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Hu S.,Chinese Academy of Sciences | Hu S.,State Key Laboratory of Cardiovascular Disease | Gao R.,Chinese Academy of Sciences | Gao R.,State Key Laboratory of Cardiovascular Disease
Coronary Artery Disease | Year: 2014

Hybrid coronary revascularization intends to combine the durability and survival advantage of the left internal mammary artery to left anterior descending coronary artery graft by a minimally invasive surgical procedure and the interventional therapy for non-left anterior descending coronary artery vessels to achieve complete revascularization. It provides a feasible and attractive alternative to conventional coronary artery bypass grafting and percutaneous coronary intervention to target multivessel coronary artery disease, and advances the individualized, patient-oriented treatment for heart disease. In initial experiences, this new approach has yielded favorable early or midterm results in selected patients with multivessel coronary artery disease. However, available data related to these outcomes following hybrid revascularization are limited to retrospective studies with relatively small sample sizes. In this review, we aim to provide an overview of hybrid revascularization, and discuss appropriate patient selection, procedure techniques, and the main literature pertaining to the hybrid revascularization. © 2014 Wolters Kluwer Health | Lippincott Williams and Wilkins.


Hsu C.-C.,National Health Research Institute | Hsu C.-C.,China Medical University at Taichung | Wang H.,State Key Laboratory of Cardiovascular Disease | Wang H.,Peking Union Medical College | And 10 more authors.
Hypertension | Year: 2015

Limited studies have examined the effects of nonsteroidal anti-inflammatory drug (NSAID) use on the risk of chronic kidney disease (CKD), especially in subjects with hypertension. Using National Health Insurance claims data in Taiwan, we conducted a propensity score-matched cohort study to investigate the relationship between NSAID use and CKD in subjects with hypertension. A total of 31976 subjects were included in this study: subjects not taking any NSAIDs in 2007 (n=10782); subjects taking NSAIDs for 1 to 89 days in 2007 (n=10605); and subjects taking NSAIDs for ≥90 days in 2007 (n=10589). We performed multivariable proportional hazard models to determine the relationship between NSAID use and CKD. The results showed that NSAID use was associated with a 1.18-fold increased risk of CKD in subjects taking NSAIDs for 1 to 89 days; and a 1.32-fold increased risk of CKD in hypertension subjects taking NSAIDs for ≥90 days, compared with subjects not taking any NSAIDs, after controlling for the confounding factors. In subgroup analyses, subjects taking NSAIDs for ≥90 days, >1 defined daily dose per day or taking NSAIDs >15 cumulative defined daily doses had a greater risk of CKD than subjects not taking any NSAID, but not for congestive heart failure, stroke, cancer, osteoarthritis, or rheumatoid arthritis. These results provide supportive evidence that NSAID use is associated with increased risk of CKD in subjects with hypertension. It is important to closely monitor the effects of NSAID use, particularly in patients with hypertension, a susceptible population for CKD.


Zhang W.,State Key Laboratory of Cardiovascular Disease | Zhang W.,Sino German Laboratory for Molecular Medicine | Chen Y.,Sino German Laboratory for Molecular Medicine | Liu P.,China Japan Friendship Hospital | And 11 more authors.
Stroke | Year: 2012

Background and Purpose-: ANRIL encodes a long antisense noncoding RNA in the INK4 locus. Although ANRIL has been proven to be associated with coronary heart disease, its roles in stroke are inconsistent, and sparse data are available regarding hemorrhagic stroke. Methods-: A Chinese case-control study was conducted, comprising 1657 cases (724 atherothrombosis, 466 lacunar infarction, and 462 hemorrhagic strokes) and 1664 controls. Stroke patients were prospectively followed-up for a median of 4.5 (range, 0.1-6.0) years. Expression of ANRIL transcripts was examined in 42 human atherosclerotic plaques. Results-: After adjustment for vascular risk factors and correction for multiple comparisons, subjects carrying the GG genotype of rs10757278 had 1.47-fold (95% CI, 1.11-1.89; P=0.05) and 1.60-fold (95% CI, 1.16-2.15; P=0.04) increased risk for atherothrombotic and hemorrhagic strokes, respectively. During the follow-up, 317 recurrent strokes and 301 deaths from all causes were documented. Subjects carrying rs10757278GG had higher risk for stroke recurrence (relative risk [RR],1.56; 95% CI,1.15-2.12; P=0.005) and cardiovascular mortality (RR, 2.0; 95% CI, 1.26-3.18; P=0.003), respectively. Rs10757274 was also associated with stroke risk and recurrence. Family history of stroke further increased the stroke risk by 2.37-fold (95% CI, 1.38-4.06; P=0.01) and recurrent stroke risk by 2.45-fold (95% CI, 1.56-3.86; P<0.0001) respectively, when compared with those carrying none of G-alleles and without family history. Finally, rs10757278 was associated with differential expression of the ANRIL transcripts. Conclusions-: Our findings indicated that the ANRIL may serve as a novel genetic marker for the risk of atherothrombotic and hemorrhagic stroke and their recurrence. © 2011 American Heart Association. All rights reserved.


Li J.,Capital Medical University | Li J.,State Key Laboratory of Cardiovascular Disease | Luo S.-H.,State Key Laboratory of Cardiovascular Disease | Tang Y.,State Key Laboratory of Cardiovascular Disease | Li J.-J.,State Key Laboratory of Cardiovascular Disease
Clinical Laboratory | Year: 2014

C-reactive protein (CRP) is a biomarker of systemic inflammation, which is also associated with pulmonary artery disease. However, the impact of CRP on cell proliferation of the pulmonary arterial wall has been investigated less. We, therefore, examined the effects and potential mechanisms of CRP on proliferation in human pulmonary artery smooth muscle cells (hPASMC). Methods: HPASMCs were cultured and stimulated by different concentrations of CRP (5-200 μg/mL) for 24 hours. The effects of CRP on proliferation of hPASMCs were examined using the BrDU incorporation assay, and the potential signal pathways including ERK1/2, Akt and NF-KB involved in hPASMCs' proliferation were evaluated by the Western blot and electrophoretic mobility shift assays. Results: CRP significantly increased proliferation of hPASMCs with a dose-dependent fashion (1.13-fold increase in CRP 5 μg/mL, and 1.84-fold increase in CRP 200 μg/mL versus controls, p < 0.05 and 0.01, respectively). Additionally, CRP could enhance the expression of Akt and ERK1/2 phosphorylation, but had no effects on total protein. Moreover, CRP resulted in the activation of NF-KB significantly, which was diminished by PI3K inhibitor wortmannin. The increased expression of phosphorylated ERK1/2 was inhibited by MEK inhibitor PD98095, whereas no such effects of NF-KB inhibitor Bay117082 on the expression of Akt and ERK1/2 was found. Conclusions: The data suggest that CRP directly impacts proliferation of hPASMCs via modulation of Akt, ERK1/2, and NF-KB pathways, which may have important implications for treating pulmonary arterial disease.


Hao Y.,State Key Laboratory of Cardiovascular Disease | Zhang H.,State Key Laboratory of Cardiovascular Disease | Yang X.,State Key Laboratory of Cardiovascular Disease | Wang L.,Brigham and Womens Hospital | Gu D.,State Key Laboratory of Cardiovascular Disease
Clinical Chemistry and Laboratory Medicine | Year: 2012

Background: The effects of fibrates on C-reactive protein (CRP) are controversial. This meta-analysis was conducted to synthesize the available clinical trial evidence and summarize the effects of fibrates on CRP concentrations. In addition, this study assessed the relationship between changes in CRP and lipid measures. Methods: A systematic search was conducted of randomized controlled trials on the effects of fibrates on CRP concentrations in the PubMed, Embase and Cochrane Library Database up to January 2011. A meta-analysis was performed using a random effect model. Meta-regression analysis was employed to assess the relationships between average change in CRP and lipid profiles. Results: Sixteen randomized controlled trials were included in the meta-analysis. Compared with placebo, treatment with fibrates significantly decreased CRP concentrations (weighted mean difference 0.47mg/L, 95 confidence interval 0.93 to 0.01mg/L, p=0.046). Fibrates significantly reduced CRP concentrations in trials with a higher baseline CRP concentrations (<3mg/L). There was a significant correlation between change in CRP and change in high-density lipoprotein cholesterol (regression coefficient or slope=2.03, 95 CI 3.20 to 0.87, p=0.001). Conclusions: Fibrates can reduce CRP concentrations and change in CRP was correlated with change in high-density lipoprotein cholesterol but not with triglyceride. These findings suggest that patients with dyslipidemia could benefit from fibrates treatment by CRP lowering and this benefit is associated with lipid profile improving. © 2012 by Walter de Gruyter Berlin Boston.

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