22 research outputs found

    Health-related Quality of Life after coronary revascularization: : A systematic review with meta-analysis

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    This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).Objective: To conduct a systematic review and meta-analysis to summarize evidence and determine the impact of coronary revascularization (CR) on cardiac patients' Health-Related Quality of Life (HRQoL), highlighting factors that may affect this outcome in patients. Methods: A systematic search of Medline (Pubmed), EMBASE, Cochrane Library, Sciverse (Science Direct and Scopus) and PsycInfo was conducted to identify studies published from January 2000 to December 2012. Data were analyzed using MIX 2.0 Pro and SPSS 20. Results: Thirty-four longitudinal studies met the inclusion criteria; these studies included 15,992 patients, of whom 8,027 had undergone PCI, 6,348 had undergone CABG and 1,617 had received medication treatment. Moderate long-term effect sizes were revealed for both CR procedures. Both percutaneous coronary interventions (PCI) and coronary artery bypass graft surgery (CABG) had significantly greater effects on HRQoL than did medication; however, the CR procedures did not differ significantly from each other. Moderators included the type of instrument used to assess HRQoL and the study quality. Benefits related to physical functioning were greater than those related to psychosocial functioning in patients treated with CABG. Conclusions: Empirical research highlights the positive effect of CR on patient HRQoL. Researchers should carefully select the instrument they use to measure HRQoL, as this may affect the results and thus conclusions. More RCTs and between-group studies employing pre-post designs should be conducted before clear conclusions can be drawn.Peer reviewedFinal Published versio

    Cardiopoietic cell therapy for advanced ischemic heart failure: results at 39 weeks of the prospective, randomized, double blind, sham-controlled CHART-1 clinical trial

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    Cardiopoietic cells, produced through cardiogenic conditioning of patients' mesenchymal stem cells, have shown preliminary efficacy. The Congestive Heart Failure Cardiopoietic Regenerative Therapy (CHART-1) trial aimed to validate cardiopoiesis-based biotherapy in a larger heart failure cohort

    Resistin decreases expression of endothelial nitric oxide synthase through oxidative stress in human coronary artery endothelial cells

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    Resistin is a newly discovered adipocyte-derived cytokine that may play an important role in insulin resistance, diabetes, adipogenesis, inflammation, and cardiovascular disease. However, it is largely unknown whether resistin impairs endothelial functions by affecting the endothelial nitric oxide synthase (eNOS) system. In this study, we determined the effect of human recombinant resistin protein on eNOS expression and regulation in human coronary artery endothelial cells (HCAECs). When cells were treated with clinically relevant concentrations of resistin (40 or 80 ng/ml) for 24 h, the levels of eNOS mRNA, protein, and activity and eNOS mRNA stability were significantly reduced. Cellular nitric oxide levels were also decreased. In addition, the cellular levels of reactive oxygen species (ROS), including superoxide anion, were significantly increased in resistin-treated HCAECs. Mitochondrial membrane potential and the activities of catalase and superoxide dismutase were reduced. Three antioxidants, seleno-l-methionine, ginsenoside Rb1, and MnTBAP (superoxide dismutase mimetic), effectively blocked resistin-induced eNOS downregulation. Meanwhile, resistin activated the mitogen-activated protein kinases p38 and c-Jun NH2-terminal kinase (JNK), and the specific p38 inhibitor SB-239063 effectively blocked resistin-induced ROS production and eNOS downregulation. Furthermore, immunoreactivity of resistin was increased in atherosclerotic regions of human aorta and carotid arteries. Thus resistin directly induces eNOS downregulation through overproduction of ROS and activation of p38 and JNK in HCAECs. Resistin-induced mitochondrial dysfunction and imbalance in cellular redox enzymes may be the underlying mechanisms of oxidative stress
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