Haichen Chu

The effect of tranexamic acid to reduce blood loss and transfusion on off-pump coronary artery bypass surgery: A systematic review and cumulative meta-analysis

STUDY OBJECTIVE To assess the safety and efficacy of tranexamic acid (TA) on off-pump coronary artery bypass (OPCAB) surgery. DESIGN Meta-analysis. SETTING Operating room, OPCAB surgery, all surgeries were elective measurements. Searching the following data sources respectively: PubMed/MEDLINE, the Cochrane Library, EMBASE and reference lists of identified articles, we performed a meta-analysis of postoperative 24h blood loss, postoperative allogeneic transfusion, re-operation for massive bleeding, postoperative mortality, and postoperative thrombotic complications. MAIN RESULTS Using electronic databases, we selected 15 randomized control trials (RCTs), carried out between 2003 and 2016, with a total of 1250 patients for our review. TA significantly reduced the postoperative 24h blood loss (mean difference -213.32ml, 95% confidence intervals, -247.20ml to -179.43ml; P<0.0001). And, TA also significantly reduced the risk of packed red blood cell (PRBCs) transfusion (risk ratio 0.62; 95% confidence intervals 0.51 to 0.76; P<0.0001) and fresh frozen plasma (FFP) transfusion (0.65; 0.52 to 0.81; P<0.001). There were no statistical significance on platelet transfusion (risk difference -0.00, 95% confidence interval -0.02 to 0.02; P=0.73) and re-operation (0.00, -0.02 to 0.02; P=1.00). No association was found between TA and morbility (risk difference -0.00, 95% confidence interval -0.02 to 0.02; P=0.99) and thrombotic complications (-0.01, -0.01 to 0.02; P=0.70). CONCLUSIONS TA reduced the probability of receiving a PRBCs and FFP transfusion during OPCAB surgery. And no association with postoperative death and thrombotic events was found. However, further trials with an appropriate sample size are required to confirm TA safety in OPCAB surgery.

Morphine postconditioning protects against reperfusion injury: the role of protein kinase c-epsilon, extracellular signal-regulated kinase 1/2 and mitochondrial permeability transition pores

Background/Aims: The purpose of this study was to investigate the implications of protein kinase C-epsilon (PKCε), Extracellular Signal-regulated Kinase 1/2 (ERK1/2) and mitochondrial permeability transition pore (mPTP) in myocardial protection induced by morphine postconditioning (MpostC). Methods: The isolated rat hearts were randomly assigned into one of eight groups. Hearts in time control (TC) group were constantly perfused for 105min. Hearts in ischemia-reperfusion (I/R) group were subjected to 45 min of ischemia followed by 1 h of reperfusion. MpostC was induced by 10 min of morphine administration at the onset of reperfusion. εV1-2 (an inhibitor of PKCε) and PD (an inhibitor of ERK1/2) was administered with or without morphine during the first 10 min of reperfusion following the 45 min of ischemia. I/R injury was assessed by functional parameters, creatine kinase-MB (CK-MB) release and infarct size (IS/AAR). Additional hearts were excised at 20 min following reperfusion to detect the membrane-specific translocation of PKCε, ERK1/2 phosphorylation, mitochondrial permeability transition (MPT) and cytochrome C (Cyt-c) release. Results: MpostC markedly reduced infarct size (IS/AAR), CK-MB release, and improved cardiac function recovery. However, these protective effects were partly abolished in the presence of εV1-2 or PD. Compared to TC group, the membrane translocation of PKCε, ERK1/2 phosphorylation, mPTP opening, and Cyt-c release were significantly increased in I/R hearts. MpostC further increased the membrane translocation of PKCε and ERK1/2 phosphorylation, and significantly inhibited mPTP opening and Cyt-c release. However, those protective effects induced by MpostC were abolished by εV1-2 or PD, which, used alone, showed no influence on reperfusion injury. Conclusions: These findings suggest that MpostC protects isolated rat hearts against ischemia-reperfusion injury via activating PKCε-ERK1/2 pathway and inhibiting mPTP opening.