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.
Coronary artery disease (CAD) is a cardiovascular disease mainly caused by atherosclerosis, which involves a variety of pathophysiological mechanisms such as lipid metabolism, inflammatory response, and endothelial dysfunction. Fetuin B is a glycoprotein secreted by the liver, which can participate in many processes such as cell inflammation, vascular calcification, and lipid metabolism, and is closely related to the pathogenesis of CAD. This article reviews the relationship between fetuin B and CAD and the mechanism of its occurrence and development, in order to provide new choices and methods for the prevention, diagnosis, and treatment of CAD.
Sclerostin, as a bone-derived secreted glycoprotein, is a suppressor of Wnt signaling pathway. Recently, adverse cardiovascular events in the treatment of osteoporosis with sclerostin inhibitors have raised concerns about the association of sclerostin with atherosclerotic heart disease. Whether the role of sclerostin in atherosclerotic heart disease is harmful or beneficial is not clear. This article reviews the progress of the mechanisms of sclerostin in vascular calcification and atherosclerotic heart disease, focusing on the relationship between sclerostin and vascular calcification, the impact of its concentration changes on atherosclerotic heart disease, and the effect of sclerostin inhibitor on cardiovascular events.
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.
Objective To investigate the predictive factors of clinical progression and short-term prognosis of cerebral infarction caused by large artery atherosclerosis (LAA). MethodsPatients with acute LAA cerebral infarction who were hospitalized in the Department of Neurology, Lianyungang Hospital of Traditional Chinese Medicine between January 2016 and May 2019 were included. On admission, the patients’ medical history was collected. The degree of neurological deficit was assessed, blood pressure, blood glucose, blood lipids, plasma homocysteine, lipoprotein-associated phospholipase A2 (Lp-PLA2) were measured, and intracranial and extracranial blood vessels related test results were collected. Within 72 hours of onset, the Scandinavian Stroke Scale (SSS) was used to determine whether the patients’ condition progressed. The modified Rankin scale was used to evaluate the short-term prognosis at 30 days of onset. The related factors of clinical progression and short-term prognosis of LAA cerebral infarction were analyzed. Results Finally, 100 patients were included. According to the SSS assessment results within 72 hours of onset, 27 cases were divided into the progression group and 73 cases in the non-progression group. There was no significant difference in gender and age between the two groups (P>0.05). According to the evaluation results of the modified Rankin scale at 30 days of onset, they were divided into 31 cases in the poor prognosis group and 69 cases in the good prognosis group. There was no significant difference in gender and age between the two groups (P>0.05). Logistic regression analysis showed that plasma Lp-PLA2 [odds ratio (OR)=1.013, 95% confidence interval (CI) (1.007, 1.018), P<0.001], SSS score [OR=0.910, 95%CI (0.842, 0.985), P=0.019], and history of hypertension [OR=5.527, 95%CI (1.241, 24.613), P=0.025] were the predictors of disease progression within 72 hours. SSS score [OR=0.849, 95%CI (0.744, 0.930), P<0.001], carotid artery stenosis [OR=9.536, 95%CI (1.395, 65.169), P=0.021] and progressive stroke [OR=8.873, 95%CI (1.937, 40.640), P=0.005] were the predictors of short-term prognosis of LAA cerebral infarction. Conclusions History of hypertension and high levels of plasma Lp-PLA2 are predictors of early progression of cerebral infarction. Carotid artery stenosis and progressive stroke are predictors of adverse outcomes in the acute phase of cerebral infarction. Neurological scores on admission was a predictor for short-term adverse outcomes in the early and acute phases.
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.
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.
Atherosclerotic plaque rupture is the main cause of many cardiovascular diseases, and biomechanical factors play an important role in the process of plaque rupture. In the study of plaque biomechanics, there are relatively few studies based on fatigue fracture failure theory, and most of them mainly focus on the whole fatigue propagation process from crack initiation to plaque rupture, while there are few studies on the influence of crack on plaque rupture at a certain time in the process of fatigue propagation. In this paper, a two-dimensional plaque model with crack was established. Based on the theory of fracture mechanics and combined with the finite element numerical simulation method, the stress intensity factor (SIF) and related influencing factors at the crack tip in the plaque were studied. The SIF was used to measure the influence of crack on plaque rupture. The results show that the existence of crack can lead to local stress concentration, which increases the risk of plaque rupture. The SIF at the crack tip in the plaque was positively correlated with blood pressure, but negatively correlated with fibrous cap thickness and lipid pool stiffness. The effect of the thickness and angle of lipid pool on the SIF at the crack tip in the plaque was less than 4%, which could be ignored. This study provides a theoretical basis for the risk assessment of plaque rupture with cracks.
Obesity, sleep disorders, psychological stress, sedentary are modifiable cardiovascular risk factors. There is growing evidence that these risk factors may accelerate the chronic inflammatory process of atherosclerosis and lead to myocardial infarction. Studies on the role of immune cells and their related immune mechanisms in atherosclerosis have shown that the above modifiable risk factors can affect the hematopoiesis of the bone marrow system, affect the production of immune cells and phenotypes, and then affect the progress of atherosclerosis. This review will focus on the effects of modifiable cardiovascular risk factors on the progression of atherosclerosis through the role of the innate immune system.
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.