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Wang Y.,Fudan University | Wang C.,Beijing Institute of Respiratory Medicine Beijing Chaoyang Hospital | Zhang J.,Shanghai JiaoTong University | Liu Z.,Cardiovascular Institute and Fu Wai Hospital | And 11 more authors.
Thrombosis Journal | Year: 2013

Background: The worldwide EINSTEIN DVT and EINSTEIN PE studies randomized 8282 patients with acute symptomatic deep-vein thrombosis (DVT) and/or pulmonary embolism (PE) and, for the first time in trials in this setting, included patients in China. This analysis evaluates the results of these studies in this subgroup of patients. Methods: A total of 439 Chinese patients who had acute symptomatic DVT (n=211), or PE with or without DVT (n=228), were randomized to receive rivaroxaban (15 mg twice daily for 21 days, followed by 20 mg once daily) or standard therapy of enoxaparin overlapping with and followed by an adjusted-dose vitamin K antagonist, for 3, 6, or 12 months. The primary efficacy outcome was symptomatic recurrent venous thromboembolism. The principal safety outcome was major or non-major clinically relevant bleeding. Results: The primary efficacy outcome occurred in seven (3.2%) of the 220 patients in the rivaroxaban group and in seven (3.2%) of the 219 patients in the standard-therapy group (hazard ratio, 1.04; 95% confidence interval 0.36-3.0; p=0.94). The principal safety outcome occurred in 13 (5.9%) patients in the rivaroxaban group and in 20 (9.2%) patients in the standard-therapy group (hazard ratio, 0.63; 95% confidence interval 0.31-1.26; p=0.19). Major bleeding was observed in no patients in the rivaroxaban group and in five (2.3%) patients in the standard-therapy group. In fragile patients (defined as age >75 years, creatinine clearance <50 mL/min, and/or body weight ≤50 kg), the principal safety outcome occurred in four (8.9%) of the 45 patients who received rivaroxaban compared with seven (15.2%) of the 46 patients who received standard therapy. Conclusions: In Chinese patients with acute symptomatic DVT and/or PE, rivaroxaban was as efficacious as enoxaparin followed by vitamin K antagonist therapy, with a similar safety profile. The relative efficacy and safety of rivaroxaban compared with enoxaparin/vitamin K antagonist were consistent with that found in the rest of the world.Trial registration number: EINSTEIN PE, ClinicalTrials.gov NCT00439777; EINSTEIN DVT, ClinicalTrials.gov NCT00440193. © 2013 Wang et al.; licensee BioMed Central Ltd. Source


Do R.,McGill University | Xie C.,Hamilton Health Sciences | Xie C.,McMaster University | Zhang X.,Hamilton Health Sciences | And 19 more authors.
PLoS Medicine | Year: 2011

Background: One of the most robust genetic associations for cardiovascular disease (CVD) is the Chromosome 9p21 region. However, the interaction of this locus with environmental factors has not been extensively explored. We investigated the association of 9p21 with myocardial infarction (MI) in individuals of different ethnicities, and tested for an interaction with environmental factors. Methods and Findings: We genotyped four 9p21 SNPs in 8,114 individuals from the global INTERHEART study. All four variants were associated with MI, with odds ratios (ORs) of 1.18 to 1.20 (1.85×10-8≤p≤5.21×10-7). A significant interaction (p = 4.0×10-4) was observed between rs2383206 and a factor-analysis-derived "prudent" diet pattern score, for which a major component was raw vegetables. An effect of 9p21 on MI was observed in the group with a low prudent diet score (OR = 1.32, p = 6.82×10-7), but the effect was diminished in a step-wise fashion in the medium (OR = 1.17, p = 4.9×10-3) and high prudent diet scoring groups (OR = 1.02, p = 0.68) (p = 0.014 for difference). We also analyzed data from 19,129 individuals (including 1,014 incident cases of CVD) from the prospective FINRISK study, which used a closely related dietary variable. In this analysis, the 9p21 risk allele demonstrated a larger effect on CVD risk in the groups with diets low or average for fresh vegetables, fruits, and berries (hazard ratio [HR] = 1.22, p = 3.0×10-4, and HR = 1.35, p = 4.1×10-3, respectively) compared to the group with high consumption of these foods (HR = 0.96, p = 0.73) (p = 0.0011 for difference). The combination of the least prudent diet and two copies of the risk allele was associated with a 2-fold increase in risk for MI (OR = 1.98, p = 2.11×10-9) in the INTERHEART study and a 1.66-fold increase in risk for CVD in the FINRISK study (HR = 1.66, p = 0.0026). Conclusions: The risk of MI and CVD conferred by Chromosome 9p21 SNPs appears to be modified by a prudent diet high in raw vegetables and fruits. Please see later in the article for the Editors' Summary. © 2011 Do et al. Source


Wang F.,Nanjing Medical University | Wang F.,Nanjing University | Fang W.,Cardiovascular Institute and Fu Wai Hospital | Fang W.,Jiangsu Institute of Nuclear Medicine | And 11 more authors.
Journal of Nuclear Medicine | Year: 2011

The C2A domain of synaptotagmin I can target apoptotic cells by binding to exposed anionic phospholipids. The goal of this study was to synthesize and develop 18F-labeled C2A-glutathione- S-transferase (GST) as a molecular imaging probe for the detection of apoptosis and to assess the response of paclitaxel chemotherapy in VX2 rabbit lung cancer. Methods: 18F-C2A-GST was prepared by labeling C2A-GST with N-succinimidyl 4-18F-fluorobenzoate (18F-SFB). 18F-C2A-GST was confirmed by high-performance liquid chromatography and sodium dodecyl sulfate polyacrylamide gel electrophoresis. The binding of 18F-C2A-GST toward apoptosis was validated in vitro using camptothecin-induced Jurkat cells. Biodistribution of 18F-C2A-GST was determined in mice by a dissection method and small-animal PET. Single-dose paclitaxel was used to induce apoptosis in rabbits bearing VX2 tumors (n = 6), and 2 VX2 rabbits without treatment served as control. 18FC2A- GST PET was performed before and at 72 h after therapy, and 18F-FDG PET/CT was also performed before treatment. To confirm the presence of apoptosis, tumor tissue was analyzed and activated caspase-3 was measured. Results: 18FC2A- GST was obtained with more than 95% radiochemical purity and was stable for 4 h after formulation. 18F-C2A-GST bound apoptotic cells specifically. Biodistribution in mice showed that 18F-C2A-GST mainly excreted from the kidneys and rapidly cleared from blood and nonspecific organs. High focal uptake of 18F-C2A-GST in the tumor area was determined after therapy, whereas no significant uptake before therapy was found in the tumor with 18F-FDG-avid foci. The maximum standardized uptake value after therapy was 0.47±0.28, significantly higher than that in the control (0.009±0.001; P < 0.001). The apoptotic index was 79.81% ± 8.73% in the therapy group, significantly higher than that in the control (5.03%±0.81%; P < 0.001). Activated caspase-3 after paclitaxel treatment increased to 69.55%±16.27% and was significantly higher than that in the control (12.26%±5.39%; P < 0.001). Conclusion: 18F-C2A-GST was easily synthesized by conjugation with 18F-SFB and manifested a favorable biodistribution. Our results demonstrated the feasibility of 18FC2A- GST for the early detection of apoptosis after chemotherapy in a VX2 lung cancer model that could imitate. Copyright © 2011 the American Physiological Society. Source


Yang Y.M.,Cardiovascular Institute and Fu Wai Hospital
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] | Year: 2010

To compare the impact of the first 24 hours mean blood glucose (MBG) level and admission glucose (AG) during hospitalization on the short term mortality and combined end point events in patients with ST-segment elevation acute myocardial infarction (STEMI). A total of 7446 Chinese STEMI patients hospitalized within 12 hours of symptom onset were included. Plasma glucose was measured at admission, 6 and 24 hours after admission, respectively. The MBG level through the first 24 hours for each patient was calculated. Patients were stratified into six groups according to their MBG levels: < 4.5, 4.5 - 5.5, 5.6 - 7.0, 7.1 - 8.5, 8.6 - 11.0 and > 11.0 mmol/L. The incidence of all-cause mortality and combined end point of death, re-infarction, cardiogenic shock, recurrence ischemia, and stroke at 7 days and 30 days post hospitalization were analyzed. Nested models were compared to determine whether logistic regression models that included MBG provided a significantly better fit than logistic regression models included AG. Compared with the MBG of 4.5 - 5.5 mmol/L group, 7-day and 30-day mortality and combined end point events increased in proportion to plasma MBG level increase. Multivariate logistic regression analysis showed that elevated MBG (equal or greater than 7.1 - 8.5 mmol/L) level is an independent predictor of 7-day and 30-day mortality and combined end point events. Nested models analysis showed that the prognostic impact of MBG is superior to AG (P < 0.001) on predicting 7-day and 30-day mortality and combined end point events in this patient cohort. Elevated MBG (≥ 7.1 mmol/L) level is an independent predictor of 7-day and 30-day mortality and combined end point events. MBG is superior to AG on predicting short-term prognosis in this patient cohort. Source


Mao Q.,National Research Institute for Family Planning | Gao L.,Chinese Peoples Liberation Army | Wang H.,China Institute of Industrial Relations | Wang Q.,Cardiovascular Institute and Fu Wai Hospital | Zhang T.,National Center for Women and Childrens Health
Asia-Pacific Journal of Public Health | Year: 2015

Published data regarding the association between alcohol dehydrogenase (ADH) 1C genotypes and breast cancer risk show conflicting results. The authors performed this meta-analysis on 1969 patients and 2244 controls from 4 (including 7 study populations) related case-control studies to estimate the association between ADH1C(rs698) genotyping information and breast cancer risk. According to the 6 eligible populations, the odds ratios (ORs) and 95% confidence intervals (CIs) for breast cancer risk for ADH1C1-2 versus ADH1C2-2, ADH1C1-1 versus ADH1C2-2 genotype, and ADH1C1 versus ADH1C2 were 1.16 (0.95-1.42), 1.17 (0.95-1.44), and 1.05 (0.96-1.16), respectively. The OR (95% CI) for ADH1C1-1 + ADH1C1-2 versus ADH1C2-2 from the 7 study populations was 1.14 (0.96-1.36). Meanwhile, genotypes of ADH1C1-1 + ADH1C1-2 increased the risk of breast cancer in drinkers (OR = 1.35; 95% CI = 1.03-1.76). This meta-analysis suggested that the ADH1C1 allele might modestly influence the effect of alcohol on breast cancer but is not an independent risk factor for breast cancer. However, more restricted prospective studies are needed. © 2012 APJPH. Source

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