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Type 2 diabetes mellitus (DM) accounts for more and more individuals worldwide. D-dimer has been demonstrated to be associated with cardiovascular diseases. The aim is to study the potential impact of D-dimer on the long-term prognosis of acute coronary syndrome (ACS) in the special population with type 2 DM.A total of 2265 consecutive patients with DM and ACS were eligible in the study. Patients were divided into four groups according to quartiles of D-dimer concentration. Univariate and multivariate Cox regression analysis were conducted to explore the prognostic value of D-dimer for future outcomes. Patients with higher level of D-dimer presented with higher percentage of major adverse cardiovascular events (MACEs) (23.7%), all-cause death (18.3%) and cardiovascular (CV) death (9.4%) in Quartile 4. In multivariate Cox regression analysis, D-dimer was demonstrated to be independently associated with MACEs, all-cause death and CV death. The prognostic value of D-dimer is still significant in subgroups of HbA1C7% and ≥7%. In Kaplan-Meier analysis, higher D-dimer showed poorer prognosis in MACEs, all-cause death and CV death (all log rank p 0.001). The area under the curve (AUC) by receiver operating characteristic (ROC) curve analysis is 0.609 for MACEs, 0.708 for all-cause death, 0.747 for CV death (p 0.001).The present study demonstrated the independent predictive value of D-dimer for outcomes in DM patients with ACS. In addition, for the first time, we explored the prognostic value in different glucose control status.

Long non-coding RNAs (lncRNAs) have been validated to mediate the development of atherosclerosis (AS). In the present study, the molecular mechanisms and functions of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in the advancement of human aortic endothelial cells (HAECs) were investigated. The levels of lncRNA-NEAT1 and miR-638 expression in clinical samples and cells were explored via quantitative reverse transcription polymerase chain reaction. Colony formation and CCK-8 assays were performed to determine the proliferative capacity of cells, and the apoptotic capacity of cells was analyzed on the basis of apoptotic cell proportion and caspase-3 activity. Then, the proportion of cells and correlations among phosphoglycerate kinase 1 (PGK1), NEAT1, and miR-638 were determined through RNA immunoprecipitation and luciferase assays and bioinformatics analysis. Moreover, the expression levels of Ki-67, proliferating cell nuclear antigen, PGK1, Bax, Bcl-2, (p)-mTOR, (p)-AKT, and β-catenin were analyzed via western blot analysis. In the serum of patients with AS and HAECs induced by oxidized low-density lipoprotein (ox-LDL), the expression level of miR-638 was decreased, whereas that of NEAT1 was increased. After ox-LDL therapy, NEAT1 knockdown suppressed HAEC proliferation and stimulated HAEC apoptosis, which could be reversed by the miR-638 inhibitor. NEAT1 inhibited miR-638 expression through direct mutual action. The following mechanical investigations revealed that PGK1 was a miR-638 target, whose expression was increased by NEAT1, a competing endogenous RNA of miR-638. Additionally, the miR-638 inhibitor contributed to proliferation and suppressed apoptosis through the activation of the AKT/mTOR signaling pathway in ox-LDL-induced HAECs. NEAT1 adjusted the AKT/mTOR signaling pathway via miR-638 in ox-LDL-induced HAECs to accelerate their proliferation and impede their apoptosis. This result revealed that NEAT1 may be valuable in the treatment of AS.

The efficacy and safety of proprotein convertase subtilisin/kexin type 9 (PCSK-9) inhibitors were confirmed by several clinical trials, but its effectiveness in routine clinical practice in China has not been evaluated. This study aims to describe the real world effectiveness of PCSK-9 inhibitors combined with statins compared with statins-based therapy among patients with very high risk of atherosclerotic cardiovascular disease (ASCVD).This is a multi-center observational study, enrolled patients from 32 hospitals who underwent percutaneous coronary intervention (PCI) from January to June in 2019. There are 453 patients treated with PCSK-9 inhibitors combined with statins in PCSK-9 inhibitor group and 2,610 patients treated with statins-based lipid lowering therapies in statins-based group. The lipid control rate and incidence of major adverse cardiovascular events (MACE) over six months were compared between two groups. A propensity score-matched (PSM) analysis was used to balance two groups on confounding factors. Survival analysis using Kaplan-Meier methods was applied for MACE.In a total of 3,063 patients, 89.91% of patients had received moderate or high-intensity statins-based therapy before PCI, but only 9.47% of patients had low-density lipoprotein cholesterol (LDL-C) levels below 1.4 mmol/L at baseline. In the PSM selected patients, LDL-C level was reduced by 42.57% in PCSK-9 inhibitor group and 30.81% (In the real world, PCSK-9 inhibitors combined with statins could significantly reduce LDL-C levels among patients with very high risk of ASCVD in China. The long-term clinical benefits for patients received PCSK-9 inhibitor to reduce the risk of MACE is still unclear and requires further study.

Background The efficacy and safety of PCSK-9 inhibitors were confirmed by several clinical trials, but its effectiveness in routine clinical practice in China is unknown. Objective To describe the real world effectiveness of initiated with PCSK-9 inhibitors combined with statins compared with statins among patients with very high risk of ASCVD and underwent percutaneous coronary intervention (PCI). Methods This is a prospective study, enrolled patients from 32 hospitals between January to June 2019. The lipid control rate and incidence of cardiovascular events over 6 months were compared between two groups. A propensity score-matched analysis was used to balance two groups on confounding factors. Survival analysis using Kaplan-Meier methods was applied for cardiovascular events. Results In a total of 3063 patients, 89.91% had received moderate or high-intensity statin therapy before PCI, but only 9.47% had LDL levels below 1.4mmol/L at baseline. In the PSM selected patients, LDL level was reduced by 42.57% in PCSK-9 inhibitor group and 30.81% (P

The present study aimed to investigate the effects of lipoprotein-associated phospholipase A2 (Lp-PLA2) on endothelial dysfunction in an in vitro cell model of atherosclerosis, and to determine whether AMP-activated protein kinase (AMPK) mediates the effects of Lp-PLA2 on endothelial dysfunction. A total of 392 patients with coronary artery disease (CAD), including various sub-conditions, were recruited, and the plasma concentrations of Lp-PLA2 were evaluated. In addition, an in vitro model of atherosclerosis was established by exposing human umbilical vein endothelial cells (HUVECs) to oxidized low-density lipoprotein (oxLDL). SB-435495 was used to inhibit Lp-PLA2, and compound C was used to suppress AMPK expression. Lp-PLA2, AMPKα and phosphorylated-AMPKα (T172) expression in HUVECs were evaluated using western blot analysis. The concentrations of nitric oxide (NO), endothelin 1 (ET-1), intercellular adhesion molecule 1 (ICAM-1) and platelet/endothelial cell adhesion molecule 1 (PECAM-1) in cell culture supernatant were determined using commercially available ELISA kits. MTT assays were employed to indicate changes in cell viability. The current study found the plasma Lp-PLA2 levels were elevated in the CAD patients with stable angina pectoris, unstable angina pectoris, acute coronary syndromes and acute myocardial infarction, compared with a healthy control population. In addition, the in vitro results showed that Lp-PLA2 expression levels were elevated in oxLDL-exposed HUVECs. Lp-PLA2 suppression could increase cell viability, induce the production of NO and decrease the secretion of ET-1, in addition to suppressing the expression of cell adhesion molecules, including ICAM-1 and PECAM-1 in oxLDL-exposed HUVECs. The expression of AMPKα and phosphorylated-AMPKα (T172) was regulated by Lp-PLA2, and AMPK suppression was able to reverse the effects of Lp-PLA2 with regard to cell viability, endothelial vasorelaxation capacity and the secretion of adhesion molecules in oxLDL-exposed HUVECs. In conclusion, the present study provides initial evidence that Lp-PLA2 is able to cause endothelial dysfunction in an in vitro model of atherosclerosis, and the effects of Lp-PLA2 on endothelial dysfunction was at least partially a result of the downregulation of AMPKα, thus contributing to the progression of atherosclerosis.

Background Reserpine is currently used by millions of Chinese hypertensive patients, in spite of the continued concern of its depressogenic effect, even when used in low dose. This study aimed to investigate the association between low-dose reserpine use and depression in older Chinese hypertensive patient. Methods In this cross-sectional, case-control study, we recruited patient aged 60 years or over who had regularly taken one or two tables of “compound reserpine and triamterene tablets (CRTTs)” for more than one year (reserpine user) from 26 community health centers located in 10 provinces in China. For each patient who took CRTTs, we selected an age (within five years) and sex matched hypertensive patient who had never taken any drugs containing reserpine (non-reserpine user) as control. Depressive symptoms were evaluated using a Chinese depression scale adapted from the Zung Self-Rating Depression Scale. Demographic, clinical data and laboratory examination results within six months were collected. Results From August 2018 to December 2018, 787 reserpine user and 787 non-reserpine user were recruited. The mean age of all study subjects was 70.3 years, with about equal numbers of males and females. The mean depression score was 40.4 in reserpine users and 40.6 in non-reserpine users (P = 0.7). The majority of study subject had a depression score < 53 (87.6% in reserpine users and 88.2% in non-reserpine users, respectively). There were no significant differences in the prevalence of mild, moderate or severe depression in reserpine users and non-reserpine users. Conclusions There is no association between low-dose reserpine use and depression in older hypertensive patient. The role of reserpine in the treatment and control of hypertension should be reconsidered; and further studies, especially randomized, controlled clinical trials to compare efficacy and safety of reserpine and other widely recommended anti-hypertensive agents are needed.

To explore the efficiency and safety of bivalirudin in patients undergoing emergency percutaneous coronary intervention via radial access.Bivalirudin reduces bleeding risks over heparin in patients undergoing PCI. However, bleeding advantages of bivalirudin in patients undergoing transradial intervention is uncertain.In the BRIGHT trial, 1,723 patients underwent emergency PCI via radial access, with 576 patients in the bivalirudin arm, 576 in the heparin arm and 571 in the heparin plus tirofiban arm. The primary outcome was 30-day net adverse clinical event (NACE), defined as a composite of major cardiac and cerebral events or any bleeding.30-day NACE occurred in 5.7% with bivalirudin, 7.8% with heparin alone (vs. bivalirudin, P = 0.159), and 10.3% with heparin plus tifofiban (vs. bivalirudin, P = 0.004). The 30-day bleeding rate was 0.9% for bivalirudin, 2.3% for heparin (vs. bivalirudin, P = 0.057), and 5.8% for heparin plus tirofiban (vs. bivalirudin, P 0.001). Major cardiac and cerebral events (4.9 vs. 5.7 vs. 4.6%, P = 0.899), stent thrombosis (0.5 vs. 0.5 vs. 0.7%, P = 0.899) and acquired thrombocytopenia (0.2 vs. 0.5 vs. 0.9%, P = 0.257) at 30 days were similar among three arms. The interaction test for PCI access and randomized treatment showed no significance on all bleeding (P 0.05).The bleeding benefit of bivalirudin was independent of artery access. Bivalirudin lead to statistical reduction on bleeding risks in comparison to heparin plus tirofiban, and only small numerical difference in comparison to heparin, with comparable risks of ischemic events and stent thrombosis in patients with acute myocardial infarction (AMI) undergoing emergency transradial PCI. © 2016 Wiley Periodicals, Inc.

Although several studies have suggested that intensive statin pretreatment could reduce the incidence of procedure-related myocardial infarction in western population, the data on the effect in Asian patients have been still limited. The aim of the study was to investigate the efficacy and safety of intensive atorvastatin load in Chinese patients undergoing elective PCI. A total of 1202 patients with stable angina or non-ST-segment elevation acute coronary syndrome (NSTE-ACS) scheduled to undergo PCI received either intensive statin treatment (80 mg atorvastatin daily × 2 days before PCI and 40 mg daily × 30 days after PCI) or usual care. The primary endpoint was incidence of major adverse cardiac events (cardiac death, myocardial infarction, or unexpected target vessel revascularization) within 30 days after PCI. Safety endpoints include the incidence of contrast induced nephropathy (CIN), ALT/AST >3 upper limit of normal (ULN), CK >5 ULN. The incidence of 30-day MACE did not significantly differ between the intensive group and control group (19.4 vs 18.3%, P = 0.63). Multivariate analysis revealed age (OR = 1.024, 95% CI 1.003–1.045, P = 0.023) and total stent length as an independent predictor of 30-day MACE (OR = 1.012, 95% CI 1.007–1.018, P < 0.0001). The incidence of CIN was comparable between intensive group and control group (4.09 vs 4.39%, P = 0.795). No significant differences were observed in other safety profile at all follow-ups between treatment groups. The ISCAP trial demonstrated that serial intensive atorvastatin therapy did not improve the clinical outcome with similar safety profile comparing with usual care among Chinese patients undergoing elective PCI.

Objective We aimed to investigate the association between the 5A/6A promoter polymorphism in the matrix metalloproteinase 3 ( MMP3 ) gene and in-stent restenosis (ISR) in a regional Chinese population. Methods A total of 818 patients who underwent primary implantation of drug-eluting stents were enrolled and received a 6-month follow-up angiography and DNA genotyping of the 5A/6A polymorphism. Results ISR was found in 36.9% of all patients (302 ISR vs. 516 no ISR). The genotype proportion of 6A6A was significantly increased in ISRs (74.2% ISR vs. 66.8% no ISR), whereas the allele frequency of 5A was significantly decreased in ISR patients (25.8%) compared with controls who did not undergo ISR (33.1%). Conclusions Our data indicate that the MMP3 6A6A genotype is a genetic susceptibility factor for ISR after coronary stent placement, but the 5A allele can lower the risk for patients within 6 months after stenting. Therefore, genotyping 5A/6A in the MMP3 promoter is suggested for patients who undergo coronary stent implantation.

Objective The aim of this study was to investigate the correlations between risk factors such as hypertension and the complex degrees of coronary arterial lesions (CAL). Methods We selected 462 patients with coronary heart disease (CHD) with confirmed the stenosis (≥50 %) in at least one major coronary artery on coronary angiography and divided them into the “CHD with hypertension” group (CHD-HT, n = 306) and the CHD group (n = 156). The characteristics of CAL and the occurrence of 2-year postoperative major adverse cardiac cerebrovascular events (MACCE) in the two groups were observed. Results The mean SYNTAX scores (SS) was higher in the CHD-HT group than in the CHD group (P

To explore diagnostic performance of mean platelet volume (MPV) for acute myocardial infarction (AMI) of patients with acute coronary syndrome (ACS).We compared MPV and other indicators of 1,524 patients with ACS. Among them, 880 patients were diagnosed with AMI, 344 were diagnosed with unstable angina pectoris and 350 were the control group.The level of MPV in ACS group was significantly higher than the control group (9.5 ± 1.34fL versus 7.9 ± 1.03fL, P0.001). Additionally, MPV of AMI group was higher than unstable angina pectoris (9.4 ± 1.30fL versus 9.2 ± 1.42fL, P0.001). Increased MPV could be identified as an early independent predictor of AMI (odds ratio = 1.957, 95% CI: 1.389-2.758, P0.001). The area under the receiver operating characteristic curves curve for MPV combined with troponin I (TnI) was 0.816, the sensitivity (68.81%) and the specificity (97.98%) at the best cut-off value were higher than using MPV or TnI alone respectively.MPV has been shown as an independent risk factor for early onset of AMI and can be applied to assist AMI diagnosis of ACS patients. Additionally, measuring MPV in conjunction with TnI levels can improve the diagnostic performance of TnI with higher sensitivity and specificity.

To investigate the association between inflammatory mediators, matrix degrading enzymes and acute coronary syndrome (ACS) and the impact of early reperfusion therapy on circulating biomarkers.Peripheral serum levels of interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP) and matrix metalloproteinase-9 (MMP-9) were determined in 134 patients with ACS. These biomarkers were serially monitored in ten patients with intravenous thrombolytic therapy (IVT).Serum levels of IL-6, hs-CRP and MMP-9 were higher in unstable angina (UA) and myocardial infarction (MI) groups than in control or SA group (p0.05). Peripheral IL-6 level in patients with MI was greater after percutaneous coronary intervention (PCI) (p0.01) or IVT (p0.05). Serial concentration determination revealed marked elevation of serum IL-6 and MMP-9 levels, both reaching peak values (like creatine kinase-MB).Elevated levels of IL-6, hs-CRP and MMP-9 provide a link between inflammation, matrix degradation and the development and progression of ACS. IL-6 and MMP-9 appear to be released mainly from vulnerable plaque or necrotic myocardium during the acute phase of MI.

Inflammatory responses in the blood vessel play a pivotal role in the pathogenesis of atherosclerosis. Eupatilin, a flavone derived from Artemisia princepsPampanini, has various pharmacological activities, including antioxidant, anti-tumor, and anti-inflammatory capacities. However, there has been no research examining the function of eupatilin on vascular inflammation. Therefore, the aim of this study was to investigate the effects of eupatilin on tumor necrosis factor (TNF)-α-induced human umbilical vein endothelial cells (HUVECs) activation and the underlying molecular mechanisms. Our findings showed that eupatilin reduced U937 cells adhesion to TNF-α-stimulated HUVECs and attenuated TNF-α-induced the expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) in HUVECs, as well as the production of intracellular reactive oxygen species (ROS). Moreover, eupatilininhibits TNF-α-induced phosphorylation of NF-kB p65 and MAPKs in HUVECs. Taken together, the results of the present study suggest that eupatilin inhibited inflammatory reaction through suppressing the ROS/MAPK-NF-ĸB pathway in HUVECs. Thus, eupatilin is proposed as an effective new anti-inflammatory agent to suppress vascular inflammation, and further prevent atherosclerosis.

‘Artificial blood vessels’ were grown in the peritoneal or pleural cavities of the dog for autologous transplantation as arterial interposition grafts. Tubing up to 250 mm long, either bare or wrapped in biodegradable polyglycolic acid (Dexon) mesh, was inserted into the body cavities using minimally invasive techniques. After 3 weeks, the tubes and their tissue capsules were harvested then the inert tubing discarded. The wall of living tissue was uniformly 1–1.5 mm thick and consisted of multiple layers of myofibroblasts that stained for α-smooth muscle actin, and extracellular matrix overlaid by a single layer of mesothelium. The bursting strength of tissue tubes with no biodegradable mesh scaffolds was in excess of 2500 mm Hg and the suture holding strength was 11.5 N. Tissue tubes (5–7 cm) were transplanted as interposition grafts into the femoral artery of the same dog in which they were grown where they remained patent until harvest at 3 to 6.5 months. Endothelial-like cells lined the lumen and the cells of wall stained for α-actin, smooth muscle myosin and smoothelin; a thick ‘neo-adventitia’ contained vasa vasorum. These studies demonstrate that peritoneal and pleural cavities of large animals can function as a bioreactor to grow tissue tubes for use as autologous vascular grafts.

Background Given the increasing number of patients who require dual antiplatelet (DAP) therapy and electrophysiological device (EPD) placement, perioperative antiplatelet management is a current challenge. In this study, we investigated the incidence of pocket hematoma formation after EPD placement in patients undergoing DAP therapy or an alternative low-molecular-weight heparin (LMWH) regimen. Methods This clinical observational study was performed from July 2010 to July 2012. In total, 171 patients were enrolled in the analysis after meeting the inclusion criteria. These patients were divided into two groups: 86 patients were treated with DAP therapy at the time of device implantation, and the DAP therapy was discontinued for 5 to 7 days and replaced with enoxaparin before device implantation in the other 85 patients. Adenosine phosphate (ADP)-mediated platelet aggregation and arachidonic acid-induced platelet aggregation were tested preoperatively. We compared the incidence of pocket hematoma between the two groups and the association of pocket hematoma development with ADP-mediated platelet aggregation and arachidonic acid-induced platelet aggregation. Results The incidence of pocket hematoma in the patients who continued DAP was lower than that in the patients who replaced the dual antiplatelet regimen with LMWH (3.49% vs. 16.47%, respectively; X2 = 6.66, P < 0.01). Among the patients who continued DAP therapies, the rate of ADP-mediated platelet aggregation inhibition in patients with pocket hematomas was higher than that in patients without pocket hematomas. None of the patients undergoing DAP or enoxaparin therapy developed pocket infection, thromboembolic events, or other serious complications. Multiple logistic regression analysis revealed that LMWH therapy was an independent risk factor for the development of pocket hematoma (RR = 0.054, 95%CI = 0.012–0.251). Furthermore, patients undergoing LMWH therapy were 5.1-fold more likely to develop pocket hematomas than were DAP-treated individuals. Conclusion Continuance of DAP therapy does not increase the risk of pocket hematoma formation after EPD placement.

to evaluate the correlation between the severity of coronary artery lesion and multiple risk factors of events of coronary heart disease (CHD) in patients with coronary arteriography (CAG) in Tianjin.A retrospective study was conducted. One thousand six hundred and twenty-nine patients with CHD as diagnosed with CAG in Tianjin Chest Hospital were enrolled in the study. Using the SYNTAX score to evaluate the outcomes of CAG, The patients wer divided into three groups, i.e. low (0-22, n=962), medium (23-32, n=446) and high (≥ 33, n=221) score groups. The relationship between the severity of CHD patients analysis.The single factor analysis results showed that the severer the coronary artery lesion, the higher the SYNTAX score, the higher the proportion of patients having one of single risk factors (old, male, smoking, hypertension, type 2 diabetes mellitus, blood lipid abnormality), the lower the high density lipoprotein cholesterol (HDL-C), and the higher the low density lipoprotein cholesterol (LDL-C), total cholesterol (TC) level, fibrinogen (FIB) content, and body mass index (BMI, all P0.01). The logistic regression analysis showed that male, old age, hypertension, typed 2 diabetes mellitus, TC were the independent risk factors in aggravating the severity of CHD. Hypertension [ odds ration (OR)=3.947, 95% confidence interval (95% CL) 1.45-10.704, P0.001] and type 2 diabetes mellitus (OR=5.760, 95% CI 2.549-13.018, P0.001) were the two most prominent predictors for CHD, while HDL-C was the protective factor for CHD (OR=0.541, 95% CI 0.295-0.992, P=0.992, P=0.004). CONCLUSION. The severity of CHD was closely related to CHD was closely related to various risk factors, among them hypertension and type 2 diabetes mellitus were the most predominant risk factors of CHD. Therefore it should be emphasized that clinicians should control blood pressure, blood glucose, and also blood lipid level in CHD patients to prevent cardiac event.

To explore the polymorphism of cholesteryl ester transfer protein (CETP) gene -629C/A among the coronary heart disease (CHD) Han population of Tianjin area and evaluate the influences of genetic factors on atorvastatin therapeutic effects and clinical outcomes in pharmacogenomics and provide theoretical rationales for individualized treatment.A total of 332 angiographically confirmed CHD patients at Tianjin Chest Hospital were recruited from October 2010 to July 2011. The CETP gene promoter polymorphism at position -629 was determined by polymerase chain reaction-restricted fragment length polymorphism (PCR-RFLP). The serum level of CETP was determined by enzyme-linked immunosorbent assay (ELISA).Lipid levels were determined at baseline and 12 months post-treatment with 20 mg/d atorvastatin in all patients. Clinical follow-up were performed for more than 1 year (range, 12-23 months). And major adverse cardiac events (MACE, including death, non-fatal infarction, revascularization and stroke) were analyzed. The Kaplan-Meier Log-rank test was used to compare MACE-free survival between different genotypes.(1) The frequencies of variant -692A allele was 0.476, AA genotype showed reduced CETP levels and higher HDL-C levels compared with CC and CA genotypes. But it did not reach statistical significance (F = 0.893, P = 0.411 and F = 1.279, P = 0.282 respectively). Although a negative trend correlation existed between serum levels of HDL-C and CETP, it did not reach statistical significance (r = -0.151, P = 0.081) . (2) After 12-month therapy of atorvastatin, CC genotype was shown to be associated with higher LDL-C, LP(a) reduction and HDL-C elevation in response to atorvastatin compared with CA and AA genotype.LDL-C levels decreased 43.5% in CC homozygotes, 25.5% in CA heterozygotes and 11.7% in AA homozygotes (P = 0.001).HDL-C levels increased 9.2% in CC homozygotes, 6.8% in CA heterozygotes and 5.5% in AA homozygotes.However the changes of HDL-C levels in three genotypes showed no significant difference (P = 0.412). (3) There was a 7.83% incidence of MACE after a mean follow-up of (18.66 ± 5.99) months. The outcomes were death (n = 3, 0.90%), non-fatal infarction (n = 7, 2.11%), revascularization (n = 13, 3.92%) and stroke (n = 3, 0.90%). The cumulative MACE free survival rates were 96.2% , 92.1% and 87.3% in CC, CA and AA genotypes respectively (Log-rank P = 0.444).Variant AA genotype shows a higher level of HDL-C s and a lowered level of CETP.However CC genotype offers a better benefit of statin therapy associated with lowered levels of LDL-C and LP(a). And the long-term clinical prognosis is not affected among three genotypes.

To investigate cholesteryl ester transfer protein (CETP) gene polymorphism -629C/A among Han Chinese patients with coronary heart disease (CHD) in Tianjin region, and to assess the influence of genetic factors on therapeutic effect of atorvastatin and clinical outcome in order to provide a pharmacogenomic basis for personalized treatment.From October 2010 to July 2011, 232 patients with angiographically confirmed CHD were recruited. Polymorphism of position -629 of CETP gene promoter was determined with polymerase chain reaction - restricted fragment length polymorphism (PCR-RFLP) method. Serum level of CETP was determined with enzyme-linked immunosorbent assay (ELISA). Lipid level in all patients was determined at baseline and after 12 months of treatment with 20 mg/d atorvastatin. Clinical follow-up was carried out for more than a year (12-23 months). Major adverse cardiac events including death, non-fatal infarction, revascularization and stroke (MACE) were recorded. A Kaplan-Meier log-rank test was used to compare MACE-free survival for individuals with various genotypes.The frequency of -629A allele was 0.408. Compared with CC or CA genotypes, individuals with AA genotype had lower CETP levels and higher high-density lipoprotein cholesterol (HDL-C) levels, albeit without statistical significance (F = 0.893, P = 0.411 and F = 1.279, P = 0.282, respectively). There also appeared to be a negative correlation between serum HDL-C and CETP levels, though no statistical significance was detected (r = -0.151, P = 0.081). After 12 months atorvastatin therapy, individuals with CC genotype had greater reduction of low-density lipoprotein cholesterol (LDL-C), reduced LP(a) and elevated HDL-C compared with CA or AA genotypes. LDL-C level has decreased by 35.41% in CC homozygotes, 18.84% in CA heterozygotes and 8.15% in AA homozygotes (P = 0.001). HDL-C level has increased by 14.37% in CC homozygotes, 10.48% in CA heterozygotes and 6.64% in AA homozygotes, respectively. However, above changes did not reach statistical significance (P = 0.470). The incidence of MACE after a mean follow-up of (18.66 ± 5.99) months was 7.76%, which included 2 (0.86%) deaths, 5 (2.16%) non-fatal infarctions, 9 (3.88%) revascularizations and 2 (0.86%) strokes. The cumulative MACE-free survival rates were 92.4%, 85.3% and 65.0% for CC, CA and AA genotypes, respectively (Log-rank P = 0.444).Our results suggested that AA variant for the -629A allele of CETP gene had higher HDL-C levels and reduced CETP levels, though patients with CC genotype appeared to have better benefited from statin therapy with reduction in LDL-C and LP(a) levels. Long-term clinical prognosis was however not affected by the 3 genotypes.

To explore the features of coronary atherosclerosis among the patients at different ages and examine their risk factors and pathological characteristics.Retrospective analysis was performed for the clinicopathologic data of 87 patients with coronary atherosclerosis confirmed through autopsy from February 1986 to December 2011 at our hospital. They were divided into 3 groups according to age (20 -40 years, n = 12; 40 -60 years, n = 24; ≥ 60 years, n = 51). Comparative analysis was performed for the degree of coronary artery stenosis and cardiac pathological changes, vulnerable plaque occurrence and morphological features of acute coronary syndrome among different patient groups.There were 56 males and 31 females with a mean age of 66.8 years (range: 23 - 80). Great statistical differences existed in the degree of coronary artery stenosis between different genders (P0.05) while there was no significant difference among the above age groups (P0.05). In the above age groups of patients with acute coronary syndrome, the incidence of big lipid core was 23.5%, 38.5% and 53.8% (χ(2) = 6.282, P = 0.043), that of thin fibrous cap 29.4%, 41.0% and 58.8% (χ(2) = 6.589, P = 0.037), that of inflammatory cell in 2 filtration 58.8%, 69.2% and 85.0% (χ(2) = 7.435, P = 0.024) and that of calcification formation 35.3%, 56.4% and 71.3% respectively (χ(2) = 8.599, P = 0.014). And the incidence of vulnerable plaque occurrence was 76.5%, 84.6% and 88.8% (χ(2) = 1.850, P = 0.397) in the above age groups.The features and risk factors of coronary atherosclerosis are different according to different ages and genders. Thus we should pay more attention to the early diagnosis and reasonable treatments of young patients and those with both mild coronary stenosis and vulnerable plaque.

To develop a simple scoring system based on preprocedural clinical features that is capable of predicting contrast-induced acute kidney injury (CI-AKI) before percutaneous coronary intervention (PCI).CI-AKI is associated with increased in-hospital morbidity and mortality, prolonged hospitalization, and long-term renal impairment. Although several scoring methods have been developed to determine risk of CI-AKI, no simple scoring method based on PCI preprocedural clinical features yet exists for Chinese patients.A total of 2,500 Chinese patients were randomly and retrospectively assigned in a 3:2 manner to create a training and validation dataset, respectively. CI-AKI was defined as an increase of ≥25% or ≥0.5 mg/dL serum creatinine within 5 days after PCI. Preprocedural clinical variables showing independent correlation to CI-AKI were used to derive the risk score from the training dataset and then subsequently tested in the validation dataset. The odds ratios from multivariate logistic regression were used to assign a weighted integer to age ≥70 years = 4, history of myocardial infarction = 5, diabetes mellitus = 4, hypotension = 6, left ventricular ejection fraction ≤45% = 4, anemia = 3, creatinine clearance rate60 mL/min = 7, decreased high-density lipoprotein1 mmol/L= 3, and urgent PCI = 3. Summation of the integers represented the total risk score.The overall incidence of CI-AKI in the training dataset was 16.4% [246/1500; 5.4% for low (≤7) and 61.3% for very high (≥17) risk scores]. The rates of CI-AKI, 1-year dialysis, and 1-year mortality increased significantly with each group (Cochran-Armitage test of trend, P0.001). The risk score facilitated appropriate classification of patients with low and high risk for CI-AKI after PCI in the validation dataset (c-statistic = 0.82).Risk classification based on the most significantly correlated parameters is useful for predicting CI-AKI before contrast exposure. The simple preprocedural score showed excellent predictive ability for identifying patients at high risk of nephropathy and those with deteriorative prognosis after PCI.

To develop a simplified risk scoring system of contrast induced nephropathy (CIN) after percutaneous coronary intervention (PCI).A retrospective study was performed on 1500 patients in the development set undergoing PCI from January 2008 to December 2009. And 1000 patients treated from January 2010 to May 2011 were selected for the validation set. Logistic regression analysis was applied to identify the risk factors of CIN. Based on the odds ratio, the sum of integers was a total risk score for each patient.(1) Among them, CIN occurred in 246 patients with an overall incidence of 16.4%. (2) Eleven identified variables were identified as the risk factors of CIN (with weighted integer): diabetes (3 scores), hypotension (3 scores), left ventricular ejection fraction (LVEF ≤ 45%) (3 scores), eGFR60 [ml×min(-1)·(1.73 m(2))(-1)] (3 scores), age70 years (2 scores), myocardial infarction (2 scores), emergency PCI (2 scores), anemia (2 scores), decreased high-density lipoprotein (HDL) concentration (1 mmol/L) (2 scores), contrast agent dose200 ml (2 scores) and low permeability contrast agent (1 score). (3) The sum of integers was a total risk score for each patient. The incidence of CIN was 5.2% in the low-risk group (≤ 4), 13.6% in the moderate-risk group (5 - 10), 32.3% in the high-risk group (11 - 14) and 59.0% in the very-high-risk group (≥ 15). (4) Good discriminative power was found in the validation population. And the risk score was strongly correlated with CIN (c-statistic = 0.82).This scoring system provides a good estimate of the risk of CIN after PCI. It may be used for the prevention and treatment of CIN.

To investigate the impact of depression on clinical outcome of patients undergoing revascularization.Self-rating depression scale (SDS) assessment was made before and after coronary artery bypass grafting (CABG, n = 345) and percutaneous coronary intervention (PCI, n = 308) procedure. Patients were divided into depression and non-depression group. All patients were followed up for 12 months after procedure for the occurrence of rehospitalization and major adverse cardiovascular events (MACE) including all-cause mortality, nonfatal myocardial infarction or target lesion revascularization.Depression was present in 40.9% (n = 141) of patients after CABG, which was significantly higher than before procedure (24.3%, P0.01). The MACE rate was significantly higher in patients with post-procedure depression [8.5% (12/141)] than in patients without depression [2.9% (6/204), P0.05] and the incidences of target lesion revascularization and rehospitalization were also significantly higher in depression patients than in non-depression patients during the 12 months follow-up (all P0.05). Depression was present in 36.4% (n = 112) of patients after PCI, which was significantly higher than that before procedure (28.6%, P0.05). The MACE rate [8.0% (9/112) vs. 2.0% (4/196)] and rehospitalization rate [12.5% (14/112) vs. 4.6% (9/196)] were significantly higher in depression patients than in patients without depression during the 12 months follow-up (P0.05). There was no significant difference on SDS score between the PCI and CABG before the procedure. However, after the procedure, the SDS score for patients undergoing CABG was significantly higher than in patients undergoing PCI (48.9 ± 9.8 vs. 45.7 ± 10.5 P = 0.01). The level of serum IL-6 was significantly higher in depression patients than in patients without depression (P0.05).Prevalence of depression is high in patients treated with revascularization procedures and is linked with poor post-procedure prognosis.

Early clinical trials with the Endeavor zotarolimus eluting stent (ZES) in western populations demonstrated low rates of target lesion revascularization with a favorable safety profile including low late stent thrombosis with up to 5 years of follow-up. The aim of this clinical registry study was to evaluate real world clinical performance of the ZES coronary system in Chinese patients.The China Endeavor Registry is a prospective, multicenter registry assessing the safety of the ZES system in a real world patient population. It was conducted at 46 centers in China in routine treatment of patients with coronary artery stenosis, including patients with clinical characteristics or lesion types that are often excluded from randomized controlled trials. The registry included 2210 adult patients who underwent single-vessel or multi-vessel percutaneous coronary intervention. The primary end point was the rate of major adverse cardiac events (MACE) at 12 months.The 12-month rate of MACE for all patients in the registry was 3.03%. Cardiac death or myocardial infarction rate was 1.28% and target lesion revascularization rate was 1.66%, non-target lesion target vessel revascularization (TVR) was 0.52%, TVR was 2.18%, and target vessel failure was 3.22%. There was only one case of emergent cardiac bypass surgery. The 12-month overall incidence of all Academic Research Consortium (ARC)-defined stent thrombosis was 0.43%.Mid-term results from the real-world China Endeavor Registry suggest that Endeavor ZES was safe and effective in Chinese patients.

To investigate the clinical autopsy results of patients died of cardiovascular disease or other disease complicated with cardiac damage.Complete autopsy was performed on 86 cases with uncertain cause of death. Through integrating clinical diagnosis and treatment with gross autopsy findings and microscopic observations, 86 autopsies were determined the major cause of death.In 86 autopsies, 69 cases were heart disease. Differences between pathological diagnosis and clinical diagnosis were compared. Twenty-seven cases were cardiac deaths, with diagnosis accordance rate of 81.5%. Forty-two cases died of non-cardiac disease but complicated with heart disease or involving the heart which accelerated the death in patients, with accordance rate of 78.6%.Scientific and correct performance of autopsy was important to determine the causes of death, to promote development of related disciplines and to improve the diagnosis and treatment of the diseases.

The role of angiotensin-converting enzyme inhibitors (ACEI) in contrast-induced acute kidney injury (CI-AKI) is controversial. Some studies pointed out that it was effective in the prevention of CI-AKI, while some concluded that it was one risk for CI-AKI, especially for patients with pre-existing renal impairment. The purpose of this study was to assess the influence of benazepril administration on the development of CI-AKI in patients with mild to moderate renal insufficiency undergoing coronary intervention.One hundred and fourteen patients with mild to moderate impairment of renal function were enrolled before coronary angioplasty, who were randomly assigned to benazepril group (n = 52) and control group (n = 62). In the benazepril group, the patients received benazepril tablets 10 mg per day at least for 3 days before procedure. CI-AKI was defined as an increase of ≥ 25% in creatinine over the baseline value or increase of 0.5 mg/L within 72 hours of angioplasty.Patients were well matched with no significant differences at baseline in all measured parameters between two groups. The incidence of CI-AKI was lower by 64% in the benazepril group compared with control group but without statistical significance (3.45% vs. 9.68%, P = 0.506). Compared with benazepril group, estimated glomerular filtration rate (eGFR) level significantly decreased from (70.64 ± 16.38) ml · min⁻¹·1.73 m⁻² to (67.30 ± 11.99) ml · min⁻¹·1.73 m⁻² in control group (P = 0.038). There was no significant difference for the post-procedure decreased eGFR from baseline (ΔeGFR) between two groups (benazepril group (0.67 ± 12.67) ml · min⁻¹·1.73 m⁻² vs. control group (-3.33 ± 12.39) ml · min⁻¹·1.73 m⁻², P = 0.092). In diabetic subgroup analysis, ΔeGFR in benazepril group was slightly lower than that in the control group, but the difference was not statistically significant.Benazepril has a protective effect on mild to moderate impairment of renal function during coronary angioplasty. It is safe to use benazepril for treatment of patients with mild to moderate impairment of renal function before coronary intervention.

To evaluate the efficacy and safety of Chinese medicinal shensongyangxin capsules in the treatment of paroxysmal atrial fibrillation.From August 2007 to July 2008, Beijing Chaoyang Hospital conducted a multicenter study, select the eleven hospital's outpatient subjects, aged 18 to 75 years old, male or female, paroxysmal atrial fibrillation (at least one electrocardiogram diagnosis) seizure frequency ≥ 2 times/month, according to the ratio 1:1:1, subjects were randomly divided into three groups: a. shensongyangxin group, taking shensongyangxin capsule 4 + propafenone analogues 150 mg, 3 times a day; b. propafenone group, taking propafenone tablets 150 mg + 4 shensongyangxin analogues, 3 times a day; shensongyangxin capsule + propafenone group, taking shensongyangxin capsule 4 + propafenone 150 mg, 3 times a day. The treatment course is 8 weeks, with 3 times of follow-up.Total of 349 cases of paroxysmal atrial fibrillation, which 117 cases in shensongyangxin group, 115 cases in propafenone group; 117 cases in shensongyangxin + propafenone group. The baseline data analysis showed that there were no significantly difference (P0.05) among the three groups of atrial fibrillation seizure frequency, vital signs, general condition, medical history, 24-hour ambulatory ECG, 12-lead normal electrocardiogram, cardiac ultrasound and symptoms. The comparison before and after (8 weeks) treatment showed that the frequency (from 6 times/m to 2 times/m in each group, P0.01), number of cases [from 46 (43.3%) to 22 (20.8%), 43 (43.4%) to 25 (25.3%), and 40 (40.6%) to 31 (29.2%), respectively P0.01] and duration time of attack of atrial fibrillation (from 4 h to 0.5 h, 4 h to 0.5 h, and 4.25 h to 0.5 h, respectively P0.01) all decreased in three groups. No significant difference among the three groups comparing the overall effect (62.3%, 58.6%, and 58.5%, respectively, P0.05), while the efficacy of TCM symptoms in shensongyangxin group (80.2%) was better than that of propafenone group (67.7%) (P0.05). Safety evaluation showed that adverse reaction rate was 1.8% in shensongyangxin group, and 8.2% and 5.4% in propafenone group and shensongyangxin + propafenone group.Shensongyangxin capsules and propafenone have comparable efficacies in the treatment of PAF. The efficacy of TCM symptoms is better than propafenone. Shensongyangxin capsules have an excellent profile of safety.

To examine the expression of angiotensin II (Ang II) receptor subtypes in human left and right atrial tissue in atrial fibrillation underlying rheumatic heart disease.Atrial tissue samples were obtained from 39 patients with rheumatic heart disease, 25 with atrial fibrillation (AF) and 14 with sinus rhythm(SR) during open heart surgery. AT1 and AT2 mRNA levels were measured with semi-quantitative reverse transcription polymerase chain reaction techniques. AT1 and AT2 protein levels were measured with immunohistochemical techniques.Compared with that of the SR group, left atrial inner diameter was significantly increased in the patients of the AF group. The AT1 mRNA and protein levels in the LA significantly increased in patients with AF compared with those in patients with SR (P0.05), whereas AT2 mRNA and protein were not significantly altered. Investigations of Ang II receptor subtypes' mRNA and protein levels in the RA did not exhibit any significant changes either in AT1 or AT2 in patients with AF and SR.AF is associated with an up-regulation of AT1 in LA, but does not appear to influence the AT2 expression. This may indicate a possible pathophysiologic role for renin-angiotensin system in the development of AF. The series of effects mediated by AT1 activation may be one of the molecular mechanisms involved in the process of atrial remodeling.

To investigate the change of the mortality of AMI and influence factors within 20 years.Clinic data of 134 AMI patients from 1980 to 1983, 354 AMI patients from 1990 to 1993 and 817 AMI patients from 2000 to 2003 were comparably analyzed.In hospital mortality of AMI was 22.4% from 1980 to 1983, 14.4% from 1990 to 1993 and 9.2% from 2000 to 2003, respectively (P0.01). The decrease of in-hospital mortality in male was more significant than in female (P0.01). The corresponding factors for decrease of mortality were younger than 60 years old, first onset of AMI, successful rescue of cardiac arrest and reperfusion management of infarction relative artery. The disadvantage factor was female.Improvement of medical and reperfusion management of AMI conduced in significant decreases of hospital mortality.

Objectives To develop a simplified risk score of contrast induced nephropathy (CIN) after percutaneous coronary intervention (PCI) for Han Chinese. Methods A retrospective study was performed on 1500 patients for the development dataset, who had undergone PCI from January 2008 to May 2010. And one thousand patients treated in the same period were selected for the validation set. Logistic regression analysis was applied to identify risk factors for CIN. Based on the OR, the sum of the integers was a total risk score for each patient. Results (1) Among the 1500 patients, CIN occurred in 246 patients and the overall incidence of CIN was 16.4%. (2) Eleven identified variables were identified as risk factors for CIN (with weighted integer): diabetes (3 score), hypotension (3 score), Left ventricular ejection fraction (LVEF≤45%) (3 score), eGFR 2 (3 score), age>70 years (2 score), myocardial infarction (2 score), emergency PCI (2 score), anaemia (2 score), decreased high-density lipoprotein (HDL) concentration ( 200 ml (2 score), low permeability contrast agent (1 score). (3) The sum of the integers was a total risk score for each patient. The incidence of CIN was 5.2% in low risk group (≤4), 13.6% in the moderate risk group (5–10), 32.3% in the high risk group (11–14) and 59.0% in the very high risk group (≥15). (4) The model demonstrated good discriminative power in the validation population, showing that the increasing risk score was strongly associated with CIN (c-statistic=0.82). Conclusions This simple scoring system proposed here provides a good estimate of the risk of CIN after PCI for Han Chinese. This risk score can be used for the prevention and treatment of CIN.

Objectives To observe the effect of different doses of atorvastatin combined with different dose of probucol on the level of serum uric acid in patients undergoing coronary angiography or percutaneous coronary intervention (PCI). Methods 208 cases enrolled in our study were randomly divided into three groups: Standard combining treatment group (n=55): Atorvastatin 20 mg qn and Probucol 0.25 g/bid; Intensively combining treatment group (n=79): Atorvastatin 40 mg qn and Probucol 0.5 g/bid, with a further dose of Atorvastatin 40 mg and Probucol 0.5 g 2 h before the angioplasty; Intensive Atorvastatin group (n=74): Atorvastatin 40 mg qn, with a futher dose of Atorvastatin 40 mg 2 h before the angioplasty. Blood urea nitrogen (BUN), serum creatinine (Scr), serum uric acid (SUA), and estimated glomerular filtration rate (eGFR) (through MDRD method) of all patients were tested at the times of 24 h before and 24 h after the procedure. Results (1) After operation, BUN of all groups decreased; Scr in Standard combining treatment group and Intensive Atorvastatin group increased significantly; while eGFR decreased only in Standard combining treatment group (p 0.05); (2) SUA in Standard combining treatment group and Intensively combining treatment group decreased significantly after operation (p 0.05). (3) For hypertensive patients, Scr in Standard combining treatment group and Intensive Atorvastatin group increased significantly (p Conclusions Preoperative combination treatment of Atorvastatin and Probucol could reduce perioperative serum uric acid9s level, what9s more with a intensive treatment of future dose of Atorvastatin 40 mg and Probucol 0.5 g 2 h before the angioplasty could also improve CIAKI. For hypertensive patients, intensively combining treatment could not only reduce serum uric acid9s level, but also improve CIAKI.