Meta-analysis of drug-eluting versus bare metal stents in patients with indications for oral anticoagulation undergoing coronary stenting.

BACKGROUND: Current expert consensus recommends the use of bare metal stent (BMS) for patients with an indication for oral anticoagulation (OAC) undergoing coronary stenting. The use of drug-eluting stents (DES) should be limited. However, there is a lack of evidence to support these recommendations. We performed a meta-analysis to compare the efficacy and safety of DES to BMS in these patients. METHODS: We searched PubMed, Embase, the Cochrane library, and relevant journals. Studies comparing the efficacy and safety of DES to BMS in patients with an indication for OAC undergoing coronary stenting were included. End points included major adverse cardiac events (MACE), death, bleeding complications, and stroke. The outcome assessments were measured by hazard ratio (HR) and its 95% confidence interval. RESULTS: We yielded 453 studies by primary searching. According to the inclusion criteria, four studies enrolling 1,522 patients were finally included. A pooled estimate of HR for MACE, all-cause mortality, myocardial infarction, and bleeding complications showed no significant differences between patients treated with DES and BMS. The risk of target vessel revascularization (TVR) was significantly decreased in the DES implanted patients in comparison with patients with a BMS implantation. CONCLUSION: For patients with an indication for OAC undergoing coronary stenting, DES might a DES can be as safely used as a BMS, and is superior in reducing the risk of TVR.

Impact of image integration on catheter ablation for atrial fibrillation using three-dimensional electroanatomic mapping: a meta-analysis.

BACKGROUND: Studies comparing the procedural and clinical outcomes of catheter ablation for atrial fibrillation (AF) guided by CartoMerge and that by Carto have achieved mixed results (Carto, Biosense Webster, Diamond Bar, CA, USA). We collected these studies and conducted a meta-analysis to determine whether CartoMerge results in better procedural and clinical outcomes. METHODS AND RESULTS: Three randomized controlled trials and two controlled observational studies were collected for analysis. The clinical and procedural outcomes of interest were AF recurrence after catheter ablation, major complications, procedure durations, and fluoroscopy time. Meta-analysis was performed using RevMan 5.0.18 software (The Cochrane Collaboration, Copenhagen, Denmark) and pooled estimates of effect were reported as risk ratios with 95% confidence intervals (CI). The overall results of this meta-analysis indicate that catheter ablation for AF guided by CartoMerge is insignificantly associated with a decreased risk of recurrences (RR = 0.76; 95% CI: 0.55-1.04; P = 0.09) and major complications (RR = 0.73; 95% CI: 0.37-1.45; P = 0.37) compared with that by Carto. CONCLUSION: The image integration using CartoMerge guiding catheter ablation for AF does not improve the main clinical outcomes significantly compared with that by Carto in centers with experienced operators.

Liquiritigenin attenuates isoprenaline­induced myocardial fibrosis in mice through the TGF­ß1/Smad2 and AKT/ERK signaling pathways.

Myocardial fibrosis is a pathological process characterized by excessive accumulation of extracellular matrix in myocardial interstitial spaces. Myocardial fibrosis is a fundamental process in ventricular remodeling and a primary contributor to the progression of heart failure. Liquiritigenin (LQ) is a flavanone compound with anti­oxidative, anti­carcinogenic, anti­inflammatory and estrogenic properties. The present study aimed to investigate the regulatory potential of LQ treatment in a mouse model of isoprenaline (ISO)­induced cardiac fibrosis and in cultured H9C2 cardiomyocytes stimulated with angiotensin II (Ang II). The treatment of ISO­induced mice with LQ significantly decreased the levels of cardiac injury­related proteins in the serum and ECM accumulation in mouse heart tissues. LQ treatment also effectively alleviated cardiac dysfunction in ISO­treated mice. Further analyses revealed that LQ inhibited ISO­induced collagen formation and activation of the transforming growth factor­ß1 (TGF­ß1)/Smad2 and protein kinase B (AKT)/extracellular signal­regulated kinase (ERK) signaling pathways. As a major pathological event in myocardial fibrosis, the apoptosis of cardiomyocytes has been considered a key mechanism contributing to impaired left ventricle performance. The pretreatment of rat cardiomyocytes with LQ significantly reduced the apoptosis of H9C2 cells, and inhibited Ang II­induced activation of the TGF­ß1/Smad2 and AKT/ERK pathways. In conclusion, the present study revealed that LQ ameliorated ISO­induced myocardial fibrosis in mice and inhibited the apoptosis of cardiomyocytes in vitro by inhibiting the TGF­ß1/Smad2 and AKT/ERK signaling pathways. These results suggested the anti­fibrotic and cardioprotective potential of LQ in fibrosis, thus supporting the use of LQ for the management of cardiomyocyte injury and myocardial fibrosis in patients with cardiac diseases.

Neferine inhibits angiotensin II-stimulated proliferation in vascular smooth muscle cells through heme oxygenase-1.

AIM: To explore the effect of neferine on angiotensin II (Ang II)-induced vascular smooth muscle cell (VSMC) proliferation. METHODS: Human umbilical vein smooth muscle cells (HUVSMCs) were used. Cell proliferation was determined by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis. Heme oxygenase (HO)-1 protein expression was tested by Western blot analysis. Extracellular signal-regulated protein kinase 1/2 (ERK1/2) activation was determined by using immunoblotting. RESULTS: Pre-incubation of HUVSMCs with neferine (0.1, 0.5, 1.0, and 5.0 micromol/L) significantly inhibited Ang II-induced cell proliferation in a concentration-dependent manner and neferine 5.0 micromol/L increased HO-1 expression by 259% compared with control. The antiproliferative effect of neferine was significantly attenuated by coapplication of zinc protoporphyrin IX (ZnPP IX, an HO-1 inhibitor) with neferine. Ang II-enhanced ERK1/2 phosphorylation was markedly reversed by neferine. By inhibiting HO-1 activity with ZnPP IX, the inhibitive effect of neferine on ERK1/2 phosphorylation was significantly attenuated. Cobalt-protoporphyrin (CoPP), an HO-1 inducer, significantly decreased Ang II-induced ERK1/2 phosphorylation and inhibited Ang II-induced cell proliferation. The ERK1/2 pathway inhibitor PD98059 significantly blocked Ang II-enhanced ERK1/2 phosphorylation and inhibited cell proliferation. CONCLUSION: These findings suggest that neferine can inhibit Ang II-induced HUVSMC proliferation by upregulating HO-1, leading to the at least partial downregulation of ERK1/2 phosphorylation.

[Study on changes of content of Tannin in Nodus Nelumbinis Rhizomatis Charcoal].

OBJECTIVE: To determine changes of content of Tannin in different Nodus Nelumbinis Rhizomatis Charcoal. METHODS: The content of Tannin of Nodus Nelumbinis Rhizomatis Charcoal was detected by UV and colorimetric method. RESULTS: The content of tannin in standard sample was the highest. CONCLUSION: It should be studied whether the tannin of Nodus Nelumbinis Rhizomatis Charcoal is the active ingredients of hemostasis.

Upregulation of heme oxygenase-1 expression by hydroxysafflor yellow A conferring protection from anoxia/reoxygenation-induced apoptosis in H9c2 cardiomyocytes.

BACKGROUND: Reperfusion therapy is widely utilized for acute myocardial infarction (AMI), so ischemia/reperfusion (I/R) of the heart is frequently encountered in clinical practice. The curative effects of reperfusion therapy for AMI are favourable in most cases, but reperfusion can also cause harmful effect to cardiomyocytes. Hydroxysafflor yellow A (HSYA) is an effective therapeutic agent to alleviate I/R injury, but the mechanisms underlying this therapeutic effect are unknown. METHODS AND RESULTS: The H9c2 cardiomyocyte cell line was incubated with or without HSYA during hypoxia, then it was reoxygenated. In the presence of HSYA, reoxygenation resulted in the upregulated expression and activity of heme oxygenase-1 (HO-1), phosphorylation of Akt, translocation of nuclear factor Nrf2, and most importantly, a reduction in A/R-induced apoptosis. An HO-1 inhibitor completely suppressed HO-1 enzymatic activity upregulated by HSYA and notably diminished the anti-apoptotic effect of HSYA. An inhibitor of PI3K, completely blocked Akt phosphorylation induced by HSYA and partly negated HSYA-induced upregulation of HO-1, translocation of nuclear factor Nrf2 and suppression of apoptosis in the H9c2 cardiomyocytes. CONCLUSIONS: Our study suggests that HSYA can provide protection to H9c2 cardiomyocytes against A/R-induced apoptosis. This protective effect largely depends on the upregulation of HO-1 expression through the PI3K/Akt/Nrf2 signaling pathway.