Eff ect of early intervention on 12-month follow-up clinical prognosis in patients with high-risk non-ST-segment elevation acute coronary syndrome / 中国介入心脏病学杂志

Objective To compare 12-month follow-up clinical outcome of an early to a delayed intervention in the management of high-risk non-ST elevation acute coronary syndrome (NSTE-ACS) patients. Methods 758 consecutive high-risk NSTE-ACS patients treated with percutaneous coronary artery intervention(PCI)were enrolled between Jauary 2015 and December 2015 in Wuhan Asia Heart Hospital. They were divided into 2 groups according to diff erent intervention time, the early PCI group(within 24 h after diagnosis,n=185)and the delayed group (more than 24 h after diagnosis, n=573).The baseline clinical data, angiographic features, data related to PCI, the 12-month follow-up major adverse cardiac events (MACE) were analyzed retrospectively. MACE were defi ned as all-cause death and recurrent nonfatal myocardial infarction. Results Primary endpoint status after 12-month follow-up were collected in 711 of 758 initially enrolled patients. Incidence of MACE was 14.5% in the early and 11.2% in the delayed PCI group(χ2=1.289,P=0.256). No signifi cant diff erences were found in the occurrence of the individual components of all-cause death and nonfatal myocardial infarction. Mean hospital stay were(7.6±3.1)d in the early and (10.7±3.8)d in the delayed PCI group(t=2.489,P=0.014). Mean medical expenses in RMB were(48.5±13.5) thousand yuan in the early and(52.8±16.4)thousand yuan in the delayed PCI group(t=2.132,P=0.038). Conclusions After 12-month follow-up,no diff erence in incidence of MACE was seen between early and delayed invasive strategy,but with shorter hospital stay and reduced medical expenses.

High-density lipoprotein cholesterol and in-hospital mortality in patients with acute aortic dissection / 华中科技大学学报（医学）（英德文版）

The association between high-density lipoprotein cholesterol (HDL-C) and mortality in patients with acute aortic dissection (AAD) is unclear. From January 2007 to January 2014, a total of 928 consecutive AAD patients who were admitted within 48 h after the onset of symptoms were enrolled in the study. Patients were divided into two groups according to whether serum HDL-C level was below the normal lower limit or not. The Cox proportional hazard regression model was used to identify the predictive value of HDL-C for in-hospital mortality in patients with AAD. As compared with normal HDL-C group (n=585), low HDL-C group (n=343) had lower levels of systolic blood pressure and hemoglobin and higher levels of leukocyte, alanine aminotransferase, blood glucose, blood urea nitrogen, creatinine and urea acid. Low HDL-C group had significantly higher in-hospital mortality than normal HDL-C group (21.6% vs. 12.6%, log-rank=10.869, P=0.001). After adjustment for baseline variables including demographics and biologic data, the increased risk of in-hospital mortality in low HDL-C group was substantially attenuated and showed no significant difference (adjusted hazard ratio, 1.23; 95% confidence interval, 0.86-1.77; P=0.259). Low HDL-C is strongly but not independently associated with in-hospital mortality in patients with AAD.

CYP2C8-derived epoxyeicosatrienoic acids decrease oxidative stress-induced endothelial apoptosis in development of atherosclerosis: Role of Nrf2 activation / 华中科技大学学报（医学）（英德文版）

The aim of the present study is to investigate how cytochrome P450 enzymes (CYP) 2C8-derived epoxyeicosatrienoic acids (EETs) regulate the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway and protect against oxidative stress-induced endothelial injuries in the development and progression of atherosclerosis. In this study, cultured human umbilical vein endothelial cells (HUVECs) were transfected with CYP2C8 or pretreated with exogenous EETs (1 μmol/L) before TNF-α (20 ng/mL) stimulation. Apoptosis and intracellular ROS production were determined by flow cytometry. The expression levels of ROS-associated NAD(P)H subunits gp91 and p47, the anti-oxidative enzyme catalase (CAT), Nrf2, heme oxygenase-1 (HO-1) and endothelial nitric oxide synthase (eNOS) were detected by Western blotting. The results showed that CYP2C8-derived EETs decreased apoptosis of HUVECs treated with TNF-α. Pretreatment with 11, 12-EET also significantly blocked TNF-α-induced ROS production. In addition, 11, 12-EET decreased oxidative stress-induced apoptosis. Furthermore, the ability of 11, 12-EET to protect cells against TNF-α-induced apoptosis via oxidative stress was abrogated by transient transfection with Nrf2-specific small interfering RNA (siRNA). In conclusion, CYP2C8-derived EETs prevented TNF-α-induced HUVECs apoptosis via inhibition of oxidative stress associated with the Nrf2 signaling.