The effect of mild induced hypothermia on outcomes of patients after cardiac arrest: a systematic review and meta-analysis of randomised controlled trials.

INTRODUCTION: Mild induced hypothermia (MIH) is believed to reduce mortality and neurological impairment after out-of-hospital cardiac arrest. However, a recently published trial demonstrated that hypothermia at 33 °C did not confer a benefit compared with that of 36 °C. Thus, a systematic review and meta-analysis of randomised controlled trials (RCTs) was made to investigate the impact of MIH compared to controls on the outcomes of adult patients after cardiac arrest. METHODS: We searched the following electronic databases: PubMed/MEDLINE, the Cochrane Library, Embase, the Web of Science, and Elsevier Science (inception to December 2014). RCTs that compared MIH with controls with temperature >34 °C in adult patients after cardiac arrest were retrieved. Two investigators independently selected RCTs and completed an assessment of the quality of the studies. Data were analysed by the methods recommended by the Cochrane Collaboration. Random errors were evaluated with trial sequential analysis. RESULTS: Six RCTs, including one abstract, were included. The meta-analysis of included trials revealed that MIH did not significantly decrease the mortality at hospital discharge (risk ratio (RR) = 0.92; 95 % confidence interval (CI), 0.82-1.04; p = 0.17) or at 6 months or 180 days (RR = 0.94; 95 % CI, 0.73-1.21; p = 0.64), but it did reduce the mortality of patients with shockable rhythms at hospital discharge (RR = 0.74; 95 % CI, 0.59-0.92; p = 0.008) and at 6 months or 180 days. However, MIH can improve the outcome of neurological function at hospital discharge (RR = 0.80; 95 % CI, 0.64-0.98; p = 0.04) especially in those patients with shockable rhythm but not at 6 months or 180 days. Moreover, the incidence of complications in the MIH group was significantly higher than that in the control group. Finally, trial sequential analysis indicated lack of firm evidence for a beneficial effect. CONCLUSION: The available RCTs suggest that MIH does not appear to improve the mortality of patients with cardiac arrest while it may have a beneficial effect for patients with shockable rhythms. Although MIH may result in some adverse events, it helped lead to better outcomes regarding neurological function at hospital discharge. Large-scale ongoing trials may provide data better applicable to clinical practice.

Preoperative Serum Fibrinogen is Associated With Acute Kidney Injury after Cardiac Valve Replacement Surgery.

Acute kidney injury (AKI) after open cardiac surgery is associated with a longer hospital stay and higher risk of mortality. We aimed to explore the association between preoperative serum fibrinogen level and risk of postoperative AKI in patients with open cardiac surgery. 3459 patients who underwent cardiac valve replacement surgery from January 2011 to September 2015 were recruited. The primary outcome was AKI, defined as AKI stage-1 or higher based on the Kidney Disease: Improving Global Outcomes (KDIGO) Guidelines. Synthetic Minority Oversampling Technique (SMOTE) was used to subsample minority groups to eliminate classification bias. 510 (14.74%) patients developed postoperative AKI. Serum fibrinogen was independently associated with AKI (OR = 1.211, 95% CI 1.080 to 1.358, p = 0.001) after adjustment of covariates. The receiver operator characteristic (ROC) curve for the outcome of AKI, after the addition of serum fibrinogen, had a c-statistic increasing from 0.72 to 0.73 (p < 0.001). This translated to a substantially improved AKI risk classification with a net reclassification index of 0.178 (p < 0.001). After SMOTE subsampling, serum fibrinogen was still independently associated with AKI grade 1 or higher (OR = 1.212, 95% CI 1.1089 to 1.347, p = 0.003). Preoperative serum fibrinogen levels were associated with the risk of postoperative AKI after cardiac valve replacement surgery.

Chemokine receptor 7 overexpression promotes mesenchymal stem cell migration and proliferation via secreting Chemokine ligand 12.

Great interest has been shown in mesenchymal stem cell (MSC) therapy in a wide variety of clinical domains. However, the therapeutic efficiency depends on the proliferation and migration of MSCs. Chemokine receptors are involved in regulating the proliferation and migration to the specific organs of MSCs in different microenvironments. CXC receptor seven (CXCR7), a newly discovered Chemokine ligand 12 (CXCL12) receptor, has organ specificity for tumour migration. We hypothesized that CXCR7 expression affects proliferation and migration of MSCs. In present study, we constructed long-term and stable mMSCs lines overexpressing and suppressing CXCR7 modifications with lentiviral vectors. The transduction efficiencies, mRNA and protein expression of CXCR7 were significantly regulated. CXCR7 gene overexpression promoted mMSCs proliferation and migration, whereas suppressing CXCR7 had the opposite effect. Additional CXCL12 improved the vertical migration of mMSCs. The overexpression of CXCR7 increased the MSC-secreted CXCL12, VCAM-1, CD44 and MMP2 levels, which contributed to the improvement of mMSC proliferation and migration. Therefore, overexpressing CXCR7 improved the proliferation and migration of mMSCs, which may be attributable to the CXCL12 secreted by MSCs, leading to a positive feedback loop for CXCL12/CXCR7 axis. Our results may provide a potential method for improving the treatment effectiveness of mMSCs by overexpressing CXCR7.