44 research outputs found

    The beneficial effects of renin–angiotensin system blockades on 2 year outcomes in coronary artery ectasia patients

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    <p><b>Objectives:</b> This study was designed to investigate the impact of renin–angiotensin system blockade (RASB) therapy with angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers on the outcomes of coronary artery ectasia (CAE).</p> <p><b>Methods:</b> The CAE patients identified by coronary angiography from our center were consecutively enrolled. We obtained the baseline discharge prescription of RASB from the medical records system and conducted follow-up through telephone interviews. Cox regression models, propensity score and subgroup analysis were used to assess the impact of RASB on all-cause mortality and non-fatal myocardial infarction. Both the unadjusted and adjusted Kaplan–Meier curves stratified by RASB therapy were plotted.</p> <p><b>Results:</b> There were 595 patients with CAE in total and 333 (56.0%) were prescribed RASB therapy. Over a 2 year follow-up time, 16 all-cause deaths and 10 non-fatal myocardial infarctions were identified. Those patients treated with RASB had a significantly lower all-cause mortality and non-fatal myocardial infarction rate with an adjusted hazard ratio of 0.32 (95% confidence interval: 0.13 to 0.77, <i>p</i> = .011). The outcome benefits of RASB therapy were further confirmed in the propensity score analysis and subgroup analysis.</p> <p><b>Conclusions:</b> This observational study suggests that RASB therapy is associated with a lower risk of all-cause mortality and non-fatal myocardial infarction in patients with CAE.</p

    Remote Ischemic Preconditioning Reduces Perioperative Cardiac and Renal Events in Patients Undergoing Elective Coronary Intervention: A Meta-Analysis of 11 Randomized Trials

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    <div><p>Background</p><p>Results from randomized controlled trials (RCT) concerning cardiac and renal effect of remote ischemic preconditioning(RIPC) in patients with stable coronary artery disease(CAD) are inconsistent. The aim of this study was to explore whether RIPC reduce cardiac and renal events after elective percutaneous coronary intervention (PCI).</p><p>Methods and Results</p><p>RCTs with data on cardiac or renal effect of RIPC in PCI were searched from <i>Pubmed</i>, <i>EMBase</i>, and <i>Cochrane library</i> (up to July 2014). Meta-regression and subgroup analysis were performed to identify the potential sources of significant heterogeneity(<i>I</i><sup>2</sup>≥40%). Eleven RCTs enrolling a total of 1713 study subjects with stable CAD were selected. Compared with controls, RIPC significantly reduced perioperative incidence of myocardial infarction (MI) [odds ratio(OR)  = 0.68; 95% CI, 0.51 to 0.91; <i>P</i> = 0.01; <i>I<sup>2</sup></i> = 41.0%] and contrast-induced acute kidney injury(AKI) (OR = 0.61; 95% CI, 0.38 to 0.98; <i>P</i> = 0.04; <i>I<sup>2</sup></i> = 39.0%). Meta-regression and subgroup analyses confirmed that the major source of heterogeneity for the incidence of MI was male proportion (coefficient  = −0.049; <i>P</i> = 0.047; adjusted <i>R<sup>2</sup></i> = 0.988; <i>P</i> = 0.02 for subgroup difference).</p><p>Conclusions</p><p>The present meta-analysis of RCTs suggests that RIPC may offer cardiorenal protection by reducing the incidence of MI and AKI in patients undergoing elective PCI. Moreover, this effect on MI is more pronounced in male subjects. Future high-quality, large-scale clinical trials should focus on the long-term clinical effect of RIPC.</p></div

    Forest plot for the incidence of myocardial infarction (MI).

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    <p>RIPC significantly decreased the risk of MI [odds ratio (OR)  = 0.68, <i>P</i> = 0.01].RIPC, remote ischemic preconditioning.</p

    Summarized study design of included randomized trials.

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    <p>Note: I/R, ischemia/reperfusion; SBP, systolic blood pressure; DBP, diastolic blood pressure; N.R, not report; RIC, remote ischemic conditioning; Ctrl, control.</p><p>Summarized study design of included randomized trials.</p

    Meta-regression plots on the incidence of MI in PCI[Male proportion (%); coefficient  = −0.049; <i>P</i> = 0.047)].

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    <p>Meta-regression plots on the incidence of MI in PCI[Male proportion (%); coefficient  = −0.049; <i>P</i> = 0.047)].</p

    AMPK knock down abolished resveratrol- and metformin-mdiated SIRT1 activation.

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    <p>HUVECs were transfected with AMPK siRNA (si-AMPK) and incubated in HG for 3days and then NG for 3 days. Resveratrol (RSV) or metformin (MET) was added into culture media during the entire 6 days of subculture. Immunoblotting and quantification of p300, SIRT1, p21, Ac-p53, and p53 protein expression (A-G). For p300, SIRT1, and p21, values were normalized to β-actin; for Ac-p53, normalized to total p53. (H) Relative ROS production. (I) Deacetylase activity of SIRT1. (J) SA β-Gal positive positivity. *<i>P</i> < 0.05.</p

    Potential source of heterogeneity for the incidence of MI in PCI.

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    <p>Note: MI, myocardial infarction; Coeff., coefficient; OR, odds ratio; CI, Confidence Interval.</p><p>Potential source of heterogeneity for the incidence of MI in PCI.</p

    Overexpression of SIRT1 or suppression of p300 inhibited transient HG-induced senescent “memory” in HUVECs.

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    <p>Cells were cultured in HG for 3 days followed by 3 days of NG media. SIRT1 plasmid (pSIRT1) or p300 siRNA (si-p300) was transfected into HUVECs twice, 12 hours prior to HG and NG incubation, respectively. After 6 days of culture, cells were harvested for further analysis. Immunoblotting and quantification of p300, SIRT1, p21, Ac-p53, and p53 protein expression after pSIRT1 transfection (A-F) or after 300 siRNA transfection (G-L). For p300, SIRT1, and p21, values were normalized to β-actin; for Ac-p53, normalized to total p53. SIRT1 activity, SA β-Gal positivity, and relative ROS production in HUVECs transfected with pSIRT1 (M-O) or p300 siRNA (P-R). *<i>P</i> < 0.05.</p
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