基因芯片技术分析老年冠心病患者的易感基因

目的 研究血管紧张素转换酶（ACE）、血管紧张素原（AGT）及内皮型一氧化氮合酶（eNOS）基因多态性与老年人冠心病（CHD）的关系.方法 选择老年CHD患者100例及对照者91例,应用基因芯片技术检测ACE、AGT和eNOS基因多态性,并比较其基因型及等位基因频率。结果 CHD组ACE DD基因型频率（28.0%）与对照组（15.4%）比较，差异有统计学意义（P＜0.05）,ACE基因多态性与老年CHD相关.AGT TT基因型频率（75.0%）与对照组（51.7%）比较，差异有统计学意义（P＜0.01）,AGT基因多态性与老年CHD相关.eNOS TT基因型频率（5.0%）与对照组（0.0%）比较,差异无统计学意义（P＞0.05）。同时携带ACE DD和AGT TT基因型或AGT TT和eNOS TT基因型者与老年CHD呈显著正相关（OR=2.9,P＜0.05,OR=1.1,P＜0.05）。结论 ACE和AGT基因多态性可能是中国老年人CHD的危险因素。     

Effects of angiotensinogen gene polymorphisms on the risk of coronary heart disease in the Chinese population: a meta-analysis

Objective Coronary heart disease （CHD） is a multifactorial disease. This meta-analysis was performed to evaluate the relationship between angiotensinogen gene polymorphisms and CHD in the Chinese population. Methods We searched literature in pubmed （1990- 2010.8） and CNKI （1990-2010.8） for all the relevant studies on 2 angiotensinogen polymorphisms （M235T and T174M） and risk of CHD. The meta-analysis software Stata 10.0 was used for ascertaining heterogeneity among individual studies and for combining all the studies. Furthermore,Egger＇s test and sensitivity analysis were performed to insure authenticity of the outcome.Results Ten associations studies on 2 angiotensinogen polymorphisms （M235T and T174M） were included in this meta-analysis. In a combined analysis, the summary per-allele odds ratio for CHD of the M235T polymorphism was 1.374 （95% confidence interval, 1.019 to 1.852） and T174M polymorphism was 4.089 （95% confidence interval, 1.697 to 9.851）. Conclusions The M235T polymorphism had weak but statistically significant association with CHD while the T174M polymorphism was more strongly associated with a CHD risk in Chinese population, but further confirmation studies are needed     

Research progress of the relationship between angiotensinogen gene polymorphisms and coronary heart disease

Coronary heart disease (CHD) is a major health problem in many countries and its pathogenesis is not yet fully understood, contributing to significant morbidity and mortality. Accumulated evidence manifest clearly that CHD is determined by a complex interplay of genetic and environmental factors. Many clinical data have showed that the renin-angiotensin system (RAS) involved in many cardiovascular diseases, such as hypertension and CHD. Angiotensinogen (AGT) is the key components of the RAS system, and two gene polymorphisms of AGT had been detected of the CHD risk: M235T and T174M. This article reviews the effects of AGT gene polymorphisms on the CHD.     

Angina, coronary risk factors and coronary artery disease in patients with valvular disease. A prospective study

The relationship between coronary risk factors and coronaryartery disease in patients with valvular heart disease was studiedprospectively in 387 consecutive patients undergoing routinecoronary arteriography prior to valve replacement. Coronary artery disease was as common in patients with mitralvalve disease (31.9%) as in those with aortic valve disease(26.8%) Although it occurs more frequently in patients withangina (45.7%) significant coronary artery disease is foundin 19.2% (47 of 245) of those without angina (P<0.001), suggestingthat the presence of angina alone is an unreliable indicatorof significant coronary disease. The prevalence and severityof significant coronary artery disease increases progressivelyas the number of coronary risk factors also increase (P<0.001)but the prevalence is low (3%) in patients in whom both anginaand coronary risk factors are absent. These findings suggestthat preoperative coronary arteriography might be omitted inthis latter group of patients.     

中国2型糖尿病人群脂联素受体1基因多态性与冠心病风险的相关性研究

目的 研究我国2型糖尿病(T2DM)人群脂联素受体1(AdipoR1)基因多态性与冠心病(CAD)风险的相关性. 方法 以307例T2DM患者为研究人群,其中205例伴有CAD,102例不伴CAD.应用聚合酶链式反应-限制性内切酶片断长度多态性(PCR-RFLP)技术或基因测序方法,研究AdipoR1 10个单倍型标记单核苷酸多态性(Haplotype-tagging SNPs)与CAD风险的关系. 结果 (1)Ad-ipoR1 SNP rs1342387 GG和AG基因型携带者均较AA型携带者发生CAD的风险显著增加(GG vsAA:校正OR'=2.491,95%CI' 1.354～6.885,P'=0.031;AG vs AA:校正OR'=3.053,95%CI' 1.085～5.718,P'=0.007).(2)SNP rs12045862基因型CC携带者与TT携带者相比,CAD的风险显著增加(校正OR'=2.751,95%CI' 1.063～7.115,P'=0.037).(3)SNPs rs1342387、rs12045862 GX/CC基因型组合携带者较非携带者CAD的风险显著增加(校正OR'=3.646,95%CI' 1.253～10.608,P'=0.018).保护性基因型组合AA/TX携带者较非携带者发生CAD的风险显著降低(校正OR'=0.260,95%CI'0.113～0.601,P'=0.002).(4)在超重和肥胖(BMI≥24)的T2DM人群中,发现肥胖与SNPs rs1342387、rs12045862对CAD的风险有相互作用(P<0.05);在总人群中发现的与CAD风险相关的SNPs rs1342387和rs12045862在这一亚组仍具有相关性;同时发现SNP rs7539542基因型CC携带者较GG携带者CAD的风险增加(校正OR'=4.714,P'=0.036). 结论 中国T2DM人群中,AdipoR1 SNPs与CAD的风险可能相关.在超重或肥胖T2DM人群中,AdipoR1 SNPs与肥胖对CAD风险的影响有协同作用.     

Association between T174M polymorphism in the angiotensinogen gene and risk of coronary artery disease: a meta-analysis

Background Angiotensinogen (AGT) T174M gene polymorphism has been suggested to be linked to risk of coronary artery disease, however, results from studies of this association have been inconsistent. In this study, we assess the relationship between AGT T174M gene polymorphism and coronary artery disease. Methods We conducted a meta-analysis of 18 case-control studies with 8,147 coronary artery disease cases and 5,344 controls in Google scholar, PubMed, Cochrane Library and China National Knowledge Infrastructure (CNKI) databases to identify eligible studies published by July, 2012. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated from these studies. Results Overall, a significant association was found between angiotensinogen T174M polymorphism and coronary artery disease risk when all studies were pooled into the meta-analysis (TT vs. MM: OR = 0.53, 95% CI = 0.40–0.71; dominant model: OR = 1.16, 95% CI = 1.01–1.35; recessive model: OR = 0.54, 95% CI = 0.40–0.72). In a stratified analysis, the results indicate a significant associa?tion in Caucasians suffering from coronary stenosis (TT vs. MM: OR = 0.38, 95% CI = 0.23–0.63; recessive model: OR = 0.39, 95% CI = 0.23–0.64). No significant increased risk for coronary artery disease was found in Asians. Conclusions The meta-analysis indicate a significant associa?tion of T174M polymorphism with coronary stenosis risk in Caucasians.     

Insulin receptor substrate-1 gene polymorphism and cardiovascular risk in non-insulin dependent diabetes mellitus and patients undergoing coronary angiography

Clustering of risk factors for cardiovascular disease related to insulin resistance may account for the increased incidence of vascular disease in these conditions and in non-diabetic subjects. To investigate the relationship between a coding polymorphism in the insulin receptor substrate-1 gene and the presence of cardiovascular risk factors, 209 patients with NIDDM and 452 subjects investigated for coronary artery disease (CAD) were studied. In the NIDDM subjects 22 (10.5%) were heterozygous at codon 972 for a polymorphism which codes for a glycine to arginine substitution and 187 (89.5%) were homozygous for the wild type. Patients with the mutation had lower levels of cholesterol compared with wild type (mean, 95% confidence intervals), 5.3 (4.9–5.8) vs 6.0 (5.9–6.2) mmol/l, respectively (P = 0.002), triglyceride 1.7 (1.4–2.1) vs 2.2 (2.0–2.4) mmol/l (P = 0.051), factor VII:C activity 109.5 (85.5–133.5) vs 133.5 (127–140)% (P = 0.057) and PAI-1 antigen, 16.0 (10.5–24.3) vs 22.2 (20.0–24.6) ng/ml (P = 0.054). There were no differences in body mass index, indices of glycaemic control, fasting insulin or the prevalence of hypertension. In patients with CAD, 55 (12.7%) were carriers of the mutation (including three homozygotes) (NIDDM vs CAD, NS). Although similar trends in cholesterol, factor VII, PAI-1 antigen and triglyceride existed between carriers of the mutation and the wild type, none reached statistical significance. The results indicate that the IRS-1 gene is not implicated in the pathogenesis of NIDDM or CAD.     

2型糖尿病合并冠心病患者对氧磷酶1基因多态性分析

目的探讨对氧磷酶1(PON1)基因多态性与2型糖尿病合并冠心病的相关性。方法使用变性高效液相色谱分析方法检测了202例2型糖尿病合并冠心病患者、177例单纯2型糖尿病患者和206名健康对照者;共检测了PON1基因G-126C、L55M和Q192R 3个多态性的基因型,比较分析3组间各基因型和等位基因频率分布的差异。结果 2型糖尿病合并冠心病组的Q192R位点R等位基因频率明显高于对照组(67.1%比60.2%,P=0.024),其他位点在各组间差异无统计学意义。结论PON1基因Q192R位点R等位基因与2型糖尿病合并冠心病发病相关。     

Association of angiotensin II type 1 receptor gene A1166C polymorphism with the presence of diabetes mellitus and metabolic syndrome in patients with documented coronary artery disease

Background

There are relatively limited data available on the genetic susceptibility to diabetes mellitus and metabolic syndrome in the Iranian population. We have therefore investigated the association between the angiotensin II type I receptor gene polymorphism (AT₁R/A1166C) and the presence of diabetes mellitus and metabolic syndrome in a well defined group of patients.

Methods

Patients with angiographically defined coronary artery disease (CAD) (n = 309) were evaluated for the presence of AT₁R/A1166C polymorphism. These patients were classified into subgroups with (n = 164, M/F: 109/55) and without (n = 145, M/F: 84/61) diabetes mellitus. The AT₁R polymorphism was assessed using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) based method.

Results

There was a higher frequency of polymorphic genotypes (AC + CC) in the diabetic compared with the non-diabetic group (p = 0.01). When determined for each gender separately, this difference remained significant in the males (p = 0.04) but not in females (p = 0.09). With regard to the allele frequencies, the C allele was significantly higher and the A allele frequency was lower in the diabetic group (p = 0.01). This remained significant after gender segregation for males (p = 0.01) but not females. In the binary logistic regression analysis, only serum fasting glucose was found as the independent predictor for the presence of diabetes in the CAD patients (β = 1.16, p < 0.001 for total population and β = 1.29, p < 0.001 for male subjects). There was no significant difference in genotype or allele frequencies between subgroups with and without metabolic syndrome, this being unaffected by gender or the definition of metabolic syndrome used apart from a significantly lower frequency of C allele in male subjects with metabolic syndrome defined by the NCEP ATP III criteria (p = 0.04).

Conclusion

The AT₁R/A1166C polymorphism may be associated with the presence of diabetes mellitus in male subjects with documented CAD.     

血管紧张素转换酶基因缺失多态性与冠状动脉病变

目的 :探讨血管紧张素转换酶 ( ACE)基因的插入 /缺失 ( insertion/deletion,I/D)多态性与冠状动脉病变的相关性。方法 :应用聚合酶链反应 ( PCR)扩增技术检测 86例行冠状动脉造影患者的 ACE基因 I/D多态性。结果 :冠状动脉异常组的 DD基因型频率 0 .41,D等位基因频率 0 .5 2 ,显著高于冠状动脉正常组的 0 .15和 0 .2 9( P <0 .0 5 ) ;DD基因型与冠状动脉病变有关 ( OR=3.97,P<0 .0 5 )。多支病变与 DD基因型的关系更为密切 ( OR=4.72 ,P<0 .0 5 )。冠状动脉正常组、单支病变组和多支病变组的 DD型频率依次为 0 .15、0 .33和 0 .46( P <0 .0 5 ) ,D等位基因频率为 0 .2 9、0 .44和 0 .5 6( P <0 .0 1)。结论 :ACE基因的 I/D多态性与冠状动脉病变及其严重程度相关 ,DD型及 D等位基因频率随冠状动脉病变及其程度的加重而逐渐升高。在冠状动脉病变患者中 DD及 ID型患者的吸烟率、甘油三酯及血压显著低于 型者 ( P <0 .0 5 ) ,说明 D等位基因及 DD基因型可能是冠心病低危人群冠状动脉病变的重要危险因素之一。     

Serum bilirubin levels, UGT1A1 polymorphisms and risk for coronary artery disease

Low levels of the antioxidative serum bilirubin are associated with vascular aging and an increased risk for coronary artery disease (CAD). UGT1A1 is the major gene influencing bilirubin concentrations. Therefore, we investigated an association of bilirubin levels and two polymorphisms in the promoter of UGT1A1 (-53(TA-repeat) polymorphism and T-3279G) in 477 patients with premature, familial CAD and 619 age- and sex-matched controls. Bilirubin concentrations were significantly lower in cases than in controls (0.62 ± 0.36 vs. 0.76 ± 0.41 mg/dl for men, p = 1.2 × 10⁻¹⁰; and 0.42 ± 0.29 vs. 0.55 ± 0.23 mg/dl, p = 1.9 × 10⁻⁹ for women). Both polymorphisms showed a strong association with bilirubin levels with higher levels for homozygote carriers of the minor allele. These associations were most pronounced in male controls and patients (p = 5.9 × 10⁻²⁶ and p = 3.4 × 10⁻¹⁶, respectively, for the -53(TA-repeat) polymorphism). Logistic regression analysis revealed low bilirubin levels but not the UGT1A1 polymorphisms to be significantly associated with CAD: OR (95% CI) 0.90 (0.86–0.94), p = 2.6 × 10⁻⁶ for men and 0.77 (0.68–0.87), p = 3.2 × 10⁻⁵ for women, respectively for each 0.1 mg/dl increase of bilirubin. These results indicate that it is rather decreased bilirubin levels in general than the changes in the genetic variation of this gene that increase the risk for CAD.     

The effect of angiotensin II type-1 receptor gene polymorphisms on doppler blood flow parameters of carotid and brachial arteries in patients with myocardial infarction

BACKGROUND: Genetic influence on Doppler blood flow parameters of carotid and brachial arteries (BA) is uncertain. We investigated the relationship between the angiotensin II type-1 receptor (AT1R) gene polymorphism and the blood flow characteristics of common carotid arteries (CCA) and BA by color Doppler ultrasound (CDUS) in patients with a first anterior acute myocardial infarction (AMI). METHODS AND RESULTS: Sixty-seven patients (15 women and 52 men), aged 25-77 years, with anterior AMI were studied. The AT1R genotypes were established. Based on the polymorphism of the AT1R, they were classified into three groups: AT1R AA genotype (Group1, n = 42 patients), AT1R AC genotype (Group 2, n = 17 patients), and AT1R CC genotype (Group 3, n = 8 patients). Peak-systolic velocity (PSV) and end-diastolic velocity (EDV) of right and left CCA, PSV of right BA, and intimal-medial thickness (IMT) of both CCA were measured by CDUS. All results evaluated statistically. The AT1R genotypes were distributed as follows: 63% AA, 25% AC, and 12% CC. PSV of BA and both CCA were higher in patients with CC and AC than AA (P < 0.05). Also, IMT of both CCA were also higher in the same groups (P < 0.05). CONCLUSIONS: Our results suggest that AT1R gene polymorphism influences Doppler blood flow parameters of both BA and CCA, and IMT of CCA. Although further studies are required.     

The TT genotype of the methylenetetrahydrofolate reductase C677T gene polymorphism is associated with the extent of coronary atherosclerosis in patients at high risk for coronary artery disease.

BACKGROUND: There are conflicting results on the relationship of N5,N10-methylenetetrahydrofolate reductase C677T gene variation in coronary artery disease and myocardial infarction. METHODS AND RESULTS: We analysed this gene variation in 2453 male Caucasians whose coronary anatomy was defined by coronary angiography. In the total sample, the C677T gene polymorphism was not associated with the presence or the extent of coronary artery disease (defined by the degree of vessel disease or by the coronary heart disease score according to Gensini). However, after excluding individuals with low risk profiles, an association between the C677T TT genotype and the Gensini score was found. This observation applies only to individuals (i) with high glucose levels, (ii) with low apolipoprotein Al/apolipoprotein B ratios, (iii) with low apolipoprotein Al/apolipoprotein B ratios and high lipoprotein (a) levels and (iv) with low apolipoprotein Al/apolipoprotein B ratios and high glucose concentrations. In patients with high glucose levels, the paraoxonase 191 A/B gene variation presupposed whether differences in Gensini scores between C677T C allele carriers and TT homozygotes became apparent, since only in paraoxonase 191 AA homoxygotes, but not in paraoxonase 191 B allele carriers, did C677T TT homozygotes have clearly higher Gensini scores than C allele carriers (two-way interaction; P = 0.013). The MTHFR C677T gene polymorphism was not associated with non-fatal myocardial infarction. CONCLUSION: The present study extends previous observations by the finding that carriers of the N5,N10-methylenetetrahydrofolate reductase C677T TT genotype with various coronary high risk profiles had clearly higher coronary heart disease scores than individuals with at least one C677T C allele.     

Role of angiotensin II type I (AT1 A1166C) receptor polymorphism in susceptibility of left ventricular dysfunction

Background

Left ventricular dysfunction (LVD) with subsequent congestive heart failure (CHF) constitutes the final common pathway for a host of cardiac disorders. The impaired LV function develops in response to an ischemic insult followed by a fall in cardiac output that leads to activation of renin-angiotensin-system (RAS). Angiotensin II type I receptor (AT1), which mediate the vasoconstrictive and salt-conserving actions of the RAS, represent interesting candidate genes for cardiovascular diseases. Therefore, we conducted an association study between single nucleotide polymorphism (SNP) in AT1 gene and LVD in CAD patients.

Methods and results

The present study recruited a total of 950 subjects including 720 angiography confirmed CAD patients and 230 healthy controls. Among 720 CAD patients, 229 with reduced left ventricle ejection fraction (LVEF ≤ 45%) were categorized as LVD. The AT1 (A1166C, rs5186) polymorphism was determined by ARMS-PCR. Our results showed that the frequency of AT1 1166AC and CC genotypes were significantly higher in LVD patients in comparison to non-LVD (LVEF >45%) patients (p value = 0.003; OR = 1.81 and p value <0.001; OR = 4.33). Further analysis showed that AT1 A1166C polymorphism was significantly associated with LV end diastole (p-value = 0.031), end systole (p-value = 0.038) dimensions, and mean LVEF (p-value = 0.035). Moreover, on comparing the AT1 A1166C polymorphism in CAD patients with healthy controls, we did not find any association both at genotypic and allelic level (p value = 0.927; OR = 1.04 and p value = 0.219; OR = 0.83) respectively.

Conclusions

Our study suggests that AT1 A1166C polymorphism may play significant role in conferring genetic susceptibility of LVD.     

Adiponectin receptor 1 and small ubiquitin-like modifier 4 polymorphisms are associated with risk of coronary artery disease without diabetes

Background The genes encoding adiponectin receptor 1 (ADIPOR1) and small ubiquitin-like modifier 4 (SUMO4) have been linked to anti-atherogenic effects, but little is known about whether polymorphisms in the two genes, acting separately or interacting, affect risk of coronary artery disease (CAD) without diabetes. Methods We genotyped 200 CAD patients without diabetes and 200 controls without CAD or diabetes at three single-nucleotide polymorphisms (SNPs) in ADIPOR1 and one SNP in SUMO4, which were chosen based on previous studies. Potential associations were also explored between these SNPs and clinical characteristics of CAD without diabetes. Results Risk alleles at three SNPs in ADIPOR1 (rs7539542-G, rs7514221-C and rs3737884-G) and the G allele at SNP rs237025 in SUMO4 significantly increased risk of CAD without diabetes, with ORs ranging from 1.79 to 4.44. Carriers of any of these four risk alleles showed similar adverse clinical characteristics. Compared with individuals with a CC or GC genotype, those with a GG genotype at rs3737884 were at significantly higher risk of CAD that affected the left anterior descending coronary artery (OR: 6.77, P = 0.009), the right coronary artery (OR: 4.81, P = 0.028) or a relatively large number of vessels (P = 0.04). Individuals carrying a risk allele at one or more of the three SNPs in ADIPOR1 as well as a risk allele at the SNP in SUMO4 were at significantly higher risk of CAD without diabetes than individuals not carrying any risk alleles (OR: 5.82, 95% CI: 1.23?27.7, P = 0.013). Conclusions SNPs in ADIPOR1 and SUMO4 are associated with elevated risk of CAD without diabetes, and SNPs in the two genes may interact to jointly affect disease risk.     

上海地区老年汉族人群护骨素基因T950C多态性与冠心病及其严重程度的相关性研究

目的探讨护骨素（osteoprotegerin,OPG）基因T950C位点基因多态性与冠心病（coronary artery dsease,CAD）及其严重程度的相关性。方法290例行冠状动脉造影患者根据造影结果,分为正常冠脉组102例和冠心病组188例。冠心病组根据病变冠脉病变支数,分为单支组57例、双支组50例、三支组68例、四支组13例;冠心病组再根据病史分为急性冠脉综合征（acute coronary syndrome,ACS）组133例和稳定型冠心病组55例。介质纯化法提取白细胞DNA,聚合酶链式反应（polymerase chain reaction,PCR）扩增包含护骨素T950C位点的DNA片段,连接酶检测反应（ligase detection reaction,LDR）检测PCR产物,识别多态性位点。结果在正常冠脉组和冠心病组之间,在正常冠脉组和ACS组之间,在ACS组和稳定型冠心病组之间,在正常冠脉组和不同病变冠脉数量组之间,护骨素基因T950C的各基因型频率和分布差别无统计意义;冠心病组CC基因型的Gensini评分要高于TT基因型的Gensini评分。结论研究中未发现护骨素基因T950C位点基因多态性与冠心病相关;T950C位点多态性与冠心病的严重程度有相关性,CC基因型的冠脉狭窄程度较TT基因型更严重。     

Angiotensin converting enzyme and angiotensin II type 1-receptor gene polymorphisms and risk of ischaemic heart disease.

OBJECTIVE: Polymorphisms in several genes of the renin-angiotensin system have been implicated as risk factors for myocardial infarction and ischaemic heart disease. In particular, it has been suggested that the angiotensin converting enzyme insertion/deletion (I/D) polymorphism and the angiotensin II type 1 receptor A1166C polymorphisms might act synergistically to increase the risk of myocardial infarction. The aim of this study was to investigate associations between the angiotensin converting enzyme I/D polymorphism and angiotensin II type 1 receptor polymorphisms and ischaemic heart disease. METHODS: We screened 331 white European patients who were recruited for routine angiographic investigation of chest pain, and 287 healthy white European controls for the angiotensin converting enzyme I/D and angiotensin II type 1 receptor A1166C polymorphisms, and related the genotype frequencies to angiotensin converting enzyme levels and the clinical phenotypes of atheroma and history of myocardial infarction. RESULTS: Angiotensin converting enzyme levels were related to I/D polymorphism but not to angiotensin II type 1 receptor polymorphism genotypes. I/D polymorphism and angiotensin II type 1 receptor genotypes did not relate individually to risk of myocardial infarction or atheroma in univariate or multivariate analysis. However, evidence of a synergistic relationship between the AC/II and CC/DD genotypes and coronary stenosis in the major arteries was found. No evidence of any relationship between these polymorphisms and history of myocardial infarction by World Health organisation (WHO) criteria was detected. CONCLUSION: These findings suggest that there is a weak relationship between the angiotensin converting enzyme I/D and angiotensin II type 1 receptor A1166C polymorphisms and coronary atheroma, but no evidence of a relationship with history of myocardial infarction.     

Association of dipeptidyl peptidase IV polymorphism,serum lipid profile,and coronary artery stenosis in patients with coronary artery disease and type 2 diabetes

Cardiovascular disease (CAD) is a devastating illness, but to date there are limited means of predicting a person''s coronary stenosis severity and their prognosis. The study was performed to investigate the relationship between dipeptidyl peptidase 4(DPP4) gene polymorphisms and serum lipid profiles, as well as the severity of coronary artery stenosis in patients with CAD and type 2 diabetes (T2DM) for the first time.Herein, 201 patients with CAD and T2DM were enrolled in the Department of Cardiology, Shandong Provincial Qianfoshan Hospital. DPP4 rs3788979 and rs7608798 single nucleotide polymorphisms (SNPs) were genotyped. The general information of all patients was collected, and the associations between DPP4 SNPs and lipid profiles were detected. At the same time, association between SNP polymorphisms and the degree of coronary artery stenosis were analyzed.There was a significant difference in apolipoprotein B (ApoB) levels (P = .011) for the rs3788979 polymorphism, while no difference was identified in other blood lipids or with other mutations. SNP mutation of A to G in rs3788979 was associated with a reduced percentage of severe coronary artery stenosis in female patients (P = .023) as well as those with nosmoking (P = .030), nodrinking (P = 0.007), and nocardiovascular family history (P = 0.015).G allele of rs3788979 is associated with a reduced ApoB level. Besides, we suggest that G allele in rs3788979 may have a cardioprotective effect and prove to be a useful and specific measure when predicting a patient''s coronary stenosis severity if diagnosed with CAD and T2DM.     

Angiotensin II type 1 receptor A1166C gene polymorphism: Absence of an association with the risk of coronary artery disease and myocardial infarction and of a synergistic effect with angiotensin-converting enzyme gene polymorphism on the risk of these diseases

Aim There is evidence that interaction between angiotensin II type1 receptor A1166C gene polymorphism and angio-tensin I-convertingenzyme Insertion/Deletion gene variation might have an effecton the risk of myocardial infarction. The study was carriedout in a population of 2244 male Caucasians, whose coronaryanatomy was defined by means of coronary angiography. We analysedthe relationship, on the risk of ischaemic heart disease, ofangiotensin II type 1 receptor A1166C gene variation, not onlyto myocardial infarction but also to coronary artery disease,and its potential interaction with angio-tensin I-convertingenzyme Insertion/Deletion gene polymorphism. Methods and Results No association was detected between angiotensin II type 1 receptorA1166C gene polymorphism and coronary artery disease. Similarly,there was no link to myocardial infarction, either in the totalpopulation or in low risk groups. In addition, most importantly,we found no interaction between angiotensin II type 1 receptorA1166C gene variation and angiotensin I-converting Insertion/Deletionpolymorphism, either in connection with the risk of coronaryartery disease or myocardial infarction. Conclusion This angiotensin II type 1 receptor A1166C gene variation isnot associated with any detectable increase in risk of ischaemicheart disease. The findings of the present study do not suggestthat, as regards risk of coronary artery disease and myocardialinfarction, there is interaction between gene polymorphism andangiotensin I-converting enzyme Insertion/Deletion gene variation.TheEuropean Society of Cardiology     

ICAM-1基因K469E多态性与冠心病关联的荟萃分析

目的 探讨细胞间黏附分子-1(Intercellular adhesion molecule-1,ICAM-1)基因K469E多态性与冠心病的关联性.方法 全面检索中英文数据库关于K469E多态性与冠心病遗传易感性关系的病例对照研究,采用Meta分析方法合并K469E与冠心病关联的OR值,结合95％CI作为每个研究结果...