Lipoprotein(a)variability is associated with mean follow-up Creactive protein in patients with coronary artery disease following percutaneous coronary intervention

BACKGROUND Increased lipoprotein(a)[lp(a)]has proinflammatory effects,which increase the risk of coronary artery disease.However,the association between lp(a)variability and follow-up C-reactive protein(CRP)level in patients undergoing percutaneous coronary intervention(PCI)has not been investigated.AIM To explore the association between lp(a)variability and mean CRP levels within the 1st year post-PCI.METHODS Results of lp(a)and CRP measurements from at least three follow-up visits of patients who had received PCI were retrospectively analyzed.Standard deviation(SD),coefficient of variation(CV),and variability independent of the mean(VIM)are presented for the variability for lp(a)and linear regression analysis was conducted to correlate lp(a)variability and mean follow-up CRP level.The relationship of lp(a)variability and inflammation status was analyzed by restricted cubic spline analysis.Finally,exploratory analysis was performed to test the consistency of results in different populations.RESULTS A total of 2712 patients were enrolled.Patients with higher variability of lp(a)had a higher level of mean follow-up CRP(P<0.001).lp(a)variability was positively correlated with the mean follow-up CRP(SD:β=0.023,P<0.001;CV:β=0.929,P<0.001;VIM:β=1.648,P<0.001)by multivariable linear regression analysis.Exploratory analysis showed that the positive association remained consistent in most subpopulations.CONCLUSION Lp(a)variability correlated with mean follow-up CRP level and high variability could be considered an independent risk factor for increased post-PCI CRP level.

Relationship between high sensitivity C-reactive protein and angiographic severity of coronary artery disease

Background Coronary artery disease(CAD)remains a leading cause of morbidity and mortality.Cytokines play a potential role in atherosclerosis pathogenesis and progression.We investigated the association between high sensitive C-reactive protein(hs CRP)and severity of CAD.Methods CAD patients were stratified according to hs CRP cut-off value into high levels hs CRP group(≥8.4 mg/L)and low levels hs CRP group(<8.4 mg/L).Severity of CAD was assessed according to artery stenosis degree and the number of vessel involved.Statistical analysis was performed using Statistical Package for the Social Sciences(SPSS,version 23.0).Results The mean age was 60.3±11.0 years.The level of hs CRP was increased and ranged from 0.2 to 1020.0 mg/L.Biochemical risk factors and severity of CAD didn’t show significant differences between the two groups.In multivariate linear analysis,cardiac troponin I(c Tn I)and serum amyloid A(SAA)were predictors of hs CRP.As shown in receiver operating characteristic(ROC)curve analysis performed in patients with ST-segment elevation myocardial infarction(STEMI)and compared to myonecrosis biomarkers,hs CRP(area under the curve(AUC):0.905;95%CI:0.844-0.966;P<0.001)could be a powerful predictor marker in evaluating the infarct size after myocardial infarction but not better than c Tn I.Conclusions Hs CRP levels were not associated with the severity of CAD but could be useful in the evaluation of myocardial necrosis in patients with STEMI.

Vitamin D Status, C-Reactive Protein and Risk of Coronary Artery Disease—A Hospital-Based Study

Coronary artery disease (CAD) is a leading cause of deaths of women and men worldwide. In this study we tried to assess the relationship between Vitamin D status and CAD. Vitamin D has a big role in the body and debate on its effect on the heart and coronary arteries still exits. C-reactive protein (CRP) is an inflammatory marker which may rise in CHD. Aim: To determine the relationship between Vitamin D status and CRP and CAD risk among patients at middle zone of the Gaza Strip. Methodology: A retrospective case-control, hospital-based study was conducted at Al-Aqsa Martyr’s Hospital in Dier El-Balah City from August 2014 to October 2014. Patients (n = 100) aged above 40 years with confirmed CAD history were recruited using a purposeful, non-random sampling. Vitamin D status assessed by food frequency questionnaire of dietary Vitamin D and serum Vitamin D. Serum Vitamin D was measured using Calbiotech’s 25-OH Vitamin D ELISA and serum CRP was measured by the latex agglutination. SPSS V.19 used for data analysis. Results: Mean of age among cases was (68.28 ± 8.01) higher than controls (57.82 ± 9.61) (P = 0.01);percent of males (54%) was higher than females (46.0%) among cases. Sun exposure and mean duration of daily exposure to sunlight were higher in cases (P > 0.05). Cases were consumed less servings of Vitamin D rich food than controls (P > 0.05). Percent of Vitamin D deficiency among cases (42%) was higher than controls (16.0%) (P = 0.002). Mean of serum Vitamin D in association with positive CRP was (79.95 ± 70.6) lower than those with negative CRP (106.06 ± 68.966) (P = 0.13). Percent of positive serum CRP among cases 30% was higher than controls 10% (P = 0.01). Conclusion: Vitamin D deficiency was associated with positive CRP in patients with CAD. Vitamin D may have an anti-inflammatory effect regarding to our results.

Stromelysin-1 Gene Promoter 5A/6A Polymorphism and Plasma C-Reactive Protein in Patients with Coronary Artery Disease and Myocardial Infarction

Objective: To study the associations of stromelysin-1 (MMP3) gene 5A/6A polymorphism with plasma high-sensitivity C-reactive protein (hs-CRP) level in coronary artery disease (CAD) and myocardial infarction (MI). Methods: The MMP3 5A/6A genotypes and plasma hs-CRP levels were determined in 405 non-CAD subjects and 395 angiography-documented CAD patients, 157 with MI and 238 with non-MI. Results: The percentage of the 5A/5A genotype was significantly (p < 0.001) greater in CAD than non-CAD subjects and in MI than non-MI patients. Plasma hs-CRP level of the 5A/5A genotype was significantly (p < 0.05) higher than that of the 6A/6A genotype in CAD and MI but not in non-MI patients. On logistic regression analysis, the odds ratio of the 5A/5A genotype for CAD was 2.11 (95% CI, 1.15 - 3.88, p < 0.05) and for MI was 3.05 (95% CI, 1.54 - 6.04, p < 0.005). Conclusions: This study showed a correlation of the 5A/5A genotype of MMP3 promoter with higher plasma hs-CRP level in CAD patients with MI.

ASSOCIATION OF INSULIN RESISTANCE AND C-REACTIVE PROTEIN WITH CORONARY ARTERY DISEASE IN PATIENTS WITH NORMAL GLUCOSE TOLERANCE

Objective To examine insulin resistance and high sensitivity C-reactive protein (hsCRP) association with clinical and angiographic severity of coronary artery disease (CAD) in patients with normal glucose tolerance. Methods In 638 consecutive patients with normal glucose tolerance, 221 had atypical chest pain and normal coronary artery (control group), 279 had stable angina and CAD (SAP group), and 138 suffered acute myocardial infarction (MI group). The degree of CAD was further divided into borderline lesion (lumen diameter narrowing 50%-69%), significant 1-, 2- or 3-vessel disease (luminal diameter narrowing ≥70%). Fasting serum glucose, insulin and hsCRP levels and lipid profiles were measured, and homeostasis model assessment for insulin resistance (HOMA-IR) was calculated. Multivariate analysis was performed to assess risk factors for 3-vessel disease or acute MI. Results Serum hsCRP, lipoprotein (a) levels, and insulin resistance index (IRI) were higher in AMI group than those in SAP and control groups. Serum hsCRP level and IRI were also higher in 3-vessel disease than those in other groups. Multivariate regression analysis revealed that insulin resistance, cigarette smoking, serum hsCRP, and lipoprotein (a) levels were independent risk factors for acute MI. Lipoprotein (a) elevation was an independent risk factor for 3-vessel disease. Conclusion Insulin resistance and high serum hsCRP level were associated with occurrence of acute MI and angiographic severity of coronary disease in patients with normal glucose tolerance.

Lack of association between cellular repressor of E1A-stimulated genes(GREG)polymorphisms and coronary artery disease in the Han population of North China

Objectives Phenotypic switching of smooth muscle cells(SMCs) plays a critical role in the pathogenesis of atherosclerotic lesions such as coronary artery disease (CAD).Accumulating evidence demonstrates(hat a cellular repressor of E1A-stimulated genes(CREG) plays a role in the maintenance of the mature phenotype of vascular SMCs. The purpose of the present study was to assess the possible association between CREG and CAD in the Han population of North China.Methods The promoter region of CREG by direct sequencing was conducted in 48 subjects.Then SNP rs2995073 and another 4 tagSNPs(rs4657669,rs3767443, rsl6859185,rs3753921) were selected for the association study.All five selected SNPs were determined in 1161 patients with angiographically proven CAD and 960 controls with normal coronary angiograms to investigate the possible involvement of CREG in CAD.Results Genotype frequencies of the five examined polymorphisms were similarly distributed between CAD group and controls(P】0.05).Further haplotype analysis also found no significant differences in the distributions between CAD group and controls(P】0.05). Conclusions This study did not show an association between common variants of CREG and CAD in the northern Chinese Han population.

Genetics of coronary artery disease and myocardial infarction

Atherosclerotic coronary artery disease(CAD) comprises a broad spectrum of clinical entities that include asymptomatic subclinical atherosclerosis and its clinical complications, such as angina pectoris, myocardial infarction(MI) and sudden cardiac death. CAD continues to be the leading cause of death in industrialized society. The long-recognized familial clustering of CAD suggests that genetics plays a central role in its development, with the heritability of CAD and MI estimated at approximately 50% to 60%. Understanding the genetic architecture of CAD and MI has proven to be difficult and costly due to the heterogeneity of clinical CAD and the underlying multi-decade complex pathophysiological processes that involve both genetic and environmental interactions. This review describes the clinical heterogeneity of CAD and MI to clarify the disease spectrum in genetic studies, provides a brief overview of the historical understanding and estimation of the heritability of CAD and MI, recounts major gene discoveries of potential causal mutations in familial CAD and MI, summarizes CAD and MIassociated genetic variants identified using candidate gene approaches and genome-wide association studies(GWAS), and summarizes the current status of the construction and validations of genetic risk scores for lifetime risk prediction and guidance for preventive strategies. Potential protective genetic factors against the development of CAD and MI are also discussed. Finally, GWAS have identified multiple genetic factors associated with an increased risk of in-stent restenosis following stent placement for obstructive CAD. This review will also address genetic factors associated with in-stent restenosis, which may ultimately guide clinical decision-making regarding revascularization strategies for patients with CAD and MI.

Bidirectional relationship between type 2 diabetes mellitus and coronary artery disease:Prospective cohort study and genetic analyses

Background:While type 2 diabetes mellitus(T2DM)is considered a putative causal risk factor for coronary artery disease(CAD),the intrinsic link underlying T2DM and CAD is not fully understood.We aimed to highlight the importance of integrated care targeting both diseases by investigating the phenotypic and genetic relationships between T2DM and CAD.Methods:We evaluated phenotypic associations using data from the United Kingdom Biobank(N=472,050).We investigated genetic relationships by leveraging genomic data conducted in European ancestry for T2DM,with and without adjustment for body mass index(BMI)(T2DM:N_(case)/N_(control)=74,124/824,006;T2DM adjusted for BMI[T2DM_(adj)BMI]:N_(case)/N_(control)=50,409/523,897)and for CAD(N_(case)/N_(control)=181,522/984,168).We performed additional analyses using genomic data conducted in multiancestry individuals for T2DM(N_(case)/N_(control)=180,834/1,159,055).Results:Observational analysis suggested a bidirectional relationship between T2DM and CAD(T2DM→CAD:hazard ratio[HR]=2.12,95%confidence interval[CI]:2.01–2.24;CAD→T2DM:HR=1.72,95%CI:1.63–1.81).A positive overall genetic correlation between T2DM and CAD was observed(r_(g)=0.39,P=1.43×10^(-75)),which was largely independent of BMI(T2DM_(adj)BMI–CAD:r_(g)=0.31,P=1.20×10^(–36)).This was corroborated by six local signals,among which 9p21.3 showed the strongest genetic correlation.Cross-trait meta-analysis replicated 101 previously reported loci and discovered six novel pleiotropic loci.Mendelian randomization analysis supported a bidirectional causal relationship(T2DM→CAD:odds ratio[OR]=1.13,95%CI:1.11-1.16;CAD→T2DM:OR=1.12,95%CI:1.07-1.18),which was confirmed in multiancestry individuals(T2DM→CAD:OR=1.13,95%CI:1.10-1.16;CAD→T2DM:OR=1.08,95%CI:1.04-1.13).This bidirectional relationship was significantly mediated by systolic blood pressure and intake of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors,with mediation proportions of 54.1%(95%CI:24.9-83.4%)and 90.4%(95%CI:29.3-151.5%),respectively.Conclusion:Our observational and genetic analyses demonstrated an intrinsic bidirectional relationship between T2DM and CAD and clarified the biological mechanisms underlying this relationship.

Elevated plasma lipoprotein-associated phospholipase A2 activity is associated with plaque rupture in patients with coronary artery disease

Background Lipoprotein-associated phospholipase A2 （Lp-PLA2） has recently been shown to be positively related to coronary events in patients with coronary artery disease （CAD）. However, direct evidence about the relationship between circulation Lp-PLA2 activity and vulnerable plaque in patients with CAD remains lacking. Methods Plasma Lp-PLA2 activity was determined in 146 consecutive patients with CAD who underwent clinically-indicated coronary angiography and preinterventional intravascular ultrasound （IVUS）. Results Eighty-three patients were included in the final analysis after the initial screening. Sixty （72.3%） were acute coronary syndrome （ACS） patients and 23 （27.7%） were stable angina pectoris （SAP） patients. Plaque rupture occurred in 39 （47.0%） patients, and 34 （87.2%） were from ACS patients and 5 （12.8%） from SAP patients. There were no significant differences in clinical and angiographic characteristics between patients with plaque rupture and those without plaque rupture, except for smoking, high-sensitive C-reactive protein （hs-CRP） level and Lp-PLA2 activity （all P 〈0.05）. IVUS measurement uncovered that patients with plaque rupture had more frequent positive remodeling （74.4% vs. 43.2%, P=0.004）, soft plaques （64.1% vs. 36.4%, P=-0.012） and higher remodeling index （1.13~0.16 vs. 0.99＋_0.11, P=0.041） as compared with those without plaque rupture. Multivariate Logistic regression analysis showed that plasma Lp-PLA2 activity was independently associated with plaque rupture after adjusting for smoking, positive remodeling and soft plaque （Model 1： odds ratio （OR） 1.13, 95% confidence interval （CO ： 1.06-1.20） or adjusting for smoking, hs-CRP level, positive remodeling and soft plaque （Model 2： OR 1.11,95%C1： 1.04-1.19）. Conclusions Plasma Lp-PLA2 activity is associated with plaque rupture in patients with CAD, independently of traditional CAD risk factors, hs-CRP level and IVUS parameters. Lp-PLA2 may be a risk marker for vulnerable plaques.

Combination of high-sensitivity C-reactive protein and homocysteine may predict an increased risk of coronary artery disease in Korean population

Background The association of emerging biomarkers such as high-sensitivity C-reactive protein （hs-CRP）,homocysteine and fibrinogen with the risk of coronary artery disease （CAD） is still uncertain in Asian population including Koreans and little is known about the combined effect of biomarkers on the risk of CAD.Methods A total of 10 650 subjects （6538 men and 4112 women） were enrolled in this study.A 10-year CAD risk was calculated using Framingham risk score modified by the National Cholesterol Education Program （NCEP） Adult Treatment Panel Ⅲ （ATP Ⅲ ） and levels of circulating hs-CRP,homocysteine and fibrinogen were measured using validated assays.Results The 10-year CAD risk gradually augmented with increase in the circulating levels of hs-CRP,homocysteine and fibrinogen.For the highest quartile of hs-CRP,odds ratio （OR） of high-risk for CAD （10-year risk ≥20%） compared with the lowest quartile was 3.97 （95% C/：2.51-6.29）.For homocysteine and fibrinogen,ORs in the highest quartile compared to the lowest quartile were 5.10 （95% Cl：3.05-8.53,P 〈0.001） and 1.46 （95% Cl：0.69-3.11,P=0.325）,respectively.OR of high-risk for CAD in both the highest quartile of hs-CRP and homocysteine was 9.05 （95% CI：5.30-15.45） compared with the below median of hs-CRP and homocysteine.Conclusions The present study demonstrated that hs-CRP and homocysteine are well associated with the 10-year CAD risk estimated using NCEP ATP Ⅲ in Koreans and combination of hs-CRP and homocysteine can have strong synergyin predicting the development of CAD.

High sensitive C-reactive protein, adiponectin, and urine albumin excretion rate in Chinese coronary artery disease patients with different glucose tolerance status

Background Serum high sensitive C-reactive protein （hs-CRP）, adiponectin levels and urine albumin excretion rate （UAER） are probably associated with inflammation and atherosclerosis. The aim of this study was to determine the three markers in coronary artery disease （CAD） subjects with different glucose tolerance status in a Chinese population and further explore the levels of the three markers in these subjects and the possible association of these markers with CAD risk factors and the severity of CAD as well. Methods A total of 242 subjects with angiographically documented CAD were recruited, and then assigned to three groups： the normal glucose tolerance （NGT） ＋ CAD group, including 100 CAD patients with NGT; the impaired glucose tolerance （IGT） ＋ CAD group, 40 CAD patients with IGT; the type 2 diabetes mellitus （T2DM） ＋ CAD group, 102 CAD patients with T2DM. Serum hs-CRP, adiponectin levels as well as UAER were measured in all subjects. Results Serum hs-CRP levels were increased in the T2DM ＋ CAD group compared with the NGT ＋ CAD group （4.71±2.59） vs （3.60±2.46） mg/L, P=0.037. Serum adiponectin levels were gradually decreased from the NGT ＋ CAD to IGT ＋ CAD to T2DM ＋ CAD groups, （5.99±1.84）, （5.82±1.72） and （4.65±1.71） mg/L, P=0.002 and 0.040 for NGT ＋ CAD and IGT ＋ CAD groups vs T2DM ＋ CAD group, respectively. While the UAER was gradually increased from the NGT ＋ CAD to IGT ＋ CAD to T2DM ＋ CAD groups, （6.42±2.51）, （6.89±2.94） and （15.03±4.22） μg/min （P 〈0.001） for NGT ＋ CAD and IGT ＋ CAD groups vs T2DM ＋ CAD group. Multiple linear stepwise regression analysis showed that waist-hip ratio （WHR） and low density lipoprotein cholesterol （LDL-C） were the significant determinants of serum hs-CRP levels; triglyceride （TG）, high density lipoprotein cholesterol （HDL-C）, age, WHR, T2DM, 2-hour serum insulin （2hINS）, sex, and apolipoprotein B were the significant determinants of serum adiponectin levels; and systolic blood pressure （SBP）, T2DM and hemoglobin A1c （HbA1c） were the significant determinants of UAER in all subjects （R^2= 0.070, 0.352, and 0.214, respectively）. However, no significant correlation was seen for hs-CRP, adiponectin and UAER with the severity of CAD. Hs-CRP levels were significantly correlated with UAER. Conclusions There was a trend of increased serum hs-CRP levels from the NGT ＋ CAD to IGT ＋ CAD to T2DM ＋ CAD groups, though it only showed significance in the T2DM ＋ CAD group compared with the NGT ＋ CAD group. Serum adiponectin levels were decreased and UAER was increased from the NGT ＋ CAD to IGT ＋ CAD to T2DM ＋ CAD groups Increased UAER and serum hs-CRP, and decreased adiponectin levels were associated with traditional CAD risk factors but failed to be correlated with the severity of CAD. Hs-CRP levels were significantly correlated with UAER.

Plasma levels of receptor interacting protein kinase-3 correlated with coronary artery disease

Background: Necroptosis plays an important role in human atherosclerosis and atheroma development. Since receptor interacting protein kinase-3 (RIP3) acts as a key mediator of necroptosis, this study aimed to explore its relationship between plasma RIP3 levels and coronary artery disease (CAD) and discover a potential new biomarker for screening CAD subtypes and severity. Methods: A total of 318 patients with CAD who had coronary angiography and 166 controls in Peking Union Medical College Hospital from September 2017 to January 2018 were enrolled in this study. Patients with CAD were divided into three subgroups: patients with stable coronary artery disease (SCAD), patients with unstable angina (UA), and patients with myocardial infarction (MI). The severity of atherosclerosis was determined by Gensini score (GSS). Logistic regression was used to determine the relationship between plasma RIP3 levels and CAD. The correlation between plasma RIP3 and GSS was calculated using multiple linear regression models. Results: Overall, plasma RIP3 levels were significantly higher than serum RIP3 levels. Plasma RIP3 levels in patients with CAD were significantly higher than those in controls. Plasma RIP3 levels were strongly associated with CAD (odds ratio: 6.00, 95% confidence interval 3.04–11.81;P < 0.001). Plasma RIP3 levels increased linearly from controls to patients with SCAD, then patients with UA, and finally to patients with MI. We found a significantly positive correlation between proportion of cases of acute coronary syndrome in subjects and their plasma RIP3 level quartile. Plasma RIP3 levels were also associated with GSS (B 0.027;standard error 0.012;P < 0.05). Conclusions: Plasma RIP3 levels were independently associated with CAD. Plasma RIP3 levels could potentially supplement clinical assessment to screen CAD and determine CAD severity.

Association between TaqIB polymorphism of cholesteryl ester transfer protein and coronary artery disease in the Chinese population

Objective: To assess whether the TaqIB polymorphism of cholesteryl ester transfer protein (CETP) is associated with coronary artery disease (CAD) in Chinese population, we performed a meta-analysis in this paper. Methods: We searched PubMed, Embase, the Science Citation Index (SCI), the China Biological Medicine database (CBM), the China National Knowledge Infrastructure (CNKI), and the Wanfang database for relevant articles. Data were extracted, and pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. Results: The lit- erature search yielded 448 studies, in which 10 case-control studies including 1 694 cases and 1 456 controls matched the selection criteria. The combined B1 and B2 allele frequencies were 0.587 and 0.413, respectively. The pooled OR was 1.10 (95% CI, 0.89-1.34) for comparing the B1B1 or B1B2 carriers with B2B2 carriers, and was 1.27 (95% CI, 1.09-1.49) in the B1B1 carriers versus B2B2 or B1B2 carriers. Conclusions: In the present study, the TaqIB poly- morphism of CETP was found to be associated with CAD in the Chinese population.

Pathogenesis of premature coronary artery disease:Focus on risk factors and genetic variants

The development of premature coronary artery disease(PCAD)is dependent on both genetic predisposition and traditional risk factors.Strategies for unraveling the genetic basis of PCAD have evolved with the advent of modern technologies.Genome-wide association studies(GWASs)have identified a considerable number of common genetic variants that are associated with PCAD.Most of these genetic variants are attributable to lipid and blood pressure-related single-nucleotide polymorphisms(SNPs).The genetic variants that predispose individuals to developing PCAD may depend on race and ethnicity.Some characteristic genetic variants have been identified in Chinese populations.Although translating this genetic knowledge into clinical applications is still challenging,these genetic variants can be used for CAD phenotype identification,genetic prediction and therapy.In this article we will provide a comprehensive review of genetic variants detected by GWASs that are predicted to contribute to the development of PCAD.We will highlight recent findings regarding CAD-related genetic variants in Chinese populations and discuss the potential clinical utility of genetic variants for preventing and managing PCAD.

Discovering hidden patterns:Association rules for cardiovascular diseases in type 2 diabetes mellitus

BACKGROUND It is increasingly common to find patients affected by a combination of type 2 diabetes mellitus(T2DM)and coronary artery disease(CAD),and studies are able to correlate their relationships with available biological and clinical evidence.The aim of the current study was to apply association rule mining(ARM)to discover whether there are consistent patterns of clinical features relevant to these diseases.ARM leverages clinical and laboratory data to the meaningful patterns for diabetic CAD by harnessing the power help of data-driven algorithms to optimise the decision-making in patient care.AIM To reinforce the evidence of the T2DM-CAD interplay and demonstrate the ability of ARM to provide new insights into multivariate pattern discovery.METHODS This cross-sectional study was conducted at the Department of Biochemistry in a specialized tertiary care centre in Delhi,involving a total of 300 consented subjects categorized into three groups:CAD with diabetes,CAD without diabetes,and healthy controls,with 100 subjects in each group.The participants were enrolled from the Cardiology IPD&OPD for the sample collection.The study employed ARM technique to extract the meaningful patterns and relationships from the clinical data with its original value.RESULTS The clinical dataset comprised 35 attributes from enrolled subjects.The analysis produced rules with a maximum branching factor of 4 and a rule length of 5,necessitating a 1%probability increase for enhancement.Prominent patterns emerged,highlighting strong links between health indicators and diabetes likelihood,particularly elevated HbA1C and random blood sugar levels.The ARM technique identified individuals with a random blood sugar level>175 and HbA1C>6.6 are likely in the“CAD-with-diabetes”group,offering valuable insights into health indicators and influencing factors on disease outcomes.CONCLUSION The application of this method holds promise for healthcare practitioners to offer valuable insights for enhancing patient treatment targeting specific subtypes of CAD with diabetes.Implying artificial intelligence techniques with medical data,we have shown the potential for personalized healthcare and the development of user-friendly applications aimed at improving cardiovascular health outcomes for this high-risk population to optimise the decision-making in patient care.

Association of common polymorphisms in the LRP6 gene with sporadic coronary artery disease in a Chinese population

Background Genetic factors contribute to the development of coronary artery disease （CAD）.Recently,a missense mutation in the low density lipoprotein receptor related protein 6 （LRP6） gene,encoding low density lipoprotein receptor related protein 6,has been implicated in an autosomal dominant form of early-onset CAD.The aim of this study was to determine whether the common variants in LRP6 are associated with sporadic CAD in Chinese.Methods A total of 766 CAD patients and 806 healthy controls were included in this study.The presence of angiographic CAD was determined by coronary angiographic analysis.Six signal nucleotide polymorphisms （SNPs） were genotyped using the polymerase chain reaction-restriction fragment length polymorphism （PCR-RFLP） technique.Results A significant association was detected between rs11054731 in LRP6 intron 2 and CAD in our cohort （P=0.001）.The CC genotype and C allele frequency in the case group were 52% and 72%.Using a dominant model of inheritance,the C allele of rs11054731 was shown to be an independent risk factor for CAD with an OR of 1.45 （95% CI：1.19-1.77,P=0.0002）.With the stratification according to the number of affected coronary arteries,an association was observed between rs11054731 and CAD （P=0.0002）.No significant association was observed between any other SNPs and the risk of CAD.Conclusion The C allele of the rs11054731 within the LRP6 gene was associated with increased risk and extent of CAD in Chinese.

Altered serum level of cartilage oligomeric matrix protein and its association with coronary calcification in patients with coronary heart disease

BackgroundCartilage oligomeric 矩阵蛋白质(COMP ) 主要在骨胳的系统和脉管的光滑的肌肉房间被发现。最近的研究证明它在血容器上有保护的功能并且能也禁止脉管的石灰化。我们在冠的心疾病( CHD )调查了浆液 COMP 病人，并且在浆液 COMP 和首先经历了多片跟随的冠的 angiography 的 233 个连续的胸疼痛病人全部的冠的 artery.MethodsA 的石灰化之间的关系在六个月以内计算了断层摄影术( MSCT )被招募并且根据缩小百分比的冠的 angiography 钠直径划分了成二个组：CHD 组(缩小 50% 的直径， n = 194 ) 并且控制组(直径变窄 <50% ， n = 39 ) 。Gensini 分数，句法分数和冠的动脉钙分数(CAC ) 是计算的。浆液 COMP 水平用 COMP 的 ELISA.ResultsThe 层次被决定比在控制组在 CHD 组是显著地更高的 155.7 (124.5-194.5 ) ng/mL 对 128.4 (113.0-159.9 ) ng/mL， P = 0.019。在 COMP， Gensini 分数，句法分数，冠的狭窄的严厉和有狭窄的冠的动脉的数字之间没有关联 >50% 。浆液 COMP 与年龄被相关(r = 0.294， P < 0.001 ) ， fasting 葡萄糖(r = 0.163， P = 0.015 ) ， HbA1c (r = 0.194， P = 0.015 ) 并且 CAC (r = 0.137， P = 0.037 ) 。逐步的线性回归分析显示出那 COMP 水平，年龄是在 CHD 病人的 CAC 的独立预言者(= 0.402， t = 2.612， P = 0.015；= 0.472， t = 3.077， P = 0.005 ) 。为预言 CHD 的 COMP 的性能在曲线(AUC ) 下面作为区域被显示出：0.632， 95% CI：0.549-0.715 和上面的 tertile CAC 是 AUC：0.602， 95% CI：在操作冠的动脉的特征(巨鸟) 曲线 analysis.ConclusionCalcification 的接收装置的 0.526-0.678 是浆液 COMP 的一个独立预言者。

C-reactive protein as a predictor for cardiac events in Chinese elderly patients with coronary heart disease

Background and objective To assess the predictive value of C-reactive protein(CRP) for major adverse cardiac events and the association between CRP level and the coronary lesion morphology and extent in patients with coronary heart disease (CHD).Methods CRP was measured on admission in 177 consecutive elderly (age≥60 years) patients with CHD who underwent coronary angiography. Patients were divided into high CRP group (CRP≥3mg/L) and normal CRP group (CRP ＜3mg/L). The association between CRP levels and the coronary lesion features, including severity of stenosis (mild, moderate, severe), extent of lesion (diffused or nondiffused), eccentricity of the plaque (eccentric or non-eccentric) were analyzed. Patients were followed up for a mean of 8 months for the occurrences of major adverse cardiac events (MACE). Results Compared with patients in normal CRP group, patients in high CRP group were more frequently to have unstable angina, multi-vessel, diffuse, eccentric lesions, positive remodeling, and non-smooth plaques (P＜0.01). Kaplan-Meier analysis showed patients in high CRP group had a significantly lower MACE-free survival rate than patients in normal CRP group (Log-rank = 12.0, P＜0.01); Cox regression analysis indicated CRP level as an independent predictor for the occurrence of MACE (OR=3.16, P＜0.05) Conclusions High CRP level is associated with more extend, severe and eccentric coronary lesions and is an independent predictor for MACE in elderly patients with CHD.

Association of GCKR Gene Polymorphisms with the Risk of Nonalcoholic Fatty Liver Disease and Coronary Artery Disease in a Chinese Northern Han Population

Background and Aims: Accumulated studies have eval-uated the effects of glucokinase regulatory protein(GCKR)gene polymorphisms on the risk of nonalcoholic fatty liver disease(NAFLD)and coronary artery disease(CAD),but the association of GCKR polymorphisms with the risk of NAFLD and CAD in the Chinese Han population have remained un-clear.The aim of this study was to investigate the association between GCKR gene polymorphisms(rs780094 and rs1260326)and the risk of NAFLD and CAD in NAFLD patients in a Chinese Northern Han population.Methods: GCKR rs780094 and rs1260326 gene polymorphisms were geno-typed by polymerase chain reaction sequencing for B-type ultrasonography-proven NAFLD patients with(n = 82)or without(n = 142)CAD,and in healthy controls(n = 152).Serum lipid profiles'levels were determined using biochemi-cal methods.Statistical analyses were conducted using SPSS 22.0 statistical software.Results: As the results showed,sig-nificant differences in the serum lipid profiles existed between each group.No significant differences were observed in the distributions of genotypes and alleles of GCKR rs780094 and rs1260326 in each group.The GCKR rs780094 T and rs1260326 T allele carriers possessed decreased body mass index value,and serum fasting plasma glucose and TG levels in the overall subjects,respectively.In addition,the GCKR rs780094 T allele carriers possessed decreased serum fasting plasma glucose level in the controls and NAFLD+CAD patients.Conclusions: GCKR rs780094 and rs1260326 poly-morphisms were found to be not associated with the risk of NAFLD nor of CAD in NAFLD patients in this Chinese Northern Han population.GCKR rs780094 T and rs1260326 T alleles could affect the body mass index value and serum fasting plasma glucose and triglyceride levels.

Oxidized phospholipids and lipoprotein-associated phospholipase A_2 as important determinants of Lp(a) functionality and pathophysiological role

Lipoprotein（a） [Lp（a）] is composed of a low density lipoprotein（LDL）-like particle to which apolipoprotein（a）[apo（a）] is linked by a single disulfide bridge. Lp（a） is considered a causal risk factor for ischemic cardiovascular disease（CVD） and calcific aortic valve stenosis（CAVS）. The evidence for a causal role of Lp（a） in CVD and CAVS is based on data from large epidemiological databases, mendelian randomization studies, and genome-wide association studies. Despite the well-established role of Lp（a） as a causal risk factor for CVD and CAVS, the underlying mechanisms are not well understood. A key role in the Lp（a） functionality may be played by its oxidized phospholipids（OxPL） content. Importantly, most of circulating OxPL are associated with Lp（a）; however, the underlying mechanisms leading to this preferential sequestration of OxPL on Lp（a） over the other lipoproteins,are mostly unknown. Several studies support the hypothesis that the risk of Lp（a） is primarily driven by its OxPL content.An important role in Lp（a） functionality may be played by the lipoprotein-associated phospholipase A_2（Lp-PLA_2）,an enzyme that catalyzes the degradation of OxPL and is bound to plasma lipoproteins including Lp（a）. The present review article discusses new data on the pathophysiological role of Lp（a） and particularly focuses on the functional role of OxPL and Lp-PLA_2 associated with Lp（a）.