目的:探索伊伐布雷定在急性前壁心肌梗死患者中早期应用的有效性和安全性。方法:选取20例急性前壁心肌梗死且成功施行直接经皮冠状动脉介入(PPCI)治疗的患者,所有患者均为窦性心律且静息心率>80次/min,收缩压>90 mm Hg,射血分数&l...目的:探索伊伐布雷定在急性前壁心肌梗死患者中早期应用的有效性和安全性。方法:选取20例急性前壁心肌梗死且成功施行直接经皮冠状动脉介入(PPCI)治疗的患者,所有患者均为窦性心律且静息心率>80次/min,收缩压>90 mm Hg,射血分数<50%。患者均在接受标准的急性心肌梗死药物治疗的基础上,院内早期联合应用伊伐布雷定(起始剂量5 mg,2次/d),比较患者入院时、出院前以及术后6个月时的心率、血压、射血分数变化,并观察不良反应发生的情况。结果:20例患者中,男性占75%(15例),平均年龄(56.8±15.5)岁。50%患者合并高血压病,55%患者有吸烟史,15%患者合并糖尿病,25%患者合并慢性阻塞性肺疾病,20%患者合并慢性肾功能不全。入院时平均心率(89.4±4.9)次/min,收缩压(121.6±18.1)mm Hg,舒张压(74.9±9.7)mm Hg,射血分数(38.7±4.0)%。12例(60%)患者在PPCI术后第2天加用伊伐布雷定。出院前心率比入院时降低[(75.9±5.3)次/min vs(89.4±4.9)次/min,P<0.01],术后6个月心率比出院前降低[(67.2±5.3)次/min vs(75.9±5.3)次/min,P<0.01],术后6个月射血分数较入院时显著提升[(45.0±5.5)%vs(38.7±4.0)%,P<0.01]。收缩压和舒张压在各时段无明显变化(均P>0.05)。观察期间未发生药物相关不良反应。结论:伊伐布雷定在急性前壁心肌梗死患者中早期应用有效、安全,尤其适用于合并心功能不全和/或β受体阻滞剂不能耐受的患者,其远期疗效和安全性需进一步观察。展开更多
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 pr...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/m L） 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（e NOS） 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（si RNA）. In conclusion,CYP2C8-derived EETs prevented TNF-α-induced HUVECs apoptosis via inhibition of oxidative stress associated with the Nrf2 signaling.展开更多
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 patient...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.展开更多
基金supported by National Nature Science Foundation of China(No.81170259)
文摘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/m L） 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（e NOS） 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（si RNA）. In conclusion,CYP2C8-derived EETs prevented TNF-α-induced HUVECs apoptosis via inhibition of oxidative stress associated with the Nrf2 signaling.
基金supported by National Natural Science Foundation of China(No.81170259)
文摘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.
