Objective To study the risk factors for in-hospital mortality in patients with acute myocardial infarction(AMI)undergoing emergency percutaneous coronary intervention(EPCI).Methods Nine hundred and eight patients with acute myocardial infarction(AMI)who underwent EPCI at Beijing Jingmei Group General Hospital between September 2016 and December 2022 were enrolled and divided into an in-hospital death group(36 cases)and a survival group(872 cases)based on in-hospital outcomes.The basic information,clinical indicators,results of coronary angiography,outcomes of EPCI,and complications were compared between the two groups.Multiple logistic regression analysis was conducted to identify the risk factors for in-hospital mortality during EPCI.Results The age and serum creatinine levels of the death group were higher than those of the survival group(P＜0.05),and the estimated glomerular filtration rate(eGFR)and hemoglobin(Hb)levels were lower than those of the survival group(P＜0.05).The proportion of diabetes mellitus,cerebral infarction,cardiogenic shock,left main culprit lesion,rapid ventricular arrhythmia,TIMI flow grade＜3 after EPCI for culprit vessel,and intra-aortic balloon pump(IABP)implantation in the death group were higher than those of the survival group(P＜0.05).The results of multiple logistic regression analysis showed that age,cardiogenic shock,TIMI flow grade＜3 after culprit vessel intervention,and rapid ventricular arrhythmia had a statistically significant impact on in-hospital mortality in EPCI(P＜0.05).Conclusion Age,cardiogenic shock,TIMI flow grade＜3 after PCI for culprit vessels,and rapid ventricular arrhythmia are independent risk factors for in-hospital mortality in EPCI patients with AMI.

Objective By analyzing the clinical symptoms, heart rate ( HR) , arterial oxygen saturation ( SaO2 ) and the number of white blood cells (WBC), we aimed to explore the implication of the above-mentioned indexes for early warning of high altitude pulmonary edema ( HAPE) .Methods Based on the Lake Louise Self-assessmeat Scoring System ( LLSS) and the scoring of respiratory symptoms, 628 subjects were divided into three groups: group A ( the healthy;score<3),group B(acute mountain sickness, AMS; score>3 and excluding HAPE),and group C (HAPE).Moreover, we analyzed the incidence of some clinical symptoms, HR and SaO2 , as well as the WBC number of some subjects in the three groups.Results The incidence of respiratory symptoms and WBC number were significantly increased in group C compared with group B(P<0.05).In addition,unlike group A and B, the mean HR in group C rose gradually in the first 3 days and was markedly increased at the third day(F=6.37,P<0.05).The mean SaO2in group C was remarkably lower than in group A and B in the first 3 days(F=8.21,F=8.77,F=9.58,P<0.01).Conclusion Those who enter high altitude for the first time with notable respiratory symptoms, WBC increase, HR maladaptation and decrease in SaO2 (>30%) have high risk of HAPE.It is of special importance to detect HAPE earlier at high altitude.

Objective To explore the role of potassium channel in cardiomyocyte apoptosis induced by ischemia/reperfusion process. Methods Cell viability,caspase-3 activity,intracellular reactive oxygen species(ROS)levels and cell membrane integrity were observed in apoptotic model of mouse cardiomyocytes induced by ischemia/reperfusion(I/R).Experiment groups included negative control,positive control(I/R)and drug treatment group(I/R + potassium channel blocker).Results (1)Potassium channel blockers potently inhibited cardiomyocyte apoptosis induced by I/R.Cell viability in Quinine(81.1%)and BaCl2(82.3%)groups were higher than in positive group (52.1%)(all P＜0.01).(2)Compared with positive control group(482.3%),potassium channel blockers(188.3% in Quinine group and 191.4% in BaCl2 group)inhibited caspase-3 activity significantly 24 hours after reperfusion(P＜0.01).(3)In both positive control and drug groups,the cell lactate dehydrogenase(LDH)leakage was less than 10% at 96 hours after reperfusion.Conclusions Potassium channel blockers can protect injured cardiomyocyte by inhibiting caspase-3 activity and ROS production in I/R process.

AIM:To investigate whether the chloride/bicarbonate (Cl-/HCO-3) exchanger is involved in staurosporine (STS) induced mouse cardiomyocyte apoptosis,and further understand the function of Cl-/HCO-3 exchanger in cell apoptosis. METHODS:To induce mouse cardiomyocyte apoptosis and to explore the effect of Cl-/HCO-3 exchanger,STS was used with two methods:⑴ different blocker,the chloride channel as well as exchanger blocker DIDS and the chloride channel blocker NPPB; ⑵ different culture medium with or without HCO-3 component. RESULTS:The cell viability and caspase-3 activity of DIDS and NPPB on STS-induced cardiomyocyte apoptosis were 59.7% and 47.2%,175.0% and 212.0% respectively with significant statistic differences (both P0.05,n=20). The cell viability and caspase-3 activity of STS-induced cardiomyocyte apoptosis in culture medium with or without HCO-3 were 29.8% and 41.6%,553.4% and 424.7%,respectively (both P