ObjectiveTo explore the association between hypertriglyceridemic waist (HTGW) and subclinical atherosclerosis among general Chinese population. MethodsPeople who took routine physical exam in the Sichuan Provincial People's Hospital were randomly selected from June 2011 to June 2012. We included those who received carotid artery ultrasonography and denied having symptoms of arterial ischemia, and screened the risk factors of cardiovascular disease (CVD) among them, including waist circumstance (WC) and triglycerides (TG). According to levels of WC and TG, the subjects were divided into three groups:Group I (those with normal levels of WC and TG); Group II (those with elevated levels of WC or TG); and Group Ⅲ (those with elevated WC and TG). ResultsA total of 484 subjects were included with average age of 47.3±11.3 years, of which, 72.1% of the subjects were male. The risk factors of CVD in Group I, Group II and Group III orderly increased, with significant differences. Then the subjects were stratified by age. For the elderly (no less than 60 years, n=75), the morbidities of subclinical atherosclerosis was 73.7% in Group I, 79.3% in Group II, and 70.4% in Group Ⅲ, respectively; and the results of univariate analysis and multivariate analysis showed that, HTGW was poorly associated with subclinical atherosclerosis in the elderly. For the young and middle-aged (less than 60 years, n=409), the morbidities were 19.8% in Group I, 35.1% in Group II, and 36.1% in Group III, respectively; after adjusting the confounding factors, Group II and Group III showed close association with subclinical atherosclerosis in the young and middle-aged when taking Group I as referent, with ORs (Group Ⅱ:1.987, 95%CI 1.073 to 3.679, P=0.029; and Group Ⅲ:2.060, 95%CI 1.020 to 4.161, P=0.044). ConclusionHTGW population has high-level risk factors of CVD which also present a tendency of aggregation. HTGW is closely associated with subclinical atherosclerosis in the young and middle-aged; while in the elderly, HTGW is poorly associated with subclinical atherosclerosis, but the morbidity of subclinical atherosclerosis is higher.
Objective To explore the risk factors of carotid artery atherosclerotic plaque in ischemic stroke patients. Methods One hundred and forty-eight patients with ischemic stoke were allocated into two groups by ultrasonographic testing (80 with plaque and 68 without plaque). The carotid artery acoustic densitometry (IMT), blood pressure, blood glucose , blood lipid, fibriongen (FIB), c-reactive protein (CRP) were tested. First, single variable analysis was conducted and then multivariate non-condition stepwise logistic model analysis was conducted. Results Carotid IMT, age , total cholesterol (TC), low density lipoprotein (LDL)-CH, FIB, CRP level and the incidence of hypertension and diabetes were significantly higher in ischemic stroke patients with carotid artery plaques than patients without plaques (P≤0.05); Multiple logistic regression analysis showed the most important risk factors of plaques were CRP (OR=3.546, P=0.035) and FIB (OR=1.074, P=0.012) level. Conclusion The main risk factors of carotid atherosclerosis plaque are almost the same as atherosclerosis, such as age , hypertension ,diabetes, hyperlipidemia , high FIB and CRP level and increase in carotid IMT. CRP and FIB may play a crucial role in the development of carotid artery atherosclerosis plaque.
ObjectiveTo explore the association of elongase of very long chain fatty acids family member 6 (ELOVL6) gene with increased risk of large-artery atherosclerosis stroke (LAA) in Han Chinese population in Chengdu.MethodsHan Chinese populations in Chengdu, Sichuan were chosen for this study using the case-control design between January 2015 and December 2017. The genotypes and haplotypes of six single nucleotides polymorphisms (SNPs) of ELOVL6 gene (rs3813825, rs17041272, rs4141123, rs9997926, rs6824447, and rs12504538) were analyzed in different genetic models in entire samples, and gene-enviromental interaction analyses were also carried out to get an insight of the risk factors for LAA. At the same time, we also analyzed the gene expression profile in peripheral blood mononuclear cells between groups.ResultsA total of 240 LAA cases and 211 healthy controls were enrolled in this study. All the enrolled subjects presented CC genotype of rs9997926, while the other five SNPs (rs3813825, rs17041272, rs4141123, rs6824447, and rs12504538) were genotyped successfully in all the enrolled subjects. rs17041272 polymorphism and TGTTG haplotype were significantly associated with LAA risk in studied population [CC/(CG+GG): odds ratio (OR)=0.640, 95% confidence interval (CI) (0.423, 0.968), P=0.034; TGTTG: OR=1.776, 95%CI (1.069, 2.951), P=0.024], and the interaction among rs17041272, rs6824447 SNPs and dyslipidemia increased susceptibility to LAA [OR=2.737, 95%CI (1.715, 4.368), P<0.001]. The ELOVL6 gene expression level was higher in LAA subjects (t=?3.167, P=0.003).ConclusionsELOVL6 gene is associated with LAA risk in Han nationality of Chinese population in Chengdu, and the interaction of gene-environmental risk factors could be of great importance in pathophysiology of LAA.
ObjectiveTo explore the risk factors affecting occurrence of arteriosclerosis obliterans (ASO) for patients with type 2 diabetes mellitus (T2DM) and to develop a nomogram predictive model using these risk factors. MethodsA case-control study was conducted. The patients with T2DM accompanied with ASO and those with T2DM alone, admitted to the First Affiliated Hospital of Xinjiang Medical University from January 2017 to December 2022, were retrospectively collected according to the inclusion and exclusion criteria. The basic characteristics, blood, thyroid hormones, and other relevant indicators of the paitents in two groups were compared. The multivariate logistic regression analysis was used to identify the risk factors for the occurrence of ASO in the patients with T2DM, and then a nomogram predictive model was developed. ResultsThere were 119 patients with T2DM alone and 114 patients with T2DM accompanied with lower extremity ASO in this study. The significant differences were observed between the two groups in terms of smoking history, white blood cell count, neutrophil count, lymphocyte count, platelet count, systemic immune-inflammation index, systemic inflammatory response index (SIRI), high-density lipoprotein cholesterol, apolipoprotein A1 (ApoA1), apolipoprotein α (Apoα), serum cystatin C, free-triiodothyronine (FT3), total triiodothyronine, FT3/total triiodothyronine ratio, fibrinogen (Fib), fibrinogen degradation products, and plasma D-dimer (P<0.05). Further the results of the multivariate logistic regression analysis revealed that the history of smoking, increased Fib level and SIRI value increased the probabilities of ASO occurrence in the patients with T2DM [OR (95%CI)=2.921 (1.023, 4.227), P=0.003; OR (95%CI)=2.641 (1.810, 4.327), P<0.001; OR (95%CI)=1.020 (1.004, 1.044), P=0.018], whereas higher levels of ApoA1 and FT3 were associated with reduced probabilities of ASO occurrence in the patients with T2DM [OR (95%CI)=0.231 (0.054, 0.782), P=0.021; OR (95%CI)=0.503 (0.352, 0.809), P=0.002]. The nomogram predictive model based on these factors demonstrated a good discrimination for predicting the ASO occurrence in the T2DM patients [area under the receiver operating characteristic curve (95%CI)=0.788 (0.730, 0.846)]. The predicted curve closely matched the ideal curve (Hosmer-Lemeshow goodness-of-fit test, χ2=5.952, P=0.653). The clinical decision analysis curve showed that the clinical net benefit of intervention based on the nomogram model was higher within a threshold probability range of 0.18 to 0.80 compared to no intervention or universal intervention. ConclusionsThe analysis results indicate that T2DM patients with a smoking history, elevated Fib level and SIRI value, as well as decreased ApoA1 and FT3 levels should be closely monitored for ASO risk. The nomogram predictive model based on these features has a good discriminatory power for ASO occurrence in T2DM patients, though its value warrants further investigation.
Objective To investigated the influence of the CYP2C9 polymorphism on lipid profile and blood concentration in epileptic children with VPA. Methods This study collected the information of healthy children and epilepsy children who were treated with VPA in the First Affiliated Hospital of Putian University during June, 2018 to March, 2021. The serum lipids of 184 cases were collected and compared between epilepsy group before and after treatment with VPA with the control group. The polymorphism of CYP2C9 gene in children with epilepsy was detected, and lipid and VPA concentration were compared after classification. Results There was no significant difference in lipid between the control group and the epilepsy group before treatment (P>0.05); The TC, HDL, LDL, TC/HDL, LDL/HDL were statistically different in VPA treatment group from the control group (P<0.05), and there were statistical differences in TG, LDL, TC/HDL, LDL/HDL between the trial group before the initiation and VPA treatment (P<0.05); There is no correlation between VPA blood concentration and lipid (P>0.05). VPA concentration, TC, HDL, LDL, TC/HDL and LDL/HDL in CYP2C9 wild-type were statistically different from heterozygous mutant. Conculsions CYP2C9 polymorphism and long-term use of VPA caused the changes in serum lipid levels in epilepsy children.
Atherosclerosis is a complex and multi-factorial pathophysiological process. Researches over the past decades have shown that the development of atherosclerotic vulnerable plaque is closely related to its components, morphology, and stress status. Biomechanical models have been developed by combining with medical imaging, biological experiments, and mechanical analysis, to study and analyze the biomechanical factors related to plaque vulnerability. Numerical simulation could quantify the dynamic changes of the microenvironment within the plaque, providing a method to represent the distribution of cellular and acellular components within the plaque microenvironment and to explore the interaction of lipid deposition, inflammation, angiogenesis, and other processes. Studying the pathological mechanism of plaque development would improve our understanding of cardiovascular disease and assist non-invasive inspection and early diagnosis of vulnerable plaques. The biomechanical models and numerical methods may serve as a theoretical support for designing and optimizing treatment strategies for vulnerable atherosclerosis.
Cardiovascular disease is a severe threat to human health and life. Among many risk factors of cardiovascular disease, genetic or gene-based ones are drawing more and more attention in recent years. Accumulated evidence has demonstrated that the loss or mutation of ataxia telangiectasia mutated (ATM) gene can result in DNA damage repair dysfunctions, telomere shortening, decreased antioxidant capacity, insulin resistance, increased lipid levels, etc., and thus can promote the occurrence of cardiovascular risk factors, such as aging, atherosclerosis and metabolic syndrome. In this review, we discusses the possible mechanisms between ATM gene and cardiovascular risk factors, which could be helpful to the related research and clinical application.
ObjectiveTo explore the differential expression of Sirtuin1 (SIRT1) in type A aortic dissection at diverse ages.MethodsThe expression of SIRT1 and monocyte chemoattractant protein-1 (MCP-1) in aortic tissue of the patients with type A aortic dissection (an aortic dissection group) and coronary heart disease (a control group) from 2019 to 2020 in the First Hospital of China Medical University was analyzed. In each group, the patients were divided into 3 subgroups according to the age (a younger subgroup, <45 years; a middle age subgroup, 45-60 years; an elderly subgroup, >60 years). The quantitative real-time PCR, Western blotting and immunochemical stainning were used to detect the mRNA or protein expression of SIRT1 and MCP-1. ResultsA total of 60 patients were included in each group, including 79 males and 41 females. There were 20 patients in the yonger, middle age and elderly subgroups for the two groups, respectively. Compared with the control group, the expression of SIRT1 mRNA decreased in the aortic dissection group (the younger subgroup: 4.54±1.52 vs. 8.78±2.57; the middle age group: 2.70±1.50 vs. 5.74±1.07; the elderly group: 1.41±1.33 vs. 3.09±1.14, P<0.001). Meanwhile, SIRT1 mRNA in the aortic dissection group declined with age (P<0.01). Compared with the control group, SIRT1 protein expression decreased significantly in the aortic dissection group (the younger group: 0.64±0.18 vs. 1.18±0.47; the middle age group: 0.43±0.26 vs. 0.69±0.32; the elderly group: 0.31±0.24 vs. 0.45±0.29, P<0.01). The Western blotting results showed that the expression of SIRT1 protein in the aortic dissection group decreased with age (P<0.01). The MCP-1 protein expression of younger and middle age patients in the aortic dissection group was increased compared with that in the control group (the younger group: 0.65±0.27 vs. 0.38±0.22; the middle age group: 1.08±0.30 vs. 0.46±0.36, P<0.001). MCP-1 expression increased with age (P<0.01). The result of immunohistochemical staining for SIRT1 protein was similar to that of Western blotting.ConclusionThe expression of SIRT1 decreases in patients with aortic dissection disease, and declines with age. SIRT1 may play an important role in the treatment and screening of type A aortic dissection.
ObjectiveTo compare mid-to long-term outcomes of selective coronary venous bypass grafting (SCVBG) using internal mammary artery (IMA) grafts and great saphenous vein (GSV) grafts for surgical treatment of diffuse right coronary artery atherosclerosis. MethodsWe retrospectively analyzed clinical data of 75 patients undergoing SCVBG in Beijing Anzhen Hospital from January 2003 to December 2012. GSV was used as grafts for SCVBG in 54 patients (GSV group), and IMA was used as grafts for SCVBG in 21 patients (IMA group). All the patients were followed up in November 2013. Their survival condition, recent relapse rate of angina, recent echocardiographic results and coronary CT angiography (CTA) were analyzed. ResultsOverall survival rate of IMA group was slightly higher than that of GSV group (100.0% vs. 83.3%), but survival curves showed no statistical difference in survival rate between the 2 groups (P=0.055). Coronary CTA showed significant blockage in GSV grafts and middle cardiac vein in patients in GSV group (n=39), while IMA grafts and middle cardiac vein in patients in IMA group (n=18) were mostly visible and patent (P < 0.001). Left ventricular ejection fraction (LVEF) of the 2 groups were significantly higher than preoperative values, but there was no statistical difference between the 2 groups. ConclusionCompared with SCVBG using GSV, SCVBG using IMA can significantly improve mid-to long-term patency of the grafts and middle cardiac vein, and is an efficacious procedure for diffuse right coronary artery atherosclerosis.
Objective To investigate the potential causal associations between 731 immune cell traits and atherosclerosis by Mendelian randomization (MR) analysis. Methods Using single nucleotide polymorphisms (SNPs) as instrumental variables, genome-wide association study (GWAS) summary statistics (GCST90001391 to GCST90002121) for 731 immune cell traits were obtained from the GWAS Catalog database, and the atherosclerosis dataset (finn-b-I9_CORATHER) was retrieved from the IEU database for MR analysis. The inverse variance weighted method, MR-Egger regression, weighted median, simple mode, and weighted mode approaches were employed to estimate the causal effects between the 731 immune cell traits and atherosclerosis, using odds ratio (OR) with 95% confidence interval (CI) as the effect size. Cochran Q test was used to assess heterogeneity. Horizontal pleiotropy was evaluated using the MR-Egger intercept test and the MR-PRESSO method. Leave-one-out analysis was conducted to examine the sensitivity of the causal estimates to individual SNPs. Results MR analysis revealed potential causal associations between 24 immune cell traits and atherosclerosis (P<0.05). Among them, human leucocyte antigen (HLA)-DR on plasmacytoid dendritic cells (DC) [OR=1.035, 95%CI (1.016, 1.054), P<0.001] and hematopoietic stem cell absolute count (HSCAC) [OR=1.049, 95%CI (1.021, 1.077), P<0.001] showed significant positive causal associations with atherosclerosis (P≤0.001), whereas CD86 on CD62L+ myeloid DC [OR=0.953, 95%CI (0.926, 0.981), P=0.001] exhibited a significant negative causal association with atherosclerosis (P≤0.001). The results of Cochran Q test, MR-Egger regression, and MR-PRESSO indicated P-values>0.05, suggesting no evidence of heterogeneity or horizontal pleiotropy in the causal estimates for these three immune cell traits. Reverse MR analysis, using the 24 immune cell traits as outcome variables, showed no evidence of causal association (P>0.05), supporting a unidirectional causal relationship from immune cells to atherosclerosis. Conclusion HLA-DR on plasmacytoid DC and HSCAC may serve as risk factors for atherosclerosis, while CD86 on CD62L+ myeloid DC may play a protective role against atherosclerosis.