Abstract:Atherosclerosis is major causes of death caused by cardiovascular disease. However, its causes are not completely clear, and its prevention and treatment methods are limited. Coronary vessels are the vessel most likely to cause atherosclerosis, and its corresponding anatomy also has special significance. This article commented the anatomy of coronary vessels, targeted treatment of atherosclerosis and treatment of atherosclerotic complications.

Abstract:Aim To observe the effect of TSB2 inhibiting the combination of heat shock protein 90 (HSP90) and endothelial nitric oxide synthase (eNOS) on the formation of atherosclerosis. Methods Human umbilical vein endothelial cells (HUVEC) were treated with TSB2 and the combination between HSP90 and eNOS was detected by co-immunoprecipitation. C57BL/6 mice and low density lipoprotein receptor knockout (LDLR－/－) mice were fed with normal diet (ND) or high fat diet (HFD) for 12 weeks while injected with phosphate buffered saline (PBS) or TSB2 intraperitoneally. The mice were divided into four groups:C57BL/6＋ ND＋PBS group, LDLR－/－＋ND＋PBS group, LDLR－/－＋HFD＋PBS group, LDLR－/－＋HFD ＋TSB2 group. Then the aorta was isolated. The combination between HSP90 and eNOS in aorta was measured. The atherosclerotic plaque in aorta and aortic sinus were determined. The production of nitric oxide (NO) and superoxide anion (O₂·－) were also detected. At the same time, L-monomethyl-arginine (L-NMMA), a competitive substrate of L-arginine, was used to determine the production of NO, and L-nitroarginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, was used to determine the production of O₂·－. Results Compared with control group, the combination between HSP90 and eNOS was decreased by 41.06% (P＜0.05) in cultured HUVEC treated with TBS2. Compared with LDLR－/－＋HFD＋PBS group,the combination between HSP90 and eNOS in the mouse aortas was decreased by 40.95% (P＜0.05) in LDLR－/－ ＋HFD＋TSB2 group, and the production of O₂·－ was decreased by 63.73% (P＜0.05) (L-NAME significantly inhibited the production of O₂·－ in LDLR－/－＋HFD＋PBS group), while the production of NO had no significant change in the mouse aortic endothelial cells (L-NMMA inhibited NO production in all groups), and the formation of atherosclerotic lesions in aortas and aortic sinus were significantly decreased by 59.39% and 68.86% (P＜0.05) respectively in LDLR－/－＋HFD＋TSB2 group. Conclusion TSB2 can reduce the O₂·－ production of uncoupled eNOS in vascular endothelial cells by inhibiting the combination of HSP90 and eNOS in aortic endothelial cells, and finally inhibits the formation of atherosclerosis.

Abstract:Aim To investigate the effects of coronary artery stenosis on cardiac pathology and myocardial metabolomics in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). Methods Coronary and ventricular sites (anterior, lateral and posterior walls of left ventricle and anterior, posterior wall of right ventricle and interventricular septum) were studied in 35 patients with ARVC undergoing heart transplantation. Coronary artery tissue sections were stained with HE and the degree of stenosis was quantitatively analyzed; slices of ventricular tissue were stained with Masson staining, and the proportion of myocadium, fiber, and adipose tissue in the heart was quantitatively analyzed after image processing. Metabolite extraction and metabolomics analysis of cardiac tissue from coronary artery supply areas were performed. Comparative analysis was conducted on the differences in myocardium, fiber and adipose tissue, and metabolomic profiles among the group of patients without coronary artery stenosis, with mild coronary artery stenosis (＜50%) and with moderate-severe coronary artery stenosis (≥50%). Results Among the 35 patients with ARVC, 10 (28.6%) had moderate-severe coronary artery stenosis, 11 (31.4%) had mild coronary artery stenosis, and 14 (40.0%) had no coronary artery stenosis. The age of patients with moderate-severe coronary artery stenosis receiving heart transplantation was significantly higher than those with mild coronary artery stenosis and those without coronary artery stenosis [(48.5±10.7) years vs. (33.8±10.5) years and (31.0±13.4) years, P＝0.015]. There was no statistically significant difference in the proportion of myocardium, fiber and adipose tissue between patients with moderate-severe, mild coronary artery stenosis and those without coronary artery stenosis in the left ventricular anterior wall, lateral wall, posterior wall, and right ventricular anterior wall, posterior wall, and interventricular septum (P＞0.05). There were 105 metabolites were detected from the metabolic profiles, which attributed to pathways of tricarboxylic acid cycle, amino acid metabolism, purine metabolism, pyrimidine metabolism, pentose phosphate metabolism, glycolysis and gluconeogenesis. Metabolomic analysis showed few differences among the three groups. There was no significant separation of the three groups on heat or in principle component analysis. Conclusion There was no difference in the proportion of myocardium, fiber and adipose tissue of the heart and metabolomic profiles among ARVC patients with moderate-severe, mild coronary artery stenosis and without coronary artery stenosis.

Abstract:Aim To investigate the clinical efficacy and safety of excimer laser atherectomy (ELA) in the treatment of infrapopliteal arteriosclerosis occlusion, in order to provide more options for intracavitary treatment for patients with infrapopliteal arteriosclerosis occlusion. Methods The clinical data of 50 patients (50 limbs) with infrapopliteal arteriosclerosis occlusion treated in the Department of Vascular Surgery of People's Hospital of Xinjiang Uygur Autonomous Region from December 2019 to December 2021 were collected retrospectively, they were divided into ELA group (n＝25) and plain old balloon angioplasty (POBA) group (n＝25) according to different treatment methods, the clinical characteristics, perioperative complications, primary patency rate, postoperative ankle brachial index (ABI) improvement, visual analogue scale (VSA) and limb salvage rate during follow-up of target vessels of the two groups were compared. Results The success rate of operation in the two groups was 100%, and there were no serious complications during the perioperative period. ABI and VAS scores in the two groups were significantly improved after treatment compared to before treatment, and the ABI in the ELA group was higher than that in the POBA group 3 days and 6 months after operation, with a statistically significant difference (P＜0.05); at 6 months after operation, the VAS score in the ELA group was lower than that in the POBA group, with a statistically significant difference (P＜0.05); during the follow-up period, the first-stage primary patency rate and limb (toe) salvage rate in the ELA group were higher than those in the POBA group (P＜0.05). Conclusion ELA is safe and feasible for the treatment of infrapopliteal arteriosclerosis occlusion, which provides more options for intracavitary treatment of inferior genicular artery lesions.

Abstract:Aim GEO database was used to explore the common pathogenesis of gout complicated with atherosclerosis (As). Methods The gene expression matrices of gout (GSE160170) and As (GSE100927) were downloaded from the GEO database, the differentially expressed genes (DEG) of gout and As were analyzed, and enrichment analysis was performed separately. After analyzing the common differentially expressed genes (CDEG), functional enrichment analysis, protein-protein interaction (PPI) network analysis, and hub genes (HG) identification were performed on them, and co-expression analysis and validation were performed on hub genes. Finally, the immune cell infiltration of gout and As was analyzed, and the correlation between hub genes and infiltrating immune cells (IIC) was explored. Results The GSE160170 dataset obtained 1 606 differentially expressed genes, while the GSE100927 dataset obtained 481 differentially expressed genes. The enrichment analysis of 22 differentially expressed genes showed that the regulation of cytokines may be the key mechanism of gout complicated with As. Six hub genes (CCR2, CD2, FCGR3A, FGD3, IL10RA, SIGLEC1) were identified using the CytoHubba plugin, and the validation results of these hub genes showed that they were still reliable. The co-expression network showed that these hub genes could affect the regulation of tumor necrosis factor superfamily cytokines. Immune cell infiltration analysis showed that the expression of NK cells in gout was significantly increased, and was significantly related to CCR2 gene. The expression of living fertilizer large cells in As was significantly increased, and was significantly related to CD2 gene. Conclusion The regulatory effect of tumor necrosis factor superfamily cytokines may be the core factor of gout complicated with As.

Abstract:Aim To investigate the effect of jaranol on platelet derived growth factor-BB (PDGF-BB)-induced proliferation and migration of vascular smooth muscle cell(VSMC) as well as its possible mechanism. Methods Human aortic vascular smooth muscle cells (HA-VSMC)were treated with 25 μg/L PDGF-BB to induce proliferation and migration. The cells were divided into normal control group (NC group), PDGF-BB group, PDGF-BB+jaranol (0,0 and 40 μmol/L) group, DMSO group. Cell counting Kit-8 (CCK-8) assay was used to assess proliferation ability of HA-VSMC, and Transwell assay was used to examin the migration ability of HA-VSMC. Western blot was used to detect the expression of autophagy related proteins including p62, LC3, mammalian target of rapamycin (mTOR) and phosphorylated mTOR (p-mTOR). Results After treatment with PDGF-BB, the proliferation and migration ability of HA-VSMC was notably upregulated (P＜0.01), while jaranol showed a significant and concentration-dependent inhibition effect on PDGF-BB-induced proliferation and migration of HA-VSMC (P＜0.05). Western blot results showed that compared with the PDGF-BB group, the protein expression levels of LC3Ⅰ and mTOR were significantly decreased in PDGF-BB+jaranol (40 μmol/L) group (P＜0.05); The expression levels of LC3Ⅱ/LC3Ⅰ, p62 and p-mTOR proteins were significantly increased (P＜0.05), and the effect of jaranol(40 μmol/L) and compound C on AMPK/mTOR signaling pathway of HA-VSMC induced by PDGF-BB was consistent. Conclusion Jaranol can inhibit the abnormal proliferation and migration of HA-VSMC invoked by PDGF-BB, its mechanism may be related to its inhibition effect of PDGF-BB-induced autophagy of HA-VSMC by regulating AMPK/mTOR signaling pathway.

Abstract:Aim To investigate the value of cranial computed tomography perfusion (CTP) imaging in evaluating conservative treatment response in patients with severe carotid artery stenosis (CAS). Methods A total of 90 patients with severe CAS were selected as the research subjects, all received conservative treatment, and they were divided into low response group and high response group according to whether cerebral ischemic disease occurred within 1 year. Regional cerebral blood volume (rCBV), regional cerebral blood flow (rCBF), regional mean transit time (rMTT), and regional time to peak (rTTP) were compared between the two groups. Cox regression model was used to analyze the independent risk factors of conservative treatment responsiveness, and nomogram was used to analyze the value of rCBV, rCBF, rTTP and rMTT in evaluating conservative treatment responsiveness, and the decision curve and clinical impact curve were verified. Results Of the 90 patients with severe CAS, 2 cases dropped out after 1 year of follow-up, and 88 cases were effectively followed up. There were 65 cases without cerebral ischemia-related complications (in the high response group) and 23 cases with cerebral ischemic diseases (in the low response group), including 15 cases of transient ischemic attacks (17.05%) and 8 cases of cerebral infarction (9.09%). After 3 months of treatment, the rCBF in the two groups was greater than that before treatment, and the rMTT and rTTP were lower than those before treatment (P＜0.05). Before treatment and 3 months after treatment, the rCBF of the low response group was lower than that of the high response group, and the rMTT and rTTP of the high response group were higher than those of the high response group (P＜0.05). The Cox regression model was used to screen out systolic blood pressure, uric acid, rCBF, rMTT and rTTP, and construct a nomogram prediction model for conservative treatment response in patients with severe CAS. The consistency index was 0.896. Calibration curve analysis showed that the prediction model predicted conservative treatment response was in good agreement with the actual conservative treatment response. Within a threshold range of 0.16 to 0.95, the net benefit rate of the combined nomogram model in assessing responsiveness to conservative treatment in patients with severe CAS was superior to testing alone. The number of people classified as high risk by the joint detection scheme and the number of true positive cases were basically the same when the threshold probability was 0.41. Conclusion CTP imaging parameters are closely related to treatment responsiveness in patients with severe CAS, and they can provide a reference for early clinical evaluation of treatment responsiveness and help ensure patient benefit.

Abstract:Aim To explore the correlation between platelet morphology parameters and the severity of coronary artery disease in patients with acute coronary syndrome (ACS). Methods 121 ACS patients who were hospitalized in the Department of Cardiovascular Medicine of Second Affiliated Hospital of University of South China from January 2019 to October 2019 were selected, and 35 patients with normal results of selective coronary angiography during the same period were selected as the control group. Mean platelet volume (MPV), platelet distribution width (PDW), and platelet large cell ratio (PLCR) were used as platelet morphology parameters. All patients underwent coronary angiography and were divided into low score (1～40 points) group, medium score (41～80 points) group, and high score (81 points and above) group. The differences in platelet morphology parameters between each group were compared to identify risk factors for high Gensini scores. Results The MPV, PDW, PLCR, male proportion, creatine kinase isoenzyme (CK-MB), N-terminal-pro brain natriuretic peptide (NT-proBNP), uric acid (UA), and cardiac troponin I (cTnI) in the ACS group were significantly higher than those in the control group (P＜0.05). PDW, MPV and PLCR gradually increased in the control group and Gensini low, medium, and high score groups (P＜0.05). Pearson correlation analysis showed a positive correlation between PDW(r＝0.814,P＜0.05), MPV (r＝0.822, P＜0.05), PLCR (r＝0.802, P＜0.05) and Gensini score. Multiple Logistic regression analysis showed that PLCR can be a risk factor for high coronary Gensini score. Conclusion PLCR, PDW and MPV are positively correlated with the severity of coronary artery disease in patients with ACS, and have potential importance in evaluating the severity of coronary artery disease.

Abstract:Aim To observe the changes in indexes of ventricular remodeling and adverse drug reactions in patients with acute myocardial infarction (AMI) before and after treatment, and evaluate the efficacy and safety of different doses of sarcubatrix/valsartan in the treatment of heart failure patients after AMI. Methods 174 patients with acute ST-segment elevation myocardial infarction (STEMI) and subnormal left ventricular ejection fraction (LVEF) ＜50% from March 2018 to March 2022 were randomly allocated to receive maximal tolerated dose of sacubitril/valsartan (titrated up to maximal tolerated dose or 200 mg, Bid, n＝80) or low dose sacubitril/valsartan (50 mg, Bid, n＝94) treatment, they also received conventional treatment. The changes in echocardiographic parameters, serum N-terminal pro-brain natriuretic peptide(NT-proBNP) and adverse drug reactions (symptomatic hypotension, hyperkalemia, kidney function decline and angioedema, et al) from baseline to 12 months after discharge were assessed. Results After treatment, there was statistically significant difference in left atrial diameter (LAD) of maximum tolerated dose group and low dose group compared with baseline (P＜0.05), however, there was no statistically significant difference between the two groups (P＞0.05). The left ventricular end diastolic diameter (LVEDD) were significantly decreased in two groups compared with baseline (P＜0.05), but there was no statistically significant difference between the two groups (P＞0.05). The left ventricular ejection fraction(LVEF) were significantly increased in both groups compared with baseline (P＜0.05), but there was no statistically significant difference between the two groups (P＞0.05). The decrease of serum NT-proBNP levels was higher in maximum tolerated dose group than that in low dose group (P＜0.05). The incidence of drug-related adverse reactions was higher in the maximum tolerated group (17.5% vs 2.1%, P＜0.05). Conclusion Compared with low dose sacubitril/valsartan group, the maximum tolerated dose group did not show significant advantages in improving cardiac remodeling and LVEF. Although it may be possible to reduce cardiovascular events by further reducing NT-proBNP levels, strict titration of the maximum tolerable dose was closely related to frequent adverse drug reactions.

Abstract:Multiple factors cause atherosclerosis, and its pathogenesis is complex and has not been fully elucidated.Polyunsaturated fatty acids, a member of the fatty acid family, are critical nutrients for mammalian growth and development. Types and intakes of polyunsaturated fatty acids, and fatty acid desaturase can affect the course of atherosclerotic disease. Fatty acid desaturase gene cluster can regulate fatty acid desaturase activity and further affect atherosclerosis. Based on the metabolic and genetic perspectives, this article reviewed the research progress of the effects of polyunsaturated fatty acids on atherosclerosis regulated by fatty acid desaturase and the relationship between genetic variants of the fatty acid desaturase gene cluster and atherosclerotic cardiovascular disease was summarized.

Abstract:Intestinal bacteria produce metabolites such as trimethylamine N-oxide (TMAO), which have been found to impact the pathological process of coronary artery atherosclerotic disease through various signaling pathways. TMAO has been shown to induce vascular endothelial cell damage, contribute to lipid deposition in the vascular wall, promote inflammation, and stimulate smooth muscle cell aging and migration. Research suggests that modulation of TMAO metabolism and associated signaling pathways may offer potential therapeutic interventions for the prevention and treatment of atherosclerotic disease. This article will provide a brief overview of the TMAO mechanism in atherosclerosis, offering new research insights for the prevention and treatment of this disease.

Abstract:As one of the common diseases caused by atherosclerosis, coronary heart disease has various and complex pathogenesis. How to prevent and treat coronary heart disease has become a global hot health issue. Studies have found that among the risk factors for coronary heart disease, various oral diseases such as periodontitis, caused by oral microbiome disorders, can greatly increase the risk of coronary heart disease. In order to explore the correlation between coronary heart disease and oral microorganisms, this paper discusses the possible pathogenic mechanism of periodontitis caused by oral microorganisms on coronary heart disease, in order to provide new ideas and references for the prevention and treatment of coronary heart disease.

Abstract:Atherosclerosis is an important factor in cardiovascular events. Relevant epidemiological surveys show that the burden of atherosclerotic cardiovascular disease in China has increased rapidly and significantly in recent years, which has brought major challenges to China's public health problems. Myocardin-related transcription factor-A (MRTF-A) plays an important role in the development of atherosclerosis, including participating in inflammatory responses, promoting lipid accumulation, and phenotypic transformation of vascular smooth muscle cells (VSMC) in the process of atherosclerosis, and exploring the correlation between MRTF-A and atherosclerosis is of great significance for finding new therapeutic targets. This article reviews the role of MRTF-A in the process of atherosclerosis lesions, which can provide a reference for targeted therapy of coronary atherosclerosis.