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PurposeDiabetic heart failure (DHF) or cardiomyopathy is a common complication of diabetes; however, the underlying mechanism is not clear. In the present study, the authors searched for differentially expressed genes associated with DHF and the molecular types of immune cells based on bioinformatics.MethodsThe RNA expression dataset of DHF was obtained from the NCBI Gene Expression Omnibus (GEO) database. After preprocessing the data, the differentially expressed genes (DEGs) between the DHF group and the non-diabetic heart failure (NHF) group were screened and intersected with immune-related genes (IRGs) in the ImmPort database. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed using the DAVID tool. The ssGSEA algorithm was used to evaluate immune infiltration of the heart tissue in each group. In addition, the protein-protein interaction (PPI) network and miRNA-mRNA network were constructed using the STRING online website and Cytoscape program. Finally, validation analysis was performed using animal models.ResultsEight immune-related core genes were identified. GO and KEGG showed that core genes were mainly enriched in angiogenesis and cytokine-cytokine receptor interaction. Immune infiltration results showed that activated dendritic cells, central memory CD4 T cells, central memory CD8 T cells, myeloid-derived suppressor cells (MDSCs), neutrophils, and regulatory T cells may be involved in DHF. Neutrophils may play a key role in the pathogenesis of HF in diabetes.ConclusionImmune-related core genes and immune infiltrating cells provide a new perspective on the pathogenesis of DHF.

BackgroundChronic endoplasmic reticulum stress (ERS) plays a crucial role in cardiovascular diseases. Thus, it can be considered a therapeutic target for these diseases. In this study, poly (D,L-lactic acid) (PDLLA) nanoparticle-eluting stents loaded with tauroursodeoxycholic acid (TUDCA), an ER stress inhibitor, was fabricated to assess their ability to reduce endothelial cell apoptosis and promote re-endothelialization after stent implantation.Materials and methodsPDLLA nanoparticles loaded with TUDCA were prepared via the emulsification-solvent evaporation method. The cumulative release rates of TUDCA were measured in vitro via high-performance liquid chromatography. The carotid arteries of rabbits were subsequently implanted with stents in vivo. The rabbits were then sacrificed after 4 weeks for scanning electron microscopy. Meanwhile, TUDCA concentration in the homogenate of the peripheral blood and distal vascular tissue after stent implantation was measured. The effect of TUDCA on ERS, apoptosis, and human umbilical vein endothelial cell (HUVEC) function was investigated in vitro by performing cell migration assay, wound healing assay, cell proliferation assays, endoplasmic reticulum (ER)-specific fluorescence staining, immunofluorescence, and western blotting.ResultsTUDCA nanoparticles were released slowly over 28 days. In addition, TUDCA-eluting stents enhanced re-endothelialization and accelerated the recovery of endotheliocytes in vivo. ERS and apoptosis significantly increased in H2O2-treated HUVECs in vitro. Meanwhile, TUDCA reduced apoptosis and improved function by inhibiting ERS in H2O2-treated HUVECs. Decreased rates of apoptosis and ERS were observed after silencing XBP-1s in H2O2-treated HUVECs.ConclusionTUDCA can inhibit apoptosis and promote re-endothelialization after stent implantation by inhibiting IRE/XBP1s-related ERS. These results indicate the potential therapeutic application of TUDCA as a drug-coated stent.

BackgroundDietary polyphenols, polypeptides, and oligosaccharides modulate inflammation and immunity by altering the composition of gut microbiota. The polyphenols and polypeptides in Chinese rice wine have protective effects against cardiovascular disease. In this study, we hypothesized that the polyphenols, polypeptides, and oligosaccharides in Chinese rice wine can ameliorate diabetic cardiomyopathy (DCM) by altering gut microbiota and metabolites.MethodsMice with DCM and high glucose cells were treated with rice wine polyphenols (RWPH), rice wine polypeptides (RWPE), and rice wine oligosaccharides. Cardiac function was evaluated by echocardiography and detection of myocardial injury markers. We observed the pathological structures using hematoxylin and eosin staining, Masson's trichrome staining, and transmission electron microscopy. The expression levels of autophagy-related proteins and stubRFP-sensGFP-LC3 fluorescence were measured to evaluate autophagy. We performed TUNEL staining and measured the levels of Bax, Bcl-2, and p53 to assess apoptosis. To analyze the effects of the rice wine functional components on the gut microbiota and metabolites of DCM mice, we performed fecal 16S-rDNA gene sequencing and serum untargeted metabolomics.ResultsOur results showed an increase in cardiac and mitochondrial function, promotion of autophagy, and inhibition of cardiomyocyte apoptosis, which indicates that RWPH and RWPE can ameliorate DCM. The abundance of Akkermansia and Desulfovibrio were reduced by the presence of RWPH and RWPE. The growth of the Lachnospiraceae_NK4A136_group and Clostridiales-unclassified were promoted by the presence of RWPH. Tryptophan metabolism-associated metabolites were increased and phenylalanine levels were reduced by the presence of RWPH and RWPE. The biosynthesis of primary bile acids was enhanced by the presence of RWPH.ConclusionBoth RWPH and RWPE provided a protective effect against DCM by promoting autophagy, inhibiting apoptosis, and reversing both gut microbiota dysbiosis and metabolic dysregulation.

Background: Dietary polyphenols help to prevent cardiovascular diseases, and interactions between polyphenols and gut microbiota are known to exist. In this study, we speculated that gut microbiota-mediated metabolite regulation might contribute to the anticardiotoxic effects of yellow wine polyphenolic compound (YWPC) in doxorubicin (DOX)-treated rats. Methods: 16S-rDNA sequencing was performed to analyze the effects of YWPC on the gut microbiota in DOX-treated rats (n=6). Antibiotics were used to investigate the contribution of the altered microbiome to the role of YWPC (n=6). Plasma metabolomics were also analyzed by untargeted gas chromatography-mass spectrometry systems. Results: YWPC ameliorated DOX-mediated cardiotoxicity, as evidenced by increased cardiac and mitochondrial function and reduced levels of inflammation and myocardial apoptosis ( P Escherichia – Shigella , Dubosiella , and Allobaculum , along with enrichment of Muribaculaceae_unclassified , Ralstonia , and Rikenellaceae_RC9_gut_group in the gut, suggested that YWPC ameliorated DOX-induced microbial dysbiosis. YWPC also influenced the levels of metabolites altered by DOX, resulting in lower arachidonic acid and linoleic acid metabolism and higher tryptophan metabolite levels ( P Conclusions: YWPC protected against DOX-induced cardiotoxicity in a gut microbiota–dependent manner. This supports the use of dietary polyphenols as a therapeutic approach for the treatment of cardiovascular diseases via microbiota regulation.

Aims Doxorubicin (DOX), a widely used powerful chemotherapeutic component for cancer treatment, can give rise to severe cardiotoxicity that limits its clinical use. Pyroptosis is characterized by proinflammation and has been defined as a new type of programmed cell death in recent years. However, whether the DOX-induced cardiotoxicity is related to pyroptosis, and if so, which genes are involved in this process is largely unknown. In this study, we sought to identify the effect of DOX on cardiomyocyte pyroptosis and further reveal the underlying regulatory mechanism. Methods and results In vitro and in vivo experiments showed that DOX treatment induced cardiomyocyte pyroptosis as evidenced by increased cell death and upregulated expression levels of NLR family pyrin domain containing 3 (NLRP3), caspase-3, IL-1β, IL-18 and GMDSD-N. Inhibition of NLRP3 rescued the DOX-induced pyroptosis. qRT-PCR showed that TINCR lncRNA was upregulated by DOX treatment and knockdown of TINCR reversed the DOX-induced pyroptosis both in vitro and in vivo. Mechanistic investigations revealed that TINCR increased NLRP3 level via recruiting IGF2BP1 to enhance NLRP3 mRNA. And the effect of TINCR on cardiomyocyte pyroptosis was attenuated by the inhibition of NLRP3 or IGF2BP1. Finally, TINCR was not involved in DOX-induced pyroptosis in cancer cells. Conclusion TINCR mediates the DOX-induced cardiotoxicity and pyroptosis in an IGF2BP1-dependent manner. Therefore, TINCR may serve as a promising therapeutic target to overcome the cardiotoxicity of chemotherapy for cancer therapy.

The role of endoplasmic reticulum (ER) stress in cardiovascular disease is now recognized. Tauroursodeoxycholic acid (TUDCA) is known to have cardiovascular protective effects by decreasing ER stress. This study aimed to assess the ability of TUDCA to decrease ER stress, inhibit dedifferentiation of vascular smooth muscle cells (VSMCs), and reduce in-stent restenosis. The effect of TUDCA on dedifferentiation of VSMCs and ER stress was investigated in vitro using wound-healing assays, MTT assays, and western blotting. For in vivo studies, 18 rabbits were fed an atherogenic diet to induce atheroma formation. Bare metal stents (BMS), BMS+TUDCA or Firebird stents were implanted in the left common carotid artery. Rabbits were euthanized after 28 days and processed for scanning electron microscope (SEM), histological examination (HE), and immunohistochemistry. In vitro TUDCA (10–1000 μmol/L) treatment significantly inhibited platelet-derived growth factor (PDGF)-BB-induced proliferation and migration in VSMCs in a concentration-dependent manner and decreased ER stress markers (IRE1, XBP1, KLF4, and GRP78). In vivo, we confirmed no significant difference in neointimal coverage on three stents surfaces; neointimal was significantly lower with BMS+TUDCA (1.6 ± 0.2 mm2) compared with Firebird (1.90 ± 0.1 mm2) and BMS (2.3 ± 0.1 mm2). Percent stenosis was lowest for BMS+TUDCA, then Firebird, and was significantly higher with BMS (28 ± 4%, 35 ± 7%, 40 ± 1%; respectively; P

The pro-aging miRNA, miR-34a, is hyperactivated in the cardiac myocardial tissues of patients and mice with diabetes, leading to diabetic cardiomyopathy (DCM). Increasing evidence suggests that dihydromyricetin (DHM) can be used to effectively treat cardiomyopathy. In this study, we investigated whether DHM affects the expression of miR-34a in DCM. The expression of miR-34a in high-glucose-induced cardiomyocytes and in the heart tissue of diabetic mice was determined by microRNA isolation and quantitative reverse transcription-polymerase chain reaction. Lipofectamine 3000 was used to transfect cardiomyocytes with miR-34a inhibitor, miR-34a mimics, and miR-control. These agents were intravenously injected into the tail vein of streptozotocin-induced diabetic mice. Autophagy and apoptosis were assessed in high-glucose-induced cardiomyocytes and cardiac tissue in diabetic mice by western blotting, immunofluorescence, Masson staining, hematoxylin and eosin staining (H&E), and electron microscopy. DHM clearly ameliorated the cardiac dysfunction in the diabetic mice. The expression of miR-34a was up-regulated in high-glucose-induced cardiomyocytes and in the hearts of diabetic mice, thus impairing autophagy. Treatment with DHM decreased the expression of miR-34a and rescued the impairment of autophagy in high-glucose-induced cardiomyocytes and in the heart tissue of diabetic mice, while the miR-34a mimic offset the effect of DHM with respect to the development of DCM by inhibiting autophagy. By decreasing the expression of miR-34a, DHM restores impaired autophagy, and thus ameliorates DCM. Therefore, DHM may potentially be used in the treatment of DCM.

Background Phenotypic switching of vascular smooth muscle cells (VSMCs) plays a key role in atherosclerosis. We aimed to investigate whether Homocysteine-responsive endoplasmic reticulum protein (Herp) was involved in VSMC phenotypic switching and affected atheroprogression. Methods To assess the role of Herp in homocysteine (Hcy)-associated atherosclerosis, Herp −/− and LDLR −/− double knockout mice were generated and fed with a high methionine diet (HMD) to induce Hyperhomocysteinemia (HHcy). Atherosclerotic lesions, cholesterol homeostasis, endoplasmic reticulum (ER) stress activation, and the phenotype of VSMCs were assessed in vivo . We used siRNAs to knockdown Herp in cultured VSMCs to further validate our findings in vitro . Results HMD significantly activated the activating transcription factor 6 (ATF6)/Herp arm of ER stress in LDLR −/− mice, and induced the phenotypic switch of VSMCs, with the loss of contractile proteins (SMA and calponin) and an increase of OPN protein. Herp −/− /LDLR −/− mice developed reduced atherosclerotic lesions in the aortic sinus and the whole aorta when compared with LDLR −/− mice. However, Herp deficiency had no effect on diet-induced HHcy and hyperlipidemia. Inhibition of VSMC phenotypic switching, decreased proliferation and collagen accumulation were observed in Herp −/− /LDLR −/− mice when compared with LDLR −/− mice. In vitro experiments demonstrated that Hcy caused VSMC phenotypic switching, promoted cell proliferation and migration; this was reversed by Herp depletion. We achieved similar results via inhibition of ER stress using 4-phenylbutyric-acid (4-PBA) in Hcy-treated VSMCs. Conclusion Herp deficiency inhibits the phenotypic switch of VSMCs and the development of atherosclerosis, thus providing novel insights into the role of Herp in atherogenesis.

Introduction A left common pulmonary vein (LCPV) is a common anatomical variant in atrial fibrillation (AF) patients. Whether an LCPV influences outcomes of repeated radiofrequency catheter ablation (RFCA) for AF has not been elucidated. Methods From a prospectively collected database, we enrolled 154 patients who received repeated RFCA for recurrent AF after the initial RFCA (56 ± 9 years, 72% paroxysmal AF, 32 patients with an LCPV, and 122 patients with typical left-sided pulmonary veins [PVs]). Median postprocedural follow-up was 26 months. The primary outcome was an episode of AF, atrial tachyarrhythmia, or atrial flutter lasting for more than 30 seconds, after the 3 months blanking period following the repeated procedure. Results After the follow-up period, 75 patients suffered recurrence after repeated ablation. In the Kaplan-Meier analysis, an LCPV was significantly associated with less recurrence (hazard ratio [HR]: 0.39; 95% confidence interval [CI]: 0.28-0.79; P = 0.005). In subgroup analysis, the significant association persisted in paroxysmal AF patients. Regarding persistent AF patients, an LCPV tended to be associated with less recurrence with no statistical significance (HR: 0.40; 95% CI: 0.20-1.03; P = 0.067). In multivariate analyses, an LCPV still independently predicted freedom from recurrence (HR: 0.44; 95% CI: 0.22-0.88; P = 0.02). Conclusion Compared with typical left-sided PVs, an LCPV was independently associated with better outcomes after repeated RFCA of AF, particularly in patients with paroxysmal AF.

The beneficial effect of Chinese rice wine on atherosclerosis has been proved, but the exact components that have the cardiovascular protective effect are still unknown. This study aimed to explore the exact ingredients in Chinese rice wine that could inhibit homocysteine (Hcy)-induced vascular smooth muscle cell (VSMC) proliferation and migration. VSMCs were divided into 7 groups: control, Hcy (1 mmol/L), Hcy + oligosaccharide, Hcy + polypeptides, Hcy + polyphenols, Hcy + alcohol, and Hcy + Chinese rice wine. methyl thiazolyl tetrazolium (MTT) assay, Transwell chambers, and wound-healing assay were used to test the proliferation and migratory ability of the VSMCs. Western blot and gelatin zymography were used to investigate the expressions and activities of metal matrix proteinase 2/9 (MMP-2/9) and tissue inhibitor of metalloproteinase 2 (TIMP-2) in VSMCs. Polypeptides and polyphenols in the Chinese rice wine reduced the proliferation and migration ability of the VSMCs. Furthermore, they also decreased the expression and activity of MMP-2/9 but had no obvious impact on the expression of TIMP-2 in each group. This study further confirms that polypeptides and polyphenols in the Chinese rice wine could inhibit Hcy-induced proliferation and migration of VSMCs and maintain the balance between matrix metalloproteinases (MMPs) and TIMPs.

Objective The objective of this study was to determine similarities in the effect of yellow wine as compared to statin and the possibility that yellow wine inhibits tumour necrosis factor- α(TNF-α)-induced nitric oxide (NO) synthesis, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and intercellular adhesion molecule-1 (ICAM-1) in cultured rat vascular endothelial cells (VECs).Methods We isolated VECs, and cultivated and purified Sprague Dawley (SD) rat thoracic aortas in vitro. We selected the optimal wine concentration using clonogenic and MTT assays to measure cell survival. Next, we divided the cells into 9 groups: (1) control, (2) TNF-α, (3) TNF- α+ rosuvastatin (10 μmol/L), (4) TNF- α+ ethanol 0.5%, (5) TNF- α+ yellow wine 0.5%, (6) TNF- α+ ethanol 1.0%, (7) TNF- α+ yellow wine 1.0%, (8) TNF- α+ ethanol 1.5%, and (9) TNF- α+ yellow wine 1.5% and they were given the corresponding treatment for 24 h. We determined NO production with nitrate reductase. We then measured...

Background If transformation from persistent atrial fibrillation (AF) to paroxysmal AF after catheter ablation had impacts on the outcome of repeated ablation was unclear. This study aimed to explore whether the type of recurrent AF after ablation for persistent AF was associated with recurrence after repeated ablation. Methods and results This was a retrospective cohort study. 116 persistent AF patients undergoing the second ablation due to a failed initial ablation were enrolled in our study. Patients with recurrent paroxysmal AF after initial ablation were categorized as Group A (47 patients) while those with recurrent persistent AF were categorized as Group B (69 patients). The study endpoint was defined as any episode of AF, atrial tachyarrhythmia or atrial flutter lasting for >30 s, after the 3 month blanking period following repeated procedure. After 3–72 months (median: 24 months) of follow-up from repeated ablation, 54 (47%) patients suffered from recurrence after repeated ablation. In univariate analyses, Group B suffered a higher risk for recurrence than those in Group A (hazard ratio: 2.05, 95% confidence interval: 1.14–3.70, P = 0.01). Besides recurrent AF type, larger left atrial dimension at repeated procedure and pulmonary vein reconnection also predicted success of repeated ablation. In multivariate analysis, patients in Group B still had a 1.91-fold higher risk for recurrence than those in Group A (HR: 1.91, 95% CI: 1.06–3.44, P = 0.03). Conclusions After persistent AF ablation, transformation from persistent AF to paroxysmal AF is independently associated with success of repeat ablation.

To provide evidence that rosuvastatin may improve insulin-resistance and inhibit atherogenesis by modulating insulin signaling, and whether this effect occurs beyond its plasma cholesterol-lowering effect. Thirty-two 6-week-old low-density lipoprotein receptor deficient mice were randomized into 4 groups (n = 8 in each group): Normal control group (NC); High fat and high fructose diet group (HFF); HFF plus rosuvastatin group (HFFR); HFFR plus mevalonic acid group (HFFRMA). After 12 weeks, we measured fasting blood sugar, fasting insulin and cholesterol levels; the morphological concentrations of the aorta and aortic sinus; the expression of insulin receptor substrate 2, phosphorylated insulin receptor substrate 2, protein kinase B, phosphorylated protein kinase B and the glucose transporter 4 in the liver. Compared with other groups, fasting blood sugar and fasting insulin increased significantly in HFF group. Furthermore, HFF group had an increase in the morphological concentrations of the aorta and aortic sinus, but there was a significant decrease in the HFFRMA group and the HFFR group. Moreover, there was a high expression of insulin receptor substrate 2, phosphorylated insulin receptor substrate 2, protein kinase B, phosphorylated protein kinase B and the glucose transporter 4 in the HFFRMA and HFFR groups, but a low expression in the HFF group. No significant differences regarding each afore-mentioned index was observed in the HFFR and HFFRMA groups. Our data show that rosuvastatin may improve insulin-resistance and inhibit atherogenesis in HFF-fed mice by partially reversing the decrease in the insulin stimulated insulin receptor substrate 2/Phosphatidylinositol 3-kinase/protein kinase B/glucose transporter 4 pathway in the liver, and that this effect is independent of its cholesterol-lowering effect.

Our previous study found that Chinese yellow wine could inhibit the production of homocysteine (HCY) induced extracellular matrix metalloproteinase-2 (MMP-2) in the cultured rat vascular smooth muscle cells. Little is known about the relationship between Chinese yellow wine and atherosclerosis or MMP-2 in vivo. Thirty-two LDL Receptor knockout mice on a high-fat and L-methionine diet developed plasma hyperhomocysteinemia and atherosclerosis. They were randomly divided into yellow wine group (n = 8), red wine group (n = 8), ethanol group (n = 8), and control group (n = 8), they were sacrificed after 14 weeks. There were no significant differences with plasma total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels in the four groups. Plasma HCY was significantly decreased in the yellow wine group compared to the other three groups (P < 0.01). Yellow wine and red wine groups significantly reduced the atherosclerosis lesion area compared to ethanol and control groups (P < 0.001). However, there was no significant discrepancy between the yellow wine group and red wine group. Compared to the control group and ethanol group, the production of MMP-2 reduced 26.8% and 23.6% in the aortic sinus and the activation of MMP-2 reduced 32.6% and 27.3% in the aortic arch in the yellow wine group; the production of MMP-2 reduced 25.7% and 22.4% in the aortic sinus and the activation of MMP-2 reduced 30.2% and 26.6% in the aortic arch in the red wine group. These results suggest that Chinese yellow wine and red wine can inhibit MMP-2 and improve atherosclerosis, and maybe both Chinese yellow wine and red wine have beneficial effects on cardiovascular disease by inhibiting MMP-2.

We describe two cases of Duchenne's cardiomyopathy with severe cardiac dysfunction, sporadic episodes of myoglobinuria induced by effort and increased levels of serum creatine kinase. Very mild signs of skeletal myopathy were clinically evident. Left ventriculography showed diffuse severe hypokinesia. Skeletal muscle biopsy demonstrated a dystrophic process. The patients had no familial background of the disease. These 2 patients might have a sporadic inheritance pattern with severe cardiac involvement.

We describe a case of dilated cardiomyopathy (DCM) caused by a coronary-pulmonary fistula and myocardial ischemia induced by the coronary steal phenomenon, which was successfully treated with coil embolization. Coronary fistulae and coronary-steal-induced ischemia are rare causes of DCM in adults with normal coronary arteries. Percutaneous treatment represents an alternative to surgery and may be offered as a relatively low-risk procedure. The choice between surgical and percutaneous treatment must take into account clinical and anatomical considerations. (Circ J 2006; 70: 1223 - 1225)

A case of a lost guide wire extending from the vena cava to the back of the neck after central venous catheterization is presented. A trainee inserted a central venous catheter via the left subclavian vein in a 40-year-old male patient after surgery, but did not notice that a guide wire was completely inserted in the vein. After 6 months, the lost guide wire was seen extending from the saphenous vein through the vena cava, right atrium, right ventricle, pulmonary artery and lung tissue to the back of neck. Although percutaneous catheterization of central veins is a routine technique, it is a procedure requiring advanced surgical skills, expert supervision, and attention to detail in order to prevent adverse effects. The present case is not only a technological problem, but also one of responsibility. The operator must hold onto the guide wire at all times until removal from the vessel, and a supervisor must make sure that trainees are aware of all possible complications.

This study aims to discuss the efficacy between Pulmonary Vein Antral Isolation (PVAI) plus High Density Left Atrial Voltage Mapping (HDVM) and pulmonary vein isolation on Paroxysmal Atrial Fibrillation (PAF). A total of 60 patients with paroxysmal atrial fibrillation underwent radioablation in our department from January 2012 to January 2014; all cases were divided into two groups: 30 patients in group A (PVAI), 30 patients in group B (PVAI+HDVM). Atrial arrthymic data including atrial premature, atrial tachycardia, atrial flutter, and atrial fibrillation were collected by routine Electrocardiogram (ECG) and 24 h-Holter every month during 1-year post-operation follow-ups. Ablation recurrence was defined as any atrial arrthymic events (atrial tachycardia, atrial flutter, atrial fibrillation) persisting for more than 30 seconds by real-time ECG record and/or 24 h-Holter 3-month after ablation. 60 cases of PVAI were operated successfully. Low-Voltage Zones (LVZs) were located on right superior pulmonary vein outside antrum in 7 cases, right inferior pulmonary vein outside in 3 cases, left anterosuperior wall in 6 cases, left anteroinferior wall in 9 cases, roof in 3 cases, upperposterior wall in 2 cases. 1-year atrial fibrillation ablation success rate were at the same level (83.3% vs. 80.0%, P>0.05). No difference were found in 3-month atrial arrthymic recurrences between two groups statistically (43.1% vs. 40.7% at 1 st month, 20.7% vs. 21.3% at 2 nd month, 21.3% vs. 20.2% at 3 rd month, P>0.05). Combination of pulmonary vein isolation with high density left atrial voltage mapping cannot improve ablation success rate of paroxysmal atrial fibrillation and increase the recurrence of atrial arrthymias.

OBJECTIVE This study aimed to find the effects of heparin on atherosclerosis and the production of matrix metalloproteinase (MMP)-2 in low-density lipoprotein receptor-deficient (LDLr(-/-)) mice. METHODS Sixteen 7-week-old LDLr(-/-) mice were randomized to receive sterile water or heparin. The levels of total cholesterol, high-density lipoprotein cholesterol, triglyceride and homocysteine were measured. Mean lesions area was calculated as the total atherosclerotic lesions area and expressed as a percentage of total luminal surface area. The lesions area was measured blindly by the same person using computer-assisted image analysis. The expression and localization of the MMP-2 was examined by immunohistochemistry. RESULTS All mice exhibited atherosclerotic lesions in the aortic sinus and aortic surface. Total cholesterol was decreased, while high-density lipoprotein cholesterol was increased in heparin compared with that in control group (P=0.001 and 0.002). Triglyceride was not significantly different between the two groups (P=0.92). The amount of atherosclerotic lesions in the aortic surface was 40.5% lower in heparin group than that in the control group (P

We describe a case of a 41-year-old woman with chest pain for 1 hour who was admitted to our emergency room with acute myocardial infarction. Coronary angiography and spiral computer tomography showed myocardial bridging and an intracoronary thrombus in the mid-segment of the left anterior descending artery. She felt better after taking aspirin, diltiazem and a beta blocker and was discharged 15 days later.

Objective To study the effects of heparin on the production of homocysteine-induced extracellular matrix metalloproteinase-2 (MMP-2) in cultured rat vascular smooth muscle cells. Methods The effects of different homocysteine levels (0 μmol/L to 1000 μmol/L) on MMP-2 production and the effects of different heparin concentrations (0 μg/mL to 100 μg/mL) on homocysteineinduced MMP-2 in cultured rat vascular smooth muscle cells were examined using gelatin zymography and Western blotting. The changes in MMP-2 were further compared with various treatments for 24 h, 48 h and 72 h. Results Homocysteine (50 μmol/L to 1000 μmol/L) increased the production of MMP-2 significantly in a dose-dependent manner. Increased production of MMP-2 induced by homocysteine was reduced by the extracellular addition of heparin in a dose-dependent manner. Production of MMP-2 with various treatment regimens for 72 h was greater than for 24 h and 48 h. Conclusions Extracellular addition of heparin decreased homocysteine-induced MMP-2 secretion. Data suggest a mechanism by which hyperhomocysteinemia is involved in the pathogenesis of coronary artery disease and demonstrate a beneficial effect of heparin on these conditions.

Objective Radiofrequency catheter ablation (RFCA) is the curative treatment of choice for many cardiac arrhythmias and may cause myocardial injury and inappropriate sinus tachycardia. This study aimed to determine the delayed injury of autonomic nerve after RFCA. Methods Spectral analysis of heart rate variation on 24-hour Holter electrocardiogram recordings was carried out in 86 cases (39 women, 47 men; mean age, 42 years; range, 17-67 years) with paroxysmal supraventricular tachycardia 1 hour before and 1 year after successful RFCA (WPW type A = 31; Wolf-Pakinson-White Syndrome type B = 9; atrioventricular [AV] nodal tachycardia = 46; group A: septal accessory pathway + AV nodal tachycardia [n = 52], group B: free wall accessory pathway [n = 34]). Results Heart rate variation data (time domain and frequency domain) in group A 1 year after RFCA; including very low frequency; low frequency (LF); high frequency (HF); R-R interval; root mean squared successive difference interval; the percentage of sinus cycles differing from preceding cycle by more than 50 milliseconds (PNN50); and δ very low frequency, δ LF, δ HF, δ root mean squared successive difference interval and δ PNN50 significantly decreased, compared with that before the procedure. LF/HF, SD of all normal-to-normal intervals, and SD of 5-minute average normal-to-normal intervals were not significantly changed after RFCA. Heart rate variation data in group B 1 year after RFCA was not significantly changed, compared with that before the procedure. Conclusion Radiofrequency catheter ablation operation in site of septal accessory pathway and AV node slow pathway can cause delayed injury of autonomic nerves. Heart rate variation decrement 1 year after RFCA and persistent inappropriate sinus tachycardia post RFCA resulted from delayed injury of cardiac vagus nerve by radiofrequency current.

A 40 year old man underwent an uncomplicated operation for adhesive intestinal obstruction caused by Crohn’s disease six months previously. After surgery, a cardiologist in his second year of training inserted a central venous catheter via the left subclavian vein. No problems with the catheterisation procedure were recorded. The trainee cardiologist was …

Background Hyperhomocysteinemia is an independent risk factor of coronary artery disease, but some studies have shown that patients with hyperhomocysteinemia are not prone to atherosclerosis. The aim of this study was to test whether homocysteine increases the production of matrix metalloproteinase-2 (MMP-2) and if extracellular additional magnesium and folic acid alters MMP-2 secretion. Methods and Results Gelatin zymography and western blotting were used to investigate the effects of different homocysteine levels (0-5,000 μmol/L) on MMP-2 production, and the effects of different folic acid concentrations (0-10 μmol/L) and magnesium concentrations (0-3.0 mmol/L) on homocysteine-induced MMP-2 in cultured rat vascular smooth muscle cells. Furthermore, the changes in MMP-2 were compared under various treatments for 24 h, 48 h and 72 h. Homocysteine (50-1,000 μmol/L) increased the production of MMP-2 significantly in a dose-dependent manner and at a high level (5,000 μmol/L) reduced the production of MMP-2. Increased production of MMP-2 induced by homocysteine was reduced by additional extracellular folic acid in a dose-dependent manner. Magnesium also reduced the increase of MMP-2 production induced by homocysteine. Production of MMP-2 under various treatments for 72 h increased more than during 24 or 48 h. Conclusions Homocysteine (50-1,000 μmol/L) significantly increased the production of MMP-2 in a dose-dependent manner. Added extracellular folic acid and magnesium decreased the homocysteine-induced MMP-2 secretion. These data suggest a beneficial effect of folic acid and magnesium on the pathogenesis of coronary artery disease. (Circ J 2006; 70: 141 - 146)

Objective To study the effects of copper and zinc on the production of homocysteine-induced extracellular matrix metalloproteinase-2 in cultured rats vascular smooth muscle cells. Methods We examined the effects of different homocysteine levels (0-1000 micromol/l) on matrix metalloproteinase-2 (MMP-2) production, and the effects of different copper and zinc concentrations (0-300 micromol/l) on homocysteine-induced MMP-2 in cultured rat vascular smooth muscle cells (VSMCs) using gelatin zymography and western blotting. We further compared the changes of MMP-2 under various treatments for 24, 48 and 72 hours. Results Homocysteine (50-1000 micromol/l) increased the production of MMP-2 significantly in a dose-dependent manner. Copper decreased the homocysteine-induced MMP-2 under these conditions in a dose-dependent manner, but zinc did not. Production of MMP-2 under various treatments for 72 h increased more than 24 h and 48 h. Conclusions Extracellular added copper decreased homocysteine-induced MMP-2 secretion.

OBJECTIVES This study sought to clarify the differences of intracellular and extracellular magnesium levels in patients with cardiac syndrome X. METHODS We evaluated the intracellular and extracellular magnesium status of 22 patients with cardiac syndrome X (group A) and 22 age--and gender--matched disorder-free control subjects (group B). Levels of magnesium were determined in serum, urine, erythrocytes, and the 24-h magnesium retention rate was calculated by a magnesium loading test. RESULTS Group A showed a higher 24-h magnesium retention rate (49.8 +/- 1.3% vs. 32.6 +/- 7.5%, p < 0.05) and a lower intracellular concentration of magnesium in erythrocytes than group B (3.7 +/- 1.4 vs. 5.6 +/- 1.3 fg/cell, p < 0.05), demonstrating the presence of magnesium deficiency in group A. There were no significant differences in the serum concentration of magnesium between groups A and B (0.87 +/- 0.23 vs. 0.83 +/- 0.15 mmol/l). CONCLUSIONS This study demonstrated that the intracellular magnesium level decreased in patients with cardiac syndrome X.

OBJECTIVE To study the clinical features, biochemical profiles, echocardiographic and electrocardiographic findings in the elderly and younger with idiopathic dilated cardiomyopathy (IDCM). METHODS We measured biochemical profiles and reviewed the clinical features, echocardiographic and electrocardiographic findings in 40 elderly (group A) and 70 younger (group B) patients with IDCM. RESULTS The aldosterone level in group A was higher than in group B (304.8 +/- 69.1 vs. 213.3 +/- 54.5 pmol/l, P < 0.05). Triiodothyronine (T3) and free T3 in group A were lower than in group B (0.78 +/- 0.21 and 2.87 +/- 0.73 vs. 1.26 +/- 0.33 nmol/l and 3.55 +/- 0.64 pmol/l, all P < 0.05). The incidence of ventricular arrhythmia in group A was lower than in group B (61.3% vs. 92.1 %, P < 0.01). The incidence of hypokalaemia and hypomagnesaemia were higher in group A (51.3% and 27.5%). 28.8% patients in group A were susceptible to digitalis intoxication. Disease duration and mean survival period in group A were longer than in group B (11.0 +/- 4.7 and 6.9 +/- 4.2 vs. 5.2 +/- 2.5 y and 3.4 +/- 2.7 y, all P < 0.05). The main cause of death in group A was congestive heart failure (78.9%) and ventricular arrhythmia (61.9%) in group B. CONCLUSIONS The prognosis in group A was better than in group B. The patients in group A usually showed low T3 syndrome. Ventricular arrhythmia in group A may be due to heart failure, electrolyte imbalance and sympathetic activation.

OBJECTIVES This study aimed to assess whether folic acid supplementation could produce longer-term (6-month) improvements in homocysteine levels and arterial endothelial function in patients with a high risk (3 or more traditional risk factors) of coronary artery disease (CAD) and hyperhomocysteinaemia. METHODS Thirty-one adults with 3 or more traditional risk factors of CAD and hyperhomocysteinaemia were selected, without CAD (the criterion of CAD is that more than one main vessel has an obstruction > or = 50%) by coronary angiography. All subjects were given folic acid (5 mg/day) for 6 months. Fasting plasma homocysteine levels were measured by high-performance liquid chromatography. Plasma folic acid and vitamin B12 levels were measured with immunoassay. Arterial endothelial function was measured as flow-mediated dilation of the brachial artery using high-resolution B-mode ultrasound. RESULTS Folic acid supplementation for 6 months was associated with a significant increase in mean (+/- SD) plasma levels of folic acid (4.6 +/- 1.4 microg/l to 9.1 +/- 2.5 microg/l; P < 0.01) and a significant decline in homocysteine levels (18.3 +/- 3.9 micromol/l to 11.5 +/- 2.8 micromol/l; P < 0.01). Flow-mediated dilation also improved significantly, from 6.8% +/- 2.1% to 8.9% +/- 1.7% (P < 0.01). CONCLUSION These results demonstrate that long-term (6-month) folic acid administration significantly declines homocysteine levels and improves arterial endothelial function and has potential implications for the prevention of atherosclerosis in adults with 3 or more traditional risk factors of CAD and hyperhomocysteinaemia.

The aim of this study was to study the relationship between plasma homocysteine (Hcy), folic acid, vitamin B12 and early coronary artery disease (early-CAD) and high coronary risk factors. The plasma Hcy levels of 58 cases with early-CAD and 31 subjects without CAD were measured using high-performance liquid chromatography (HPLC) with fluorescence detection. Plasma folic acid and Vitamin B12 levels were measured with radioassay method. The plasma Hcy level was significantly higher in the early-CAD patients than in the controls [(13.7 +/- 5.1) micromol/L vs (10.3 +/- 5.7) micromol/L]. The plasma folic acid and Vitamin B12 levels were significantly lower in the early-CAD patients than in the controls. The plasma Hcy level was higher in patients with more than 3 risk factors of CAD than in patients with 1 or 2 risk factors and in the controls [(17.3 +/- 5.1) micromol/ L vs (12.9 +/- 4.8) micromol/L, (7.8 +/- 2.5) micromol/L]. Other than gender, all classical coronary risk factors were related to the elevated Hcy level. Hcy levels were elevated in patients with early-CAD and with high risk factors. Hyperhomocysteinemia plays an important role in the pathogenesis of CAD.

This study sought to clarify the relationship between the degree of intracellular magnesium deficiency and the frequency of anginal attacks in women with variant angina. We evaluated the intracellular and extracellular magnesium status of twelve women with variant angina: group A (≥ 4 attacks/week, n = 5) and group B (< 4 attacks/week, n = 7). Magnesium levels were determined in serum, urine, and erythrocytes, and the 24-h magnesium retention rate was calculated by magnesium loading test. Group A showed a higher 24-h magnesium retention rate (58.2 ± 9.1% vs. 31.3 ± 4.4%; p < 0.01) and a lower intracellular concentration of magnesium in erythrocytes than group B (3.1 ± 1.1 vs. 5.0 ± 0.8 fg/cell; p < 0.05), demonstrating the presence of magnesium deficiency in group A. The 24-h magnesium retention rate and intracellular concentrations of magnesium in erythrocytes correlated well with the activity of variant angina (r = 0.61, p < 0.01; and r = –0.74, p < 0.01, respectively) for these patients. This study demonstrates that the degree of intracellular magnesium deficiency in women with variant angina is closely related to the frequency of chest pain.

A 56-year-old woman hit by the heavy objects was admitted to the emergency room. ECG changes and increased CK-MB and troponin I suggested acute myocardial infarction. Three weeks later, coronary angiography was performed and revealed a spiral intimal dissection in the proximal left anterior descending coronary artery. Patient underwent angioplasty and percutaneous coronary intervention (PCI) in the left anterior descending artery. She felt good and discharged on 7 days later after procedure.

Objective To investigate the characteristics of supraventricular tachycardia affiliated with left concealed atrioventrieular accessory pathway (AP) with rapid rate dependent ventriculoatrial conduction and the experience of electrophysiological (EP) study and radiofrequency catheter ablation (RFCA) in these cases. Methods 8 patients, 5 male, 3 female, aged from 24 to 62 years, who all had symptoms of paroxysmal palpitation and whose ECG recorded at the onset of tachycardia all manifested as narrow QRS complex, underwent electrophysiologic study and RFCA by the routine method, which including the properties of ventriculoatrial conduction while pacing (s 1 s 1 ) were performed in right ventricular apex (RVA) and left ventricle, mapping AP and RFCA. Result 8 cases were all left concealed atrioventrieular AP. In all patients that special kind of atrioventrieular AP with rapid rate dependent ventriculoatrial conduction were demonstrated to exist by EP study and the atrio-ventrieular reentrant tachycardia with the earliest atrial activated site located were induced. When pacing with slow rate in RVA, there were no ventriculoatrial conduction by AP; when pacing with fast rate, there were internal ventriculoatrial conduction by AP and when pacing with faster rate, there were 1:1 ventriculoatrial conduction by AP. Ablation were identified during rapid rate ventricular pacing and a successful ablation was attained in every patient. Conclusion Rapid rate dependent conduction of left concealed atrioventricular accessory pathway is existent and it can also induce atrioventrieular reentrant tachycardia. We should pay attention to it avoiding missed diagnosis.

Objectives In the last few years awareness of ventricular electrical storm has increased. The clinical onest of ventricular electrical storm is dangerous. Electrical storm typically has a poor outcome. The mechanisms that trigger ventricular electrical storm are poorly understood. Managing its acute presentation is a challenge, and mortality is high both in the acute phase and in the long term. Here we analyse the cause and management of ventricular electrical storm. Methods We conducted a restrospective analysis during last 5 years in our hospital. To review and assess the causes, differential diagnosis and treatment with ventricular electrical storm (VES). VES was defined by 2 or more sustained episodes of ventricular tachycardia or ventricular fibrillation within 24 hours. Results A total of 16 cases (male 11 cases, mean age 49.6 ± 4.5 years (range from 17∼70) with ventricular electrical storm (ES) were included. Causes of ventricular ES included: Acute myocardial infarction (n = 7), Brugada syndrome (n = 1), Dilated cardiomyopathy (n = 3), Hypertrophic obstructive cardiomyopathy after percutaneous transluminal septal myocardial ablation (n = 1), Hypokalemia accompany with QT prolongation (n = 1), Acute myocarditis (n = 1), Aconitine poisoning (n = 1), Cerebral haemorrhage (n = 1). All patients were treated with electrical conversion or defibrillation emergently with averagely 4.2 times. 3 cases were died, 13 cases were survival after therapies mentioned as follows : One was treated with potassium and magnesium supplement; 5 cases were received intravenous injection of amiodarone, lidocaine and magnesium sulfate; 7 cases were resistant to the antiarrhythmic drugs mentioned above, and were successful management by intravenous injection of esmolol. After the ventricular ES subsided, 3 cases accepted ICD implantation, 11 cases treated with amiodarone and betaloc oral maintenance. None of VES recurrence were monitored during a half year follow-up. Conclusions Ventricular electrical storm often occurs in patients who have structural heart disease, Especially in patients with myocardial ischaemia. Electrical conversion or defibrillation is the first step in order to maintain the haemodynamic stable. other management involves determining and correcting the underlying ischaemia, electrolyte imbalances, or other causative factors. Combining use of antiarrhythmic drugs is necessary, The early use of beta-blocking agent especially esmolol is essential.

Aims In this article, we determined the influence of chronic high glucose concentration on human cardiac fibroblasts functions and the effects of 606A and imidaprilat in these responses. Methods Human cardiac fibroblasts were long-time exposure in normal or high glucose media in the absence or presence of 606A or imidaprilat. MMP-2 activities were determined by using in-gel zymography. Collagen χ synthesis was evaluated by ELISA. Results show that chronic high glucose concentration inhibits the activity of MMP-2 and accelerates collagen χ synthesis. When Equimolar mannitol was used as an osmotic control, the activity inhidition of MMP-2 were also observed. Inhibition of MMP-2 activity and enhancement of collagen χ synthesis were reserved incompletely by 606A. But complete reservation of MMP-2 activity and collagen χ synthesis was observed by using imidaprilat in cultured media in the experiments. Conclusions Chronic high glucose inhibits the activity of MMP-2 and increases collagen χ synthesis by means of regulating MMP-2 mRNA expression in human cardiac fibroblasts through osmotic and non-osmotic pathways. Inhibition of MMP-2 activity and enhancement of collagen χ synthesis were reserved incompletely by 606A. But complete reservation of MMP-2 activity and collagen χ synthesis was observed by using imidaprilat in cultured media in the experiments.

Aims To determine the influence of high glucose and interleukin 1β (IL-1β) on human cardiac fibroblasts functions and the effects of eplerenone in these responses. Methods and results Human cardiac fibroblasts were cultured in normal or high glucose media in the absence or presence of IL-1β and/or eplerenone. MMP-2 activities were determined by using in-gel zymography. mRNA expression of MMP-2 and TIMP-2 were evaluated by rt-PCR. Results show that high glucose stimulates the activity of MMP-2 and accelerates MMP-2 mRNA synthesis. When Equimolar mannitol was used as an osmotic control, the activity enhancement of MMP-2 were also observed. We have also found that MMP-2 activity and mRNA expression were improved significantly (∼2×) by using the combination of high glucose and IL-1β as compared with using high glucose or IL-1β alone. Increase of MMP-2 activity and mRNA expression were blocked by eplerenone, that is, neither high glucose nor IL-1β has impacted TIMP-2 mRNA expression in the experiments. Conclusions High glucose increases the activity of MMP-2 by means of regulating MMP-2 mRNA expression in human cardiac fibroblasts through osmotic and non-osmotic pathways. Combining IL-1β with high glucose was found to increase significantly the MMP-2 activity and mRNA expression in human cardiac fibroblasts as compared with using IL-1β or high glucose in dividedly. However, such induced effects can be readily normalised by the use of Eplerenone.

Blunt chest trauma can cause several forms of cardiac injury. of these, coronary artery dissection and acute myocardial infarction is a rare complication. We report two cases of the left anterior descending coronary artery dissection and acute myocardial infarction after blunt chest trauma.

Blunt chest trauma can cause several forms of cardiac injury. Of these, coronary artery dissection and acute myocardial infarction is a rare complication. We report two cases of the left anterior descending coronary artery dissection and acute myocardial infarction after blunt chest trauma.

Objective To measure the relationship between responses of blood pressure to exercise stress and changes of endothelium dependent vasodilatation in rest blood pressure well-controlled patients with hypertension. Method 60 rest blood pressure were well-controlled patients with hypertension were divided into two groups: exercise hypertension (Group A) and normal exercise blood pressure (Group B), and 30 normal persons were cotrol group (Group C). Endothelium-dependent vasodilatation was assessed in the brachial artery by high resolution ultrasound technique before exercise and exercise stress test was assessed by 6-min walking test. Blood pressure (BP) and heart rate was measured before, at the time of the end of exercise and at 10, 20, 30 min after exercise. The serum concentrations of nitric oxide (NO), endothelin -1(ET-1) were measured before exercise and at the time of the end of exercise. Result Compared with group B and Group C, FMD% in Group A significantly decreased (p Conclusion BP could increase after exercise in rest blood pressure well-controled patients with hypertension. Endothelium dependent vasodilatation, the serum concentrations of NO, but not the serum concentrations of ET-1 could be related to change of DBP and SBP.

Matrix metalloproteinases (MMPs) that participate in extracellular matrix degradation have been involved in atherosclerotic plaque growth and instability. It has been demonstrated that statins could inhibit secretion of metalloproteinases from vascular smooth muscle cells and macrophages in vitro. This study investigated the effects of rosuvastatin on sterol synthesis and the expression of matrix metalloproteinases in LDLR-deficient mice. Methods: LDLR-deficient mice on a high-fat and high-cholesterol diet developed plasma hyperlipemia and atherosclerosis. They were randomly given into rosuvastatin group (n=8), control group (n=8), and they were sacrificed after 12 weeks. We examined the levels of plasma lipid; the expression of MMP-2 and MMP-9 with zymography; the morphological of the aorta artery; theH&E and immunohistochemicalwith aorta sinus. Conclusions: Rosuvastatin inhibits MMP-2 and MMP-9 expression and improves the progression of atherosclerosis in LDLR-deficient mice exposed to a high-fat and high-cholesterol diet. This may be one of the pleiotropic effects of rosuvastatin and benefits the therapy of many kinds of dyslipidemia, including familial hypercholesterolemia.

Objectives This work aimed to study the delayed electrocardiographic changes, including Q-T interval, corrected Q-T dispersion, and heart rate variability (HRV) 3 years after percutaneous transluminal septal myocardial ablation (PTSMA), in symptomatic patients with hypertrophic obstructive cardiomyopathy (HOCM). Methods In 26 patients (11 women, 15 men; average age, 37.4 ± 11.2 years) with symptomatic and medically refractory HOCM, 1.4 ± 0.5 septal branches were occluded with an injection of 3.8 ± 1.3 mL of alcohol (95%) to ablate the hypertrophied interventricular septum. Baseline and 3 days and 3 years postprocedure 24-hour Holter electrocardiographic findings were determined. Results One patient developed complete atrioventricular block requiring permanent pacing. The PR interval was significantly prolonged 3 days after ablation, but recovered 3 years postprocedure. Three days after the procedure, all patients developed right bundle branch block, which was present in 24 patients after 3 years. The QRS duration was significantly prolonged 3 days after ablation and during 3 years of follow-up. There was significant and persistent prolongation of QT interval and transient prolongation of corrected QT dispersion 3 days after ablation and returned to preablation values 3 years postprocedure, but JT interval and corrected JT dispersion were not significantly changed after PTSMA. Heart rate variability data (time domain and frequency domain) 3 days and 3 years after PTSMA, including low frequency, high frequency, root mean squared successive difference interval, and the percent of sinus cycles differing from the preceding cycle by more than 50 milliseconds, significantly increased compared to that before the procedure. Low frequency/high frequency, SD of all normal-to-normal intervals, and SD of 5-minute average normal-to-normal intervals were not significantly changed after PTSMA. Conclusions Percutaneous transluminal septal myocardial ablation for HOCM induces significant delayed electrocardiographic changes in most patients. The changes include QRS prolongation, new right bundle branch block, persistent QT prolongation, transient QT dispersion and PR prolongation, and changes in HRV data. Electrocardiographic long-term follow-up of a larger series of patients is required to determine the conclusive therapeutic significance.

To explore the active ingredients in Chinese yellow wine which could inhibit the progress of atherosclerosis in LDLR knockout mice. Six weeks old LDLR-/- male mice (n=56) were randomly allocated into 7 groups (8 mice in each group): normal control group (NC), high fat group (HF), high fat and

To determine similarities in effect of yellow wine as compared statin and the possibility that yellow wine on rat vascular endothelial cells induced by TNF-α. Isolation, cultivation, purification and identification of vascular endothelial cells of rat thoracic aorta in vitro were conducted. The