A systematic review and meta-analysis of the impact of the left atrial appendage closure on left atrial function.

BACKGROUND: Left atrial (LA) appendage closure (LAAC) is effective in patients with atrial fibrillation who are not candidates for long-term anticoagulation. However, the impact of LAAC on LA function is unknown. The aim of this study is to evaluate the impact of LAAC on atrial function. METHODS: This meta-analysis was conducted according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. A search strategy was designed to utilize PubMed/Medline, EMBASE, and Google scholar for studies showing the effect of LAAC on the LA function from inception to November 20, 2021. The standardized mean difference (SMD) was calculated from the means and standard deviations. RESULTS: Of 247 studies initially identified, 8 studies comprising 260 patients were included in the final analysis. There was a significant increase in LA emptying fraction following LAAC compared with preoperative function (SMD: 0.53; 95% confidence interval [CI]: 0.04-1.01; p = .03; I2  = 75%). In contrast, there were no significant differences in LA volume (SMD: -0.07; 95% CI: -0.82-0.69; p = .86; I2  = 92%) peak atrial longitudinal strain (SMD: 0.50; 95% CI: -0.08-1.08; p = .09; I2  = 89%), peak atrial contraction strain (SMD: 0.38; 95% CI: -0.22-0.99; p = .21; I2  = 81%), strain during atrial contraction (SMD: -0.24; 95% CI: -0.61-0.13; p = .20; I2  = 0%), strain during ventricular systole (SMD: 0.47; 95% CI: -0.32-1.27; p = .24; I2  = 89%), strain during ventricular diastole (SMD: 0.09; 95% CI: -0.32-0.51; p = .66; I2  = 65%). CONCLUSION: LAAC is associated with improvement in the left atrial emptying fraction, but did not significantly influence other parameters

PloS one

The vasculoprotective properties of delphinidin are driven mainly by its action on endothelial cells. Moreover, delphinidin displays anti-angiogenic properties in both in vitro and in vivo angiogenesis models and thereby might prevent the development of tumors associated with excessive vascularization. This study was aimed to test the effect of delphinidin on melanoma-induced tumor growth with emphasis on its molecular mechanism on endothelial cells. Delphinidin treatment significantly decreased in vivo tumor growth induced by B16-F10 melanoma cell xenograft in mice. In vitro, delphinidin was not able to inhibit VEGFR2-mediated B16-F10 melanoma cell proliferation but it specifically reduced basal and VEGFR2-mediated endothelial cell proliferation. The anti-proliferative effect of delphinidin was reversed either by the MEK1/2 MAP kinase inhibitor, U-0126, or the PI3K inhibitor, LY-294002. VEGF-induced proliferation was reduced either by U-0126 or LY-294002. Under these conditions, delphinidin failed to decrease further endothelial cell proliferation. Delphinidin prevented VEGF-induced phosphorylation of ERK1/2 and p38 MAPK and decreased the expression of the transcription factors, CREB and ATF1. Finally, delphinidin was more potent in inhibiting in vitro cyclic nucleotide phosphodiesterases (PDEs), PDE1 and PDE2, compared to PDE3-PDE5. Altogether delphinidin reduced tumor growth of melanoma cell in vivo by acting specifically on endothelial cell proliferation. The mechanism implies an association between inhibition of VEGF-induced proliferation via VEGFR2 signalling, MAPK, PI3K and at transcription level on CREB/ATF1 factors, and the inhibition of PDE2. In conjunction with our previous studies, we demonstrate that delphinidin is a promising compound to prevent pathologies associated with generation of vascular network in tumorigenesis

Tumour growth inhibition and anti-angiogenic effects using curcumin correspond to combined PDE2 and PDE4 inhibition

International audienc

Delphinidin Inhibits Tumor Growth by Acting on VEGF Signalling in Endothelial Cells.

The vasculoprotective properties of delphinidin are driven mainly by its action on endothelial cells. Moreover, delphinidin displays anti-angiogenic properties in both in vitro and in vivo angiogenesis models and thereby might prevent the development of tumors associated with excessive vascularization. This study was aimed to test the effect of delphinidin on melanoma-induced tumor growth with emphasis on its molecular mechanism on endothelial cells. Delphinidin treatment significantly decreased in vivo tumor growth induced by B16-F10 melanoma cell xenograft in mice. In vitro, delphinidin was not able to inhibit VEGFR2-mediated B16-F10 melanoma cell proliferation but it specifically reduced basal and VEGFR2-mediated endothelial cell proliferation. The anti-proliferative effect of delphinidin was reversed either by the MEK1/2 MAP kinase inhibitor, U-0126, or the PI3K inhibitor, LY-294002. VEGF-induced proliferation was reduced either by U-0126 or LY-294002. Under these conditions, delphinidin failed to decrease further endothelial cell proliferation. Delphinidin prevented VEGF-induced phosphorylation of ERK1/2 and p38 MAPK and decreased the expression of the transcription factors, CREB and ATF1. Finally, delphinidin was more potent in inhibiting in vitro cyclic nucleotide phosphodiesterases (PDEs), PDE1 and PDE2, compared to PDE3-PDE5. Altogether delphinidin reduced tumor growth of melanoma cell in vivo by acting specifically on endothelial cell proliferation. The mechanism implies an association between inhibition of VEGF-induced proliferation via VEGFR2 signalling, MAPK, PI3K and at transcription level on CREB/ATF1 factors, and the inhibition of PDE2. In conjunction with our previous studies, we demonstrate that delphinidin is a promising compound to prevent pathologies associated with generation of vascular network in tumorigenesis

Impact of Adjuvant Use of Midodrine to Intravenous Vasopressors: A Systematic Review and Meta-Analysis

Purpose. To evaluate the efficacy and safety of midodrine use in intensive care units (ICU) to facilitate weaning off intravenous vasopressors (IVV). Methods. We searched PubMed/MEDLINE, Cochrane library, and Google Scholar (inception through October 18th, 2020) for studies evaluating adjuvant use of midodrine to IVV in the ICU. The outcomes of interest were ICU length of stay (LOS), hospital LOS, mortality, IVV reinstitution, ICU readmission, and bradycardia. Estimates were pooled using the random-effects model. We reported effect sizes as standardized mean difference (SMD) for continuous outcomes and risk ratios (RRs) for other outcomes with a 95% confidence interval (CI). Results. A total of 6 studies were found that met inclusion criteria and had sufficient data for our quantitative analysis (1 randomized controlled trial and 5 retrospective studies). A total of 2,857 patients were included: 600 in the midodrine group and 2,257 patients in the control group. Midodrine use was not associated with a significant difference in ICU LOS (SMD 0.16 days; 95% CI −0.23 to 0.55), hospital LOS (SMD 0.03 days; 95% CI −0.33 to 0.0.39), mortality (RR 0.87; 95% CI 0.52 to 1.46), IVV reinstitution (RR 0.47; 95% CI 0.17 to 1.3), or ICU readmission (RR 1.03; 95% CI 0.71 to 1.49) when compared to using only IVV. However, there were higher trends of bradycardia with midodrine use that did not reach significance (RR 7.64; 95% CI 0.23 to 256.42). Conclusion. This meta-analysis suggests that midodrine was not associated with a significant decrease in ICU LOS, hospital LOS, mortality, or ICU readmissions

Sex Differences in the Clinical Outcomes of Patients with Takotsubo Stress Cardiomyopathy: A Meta-analysis of Observational Studies.

The incidence of takotsubo stress cardiomyopathy (TSCM) in males is low compared to females. Sex-based differences in clinical outcomes of TSCM are not well characterized. The aim of this meta-analysis was to analyze whether sex-based differences are observed in TSCM clinical outcomes. A comprehensive literature search of Pubmed, Embase, Cochrane Library database, and Web of Science was performed from inception to June 20, 2022, for studies comparing the clinical outcomes between males versus females in TSCM. The primary outcome of interest was in-hospital all-cause mortality and cardiogenic shock. The secondary outcomes were cardiovascular mortality, receipt of mechanical ventilation, intra-aortic balloon pump, and occurrence of ventricular arrhythmia, and left ventricular thrombus. A random-effects model was used to calculate the risk ratios (RR) and confidence intervals (CI). Heterogenicity was assessed using the Higgins I index. Twelve observational studies involving 51,213 patients (4,869 males, and 46,344 females) were included in the meta-analysis. Male sex was associated with statistically significant higher in-hospital all-cause mortality when compared to females in patients with TSCM (RR 2.17; 95% CI 1.77-2.67; P < 0.001) The rate of cardiogenic shock was significantly higher in males with TSCM as compared to females (RR 1.66; 95% CI 1.29-2.12; P < 0.001). Our meta-analysis showed a difference in the clinical outcomes of TSCM between men and women. Males sex was associated with a two-fold greater in-hospital all-cause mortality risk compared to female sex. The higher mortality risk associated with male sex deserves further study, and particularly whether it represents later recognition of the condition and disparities in treatments. [Abstract copyright: Copyright © 2023. Published by Elsevier Inc.

Long-term Outcomes of Acute Myocardial Infarction in Pre-existing Coronary Artery Ectasia: A Systematic Review and Meta-Analysis

Coronary artery ectasia is associated with an increased risk of acute myocardial infarction. This meta-analysis evaluates outcomes following acute myocardial infarction in patients with pre-existing coronary artery ectasia. A search strategy was designed to utilize PubMed/Medline, EMBASE, and Google scholar for studies including the outcomes of acute myocardial infarction in patients with coronary artery ectasia from inception to February 10, 2022. We reported effect sizes as odds ratio (OR) with a 95% confidence interval (CI). We used I2 statistics to estimate the extent of unexplained statistical heterogeneity. There were 7 studies comprising 13,499 patients in the final analysis. There was no significant difference between patients with coronary ectasia and patients without coronary ectasia in terms of all-cause mortality (OR 0.95; 95% CI 0.58 to 1.56; P = 0.79; I2 = 0%), major adverse cardiovascular events (MACE; OR 4.04; 95% CI 0.34 to 47.57; P = 0.17; I2 = 95%), myocardial re-infarction (OR 2.13; 95% CI 0.83 to 5.47; P = 0.08; I2 = 59%), target vessel revascularization (OR 1.31; 95% CI 0.69 to 2.48; P = 0.21; I2 = 0%), or requiring mechanical supportive devices (OR 1.32; 95% CI 0.22 to 7.83; P = 0.57; I2 = 56%). Acute myocardial infarction in the presence of coronary artery ectasia is not associated with an increased risk of death, MACE, myocardial infarction, or the need for mechanical circulatory support