Affiliated Hospital of Ningxia Medical College
Affiliated Hospital of Ningxia Medical College
Zheng B.,Peking University |
Jiang J.,Peking University |
Liu H.,General Hospital of Chinese Peoples Armed Police Forces |
Zhang J.,Hebei Medical University |
And 24 more authors.
European Heart Journal, Supplement | Year: 2015
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. © 2015 Published on behalf of the European Society of Cardiology. All rights reserved.
He Q.-Y.,Peking University |
Feng J.,Tianjin Medical University |
Zhang X.-L.,Tianjin Medical University |
Liang Z.-A.,Nanjing Medical University |
And 17 more authors.
Chinese Medical Journal | Year: 2012
Background The nocturnal nondipping and elevated morning blood pressure (BP) in patients with obstructive sleep apnea syndrome (OSAS) have not yet been well investigated in Chinese patients. This study aimed to describe the BP profile, and to elucidate the relationships between daytime BP and nighttime BP, and between evening BP and morning BP in patients with OSAS. Methods Twenty teaching hospital sleep centers in China were organized by the Chinese Medical Association to participate in this study and 2297 patients were recruited between January 2004 and April 2006. BP assessments were made at four time points (daytime, evening, nighttime and morning) and polysomnography (PSG) was performed and subjects were classified into four groups by their apnea-hypopnea index (AHI): control, n=213 with AHI <5; mild, n=420 with AHI ≥5 and <15; moderate, n=460 with AHI ≥15 and <30; and severe, n=1204 with AHI ≥30. SPSS 11.5 software package was used for statistical analysis and figure drawing. Results All the average daytime, nighttime, evening and morning BPs were positively correlated with AHI and negatively correlated with nadir nocturnal oxygen saturation. The ratios of nighttime/daytime and morning/evening average BP were positively correlated with AHI. The ratio of nighttime/daytime systolic BP became a "reversed BP dipping" pattern until the classification reached severe, while the ratio of nighttime/daytime diastolic BP became reversed at moderate. Similarly, the ratio of morning/evening diastolic BP becomes reversed even at mild. Conclusions OSAS may result in higher BP levels at all four time points. The ratios of nighttime/daytime and morning/evening BP increase with increased AHI. The increasing of diastolic BP, which is inclined to rise more quickly, is not parallel with increasing systolic BP.
Han Y.,Shenyang Northern Hospital |
Zhu G.,WuHan Asia Heart Hospital |
Han L.,CangZhou Central Hospital |
Hou F.,Changchun Central Hospital |
And 19 more authors.
Journal of the American College of Cardiology | Year: 2014
Objectives This study sought to evaluate the safety and efficacy of rosuvastatin in preventing contrast-induced acute kidney injury (CI-AKI) in patients with diabetes mellitus (DM) and chronic kidney disease (CKD). Background CI-AKI is an important complication after contrast medium injection. While small studies have shown positive results with statin therapy, the role of statin therapy in prevention of CI-AKI remains unknown. Methods We randomized 2,998 patients with type 2 DM and concomitant CKD who were undergoing coronary/peripheral arterial angiography with or without percutaneous intervention to receive rosuvastatin, 10 mg/day (n = 1,498), for 5 days (2 days before, and 3 days after procedure) or standard-of-care (n = 1,500). Patients' renal function was assessed at baseline, 48 h, and 72 h after exposure to contrast medium. The primary endpoint of the study was the development of CI-AKI, which was defined as an increase in serum creatinine concentration ≥0.5 mg/dl (44.2 μmol/l) or 0.25% above baseline at 72 h after exposure to contrast medium. Results Patients randomized to the rosuvastatin group had a significantly lower incidence of CI-AKI than controls (2.3% vs. 3.9%, respectively; p = 0.01). During 30 days' follow-up, the rate of worsening heart failure was significantly lower in the patients treated with rosuvastatin than that in the control group (2.6% vs. 4.3%, respectively; p = 0.02). Conclusions Rosuvastatin significantly reduced the risk of CI-AKI in patients with DM and CKD undergoing arterial contrast medium injection. (Rosuvastatin Prevent Contrast Induced Acute Kidney Injury in Patients With Diabetes [TRACK-D]; NCT00786136).
PubMed | Jinan Military General Hospital, Shenyang Northern Hospital, WuHan Asia Heart Hospital, General Hospital of Armed Police Forces and 14 more.
Type: Comparative Study | Journal: Journal of the American College of Cardiology | Year: 2014
This study sought to evaluate the safety and efficacy of rosuvastatin in preventing contrast-induced acute kidney injury (CI-AKI) in patients with diabetes mellitus (DM) and chronic kidney disease (CKD).CI-AKI is an important complication after contrast medium injection. While small studies have shown positive results with statin therapy, the role of statin therapy in prevention of CI-AKI remains unknown.We randomized 2,998 patients with type 2 DM and concomitant CKD who were undergoing coronary/peripheral arterial angiography with or without percutaneous intervention to receive rosuvastatin, 10 mg/day (n = 1,498), for 5 days (2 days before, and 3 days after procedure) or standard-of-care (n = 1,500). Patients renal function was assessed at baseline, 48 h, and 72 h after exposure to contrast medium. The primary endpoint of the study was the development of CI-AKI, which was defined as an increase in serum creatinine concentration 0.5 mg/dl (44.2 mol/l) or 0.25% above baseline at 72 h after exposure to contrast medium.Patients randomized to the rosuvastatin group had a significantly lower incidence of CI-AKI than controls (2.3% vs. 3.9%, respectively; p = 0.01). During 30 days follow-up, the rate of worsening heart failure was significantly lower in the patients treated with rosuvastatin than that in the control group (2.6% vs. 4.3%, respectively; p = 0.02).Rosuvastatin significantly reduced the risk of CI-AKI in patients with DM and CKD undergoing arterial contrast medium injection. (Rosuvastatin Prevent Contrast Induced Acute Kidney Injury in Patients With Diabetes [TRACK-D]; NCT00786136).
PubMed | Tianjin Chest Hospital, General Hospital of Shenyang Military Command, Affiliated Hospital of Ningxia Medical College, Shenyang Medical College and 3 more.
Type: | Journal: Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions | Year: 2016
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.
Ang E.,University of Western Australia |
Liu Q.,University of Western Australia |
Qi M.,Affiliated Hospital of Ningxia Medical College |
Liu H.G.,Guangxi Medical University |
And 4 more authors.
Journal of Cellular Biochemistry | Year: 2011
Osteolytic bone diseases such as osteoporosis have a common pathological feature in which osteoclastic bone resorption outstrips bone synthesis. Osteoclast formation and activation are regulated by receptor activator of nuclear factor kB ligand (RANKL). The induction of RANKL-signaling pathways occurs following the interaction of RANKL to its cognate receptor, RANK. This specific binding drives the activation of downstream signaling pathways; which ultimately induce the formation and activation of osteoclasts. In this study, we showed that a natural immunomodulator, mangiferin, inhibits osteoclast formation and bone resorption by attenuating RANKL-induced signaling. Mangiferin diminished the expression of osteoclast marker genes, including cathepsin K, calcitonin receptor, DC-STAMP, and V-ATPase d2. Mechanistic studies revealed that mangiferin inhibits RANKL-induced activation of NF-kB, concomitant with the inhibition of IkB-α degradation, and p65 nuclear translocation. In addition, mangiferin also exhibited an inhibitory effect on RANKL-induced ERK phosphorylation. Collectively, our data demonstrates that mangiferin exhibits anti-resorptive properties, suggesting the potential application of mangiferin for the treatment and prevention of bone diseases involving excessive osteoclastic bone resorption. © 2010 Wiley-Liss, Inc.
Yang Y.-J.,Affiliated Hospital of Ningxia Medical College |
Zheng X.-W.,Affiliated Hospital of Ningxia Medical College |
Yang G.-L.,Affiliated Hospital of Ningxia Medical College |
Cheng D.-Y.,University of Sichuan |
Zhang P.,Affiliated Hospital of Ningxia Medical College
Journal of Sichuan University (Medical Science Edition) | Year: 2012
Objective To investigate the expression of thrombospondin-1 (TSP-1) in serum and pulmonary arterioles of rats with hypoxic pulmonary hypertension. Methods Twenty male Wistar rats were divided into two groups and exposed to air and isobaric hypoxia for 3 weeks respectively. The mean pulmonary artery pressure (mPAP) was measured by right cardiac catheterization. The rates of wall thickness/external diameter (WT%) and wall area/total vascular area (WA%) were calculated. The TSP-1 level in serum was measured by enzyme-linked immunosorbent assay. TSP-1 mRNA expression in lung tissue was evaluated by quantitative PCR. Results The pulmonary artery pressure increased in the hypoxia exposed rats. The chronic hypoxia also elicited the thicking of the wall and the narrowing of the lumen of pulmonary arterioles. It led to the increases of pulmonary artery pressure, the index of right ventricular hypertrophy [RV/(LV + S)], WA% and WT% compared to the controls (mPAP:(2. 86±0. 39) kPa vs. (1. 35±0. 28) kPa; RV/(LV+S): (43. 53± 3. 38)% vs. (23. 68±3. 48)%; WT%; (35. 24±11.20)% vs. (23. 63±9. 74)%, WA%: (55. 09±12. 38)% vs. (41.62±12. 83)% respectively, P<0. 05) In hypoxic group, the expression of TSP-1 mRNA in the lung was significantly up-regulated, the expression level of TSP-I in serum was higher than that in control group (P<0. 01). Linear correlation analysis showed that TSP-1 mRNA was positively associated with WT%, WA% and mPAP (r = 0.748, 0. 686,0. 942 respectively, P<0. 05). Conclusion The TSP-1 may play an important role in the pathogenesis process of hypoxic pulmonary vascular remodeling and pulmonary hypertension.