14 published studies including 5746 CHD cases and 19,120 controls. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were assessed for association using a random-effects or fixed-effects model using STATA version 10 (StataCorp LP, College Station, TX, USA).

RESULTSOverall, the analysis showed that carriers of APOE ε2 allele decreased risk for CHD (ε2 allele vs. ε3 allele: OR = 0.82, 95% CI: 0.75-0.90, P < 0.001; ε2 carriers vs. ε3 carriers: OR = 0.81, 95% CI: 0.73-0.89, P < 0.001), compared with those carrying ε3 allele, especially in Caucasian population. However, those with ε4 allele had a significant increased risk for CHD (ε4 allele vs. ε3 allele: OR = 1.34, 95% CI: 1.15-1.57, P < 0.001), especially in Mongoloid population. Potential publication bias was observed in the genetic model of ε4 versus ε3, but the results might not be affected deeply by the publication bias. When we accounted for publication bias using the trim and fill method, the results were not materially alerted, suggesting the stability of our results.

CONCLUSIONSTaken together, our meta-analysis supported a genetic association between APOE gene and CHD. ε4 increased the risk of CHD, whereas ε2 decreased the risk of CHD.

Apolipoproteins E ; genetics ; Coronary Disease ; genetics ; Genetic Predisposition to Disease ; Humans ; Polymorphism, Genetic

Coronary heart disease is one of the most important causes of death in human, and consumes vast medical resources. Percutaneous coronary intervention (PCI) has been a significant breakthrough for its treatment. However, clinical application has been hampered by in-stent restenosis (ISR). Although drug eluting stent (DES) has reduced the occurrence of restenosis, incidence of ISR is still about 5% to 10%. The main reasons for restenosis after PCI are hyperplasia of vascular endothelial cells and smooth muscle cell migration. The exact mechanism of personalized differences in restenosis is not clear yet, but there may be a variety of risk factors. In addition to aging, smoking and diabetes, an increasing number of studies have found that genetic and epigenetic factors play an important role in ISR. In this article, authors have reviewed genetic and epigenetic factors on the progression of ISR, which may help to determine the genetic risk factors in patients with ISR after PCI.
Angioplasty, Balloon, Coronary ; methods ; Coronary Restenosis ; etiology ; genetics ; Disease Progression ; Epigenomics ; methods ; Humans ; Stents ; Treatment Outcome