期刊文献+
共找到5篇文章
< 1 >
每页显示 20 50 100
瑞舒伐他汀强化治疗外周动脉粥样硬化的疗效观察 被引量:1
1
作者 朱蕾 林泽鹏 +1 位作者 张荣奎 张志伟 《现代医院》 2017年第4期579-580,583,共3页
目的观察强化剂量瑞舒伐他汀治疗外周动脉粥样硬化的临床疗效。方法选择2016年1月—2016年7月间于XX医院就诊的80例外周动脉粥样硬化患者作为研究对象,随机平均分为常规治疗组和试验组。常规治疗组采用常规剂量瑞舒伐他汀进行治疗,剂量... 目的观察强化剂量瑞舒伐他汀治疗外周动脉粥样硬化的临床疗效。方法选择2016年1月—2016年7月间于XX医院就诊的80例外周动脉粥样硬化患者作为研究对象,随机平均分为常规治疗组和试验组。常规治疗组采用常规剂量瑞舒伐他汀进行治疗,剂量为10 mg/次,qd;试验组采用强化剂量瑞舒伐他汀进行治疗,剂量为20 mg/次,qd;疗程为期半年,疗程结束后,检测两组患者血脂情况(总胆固醇;甘油三酯;低密度脂蛋白;高密度脂蛋白)和外周动脉粥样斑块(斑块大小厚度;中膜厚度)。试验组患者的总胆固醇;甘油三酯,低密度脂蛋白水平分别为(4.17±1.32)mmol/L、(1.54±0.56)mmol/L、(1.92±0.65)mmol/L,均低于常规治疗组的(5.54±1.21)、(1.94±0.62)、(3.73±1.03)mmol/L(P<0.05),试验组高密度脂蛋白水平为(2.08±0.46)mmol/L,高于常规治疗组的(1.65±0.37)mmol/L(P<0.05)治疗后,试验组斑块大小;斑块厚度,中膜厚度分别为(0.056±0.012)cm^2;(1.21±0.32)mm、(1.71±0.21)mm,均小于常规治疗组的(0.073±0.011)cm^2;(1.45±0.52)mm、(1.87±0.27)mm(均P<0.05)。结论瑞舒伐他汀能有效治疗外周动脉粥样硬化,强化剂量的瑞舒伐他汀对血脂水平和斑块情况的改善更加明显。 展开更多
关键词 瑞舒伐他汀 强化治疗 外周动脉粥样硬化
在线阅读 下载PDF
2型糖尿病合并高血压患者外周动脉粥样硬化危险因素分析 被引量:3
2
作者 郭雅丽 姚群英 +2 位作者 梁彩红 何爱萍 温剑峰 《中国实用医药》 2020年第23期38-40,共3页
目的分析2型糖尿病合并高血压患者外周动脉粥样硬化的危险因素。方法200例2型糖尿病合并高血压患者,按是否发生外周动脉粥样硬化分为研究组(发生外周动脉粥样硬化)和对照组(未发生外周动脉粥样硬化),各100例。回顾分析两组患者的临床资... 目的分析2型糖尿病合并高血压患者外周动脉粥样硬化的危险因素。方法200例2型糖尿病合并高血压患者,按是否发生外周动脉粥样硬化分为研究组(发生外周动脉粥样硬化)和对照组(未发生外周动脉粥样硬化),各100例。回顾分析两组患者的临床资料,采用Logistic回归分析2型糖尿病合并高血压患者发生外周动脉粥样硬化的危险因素。结果对照组年龄(65.13±3.21)岁小于研究组的(67.28±5.63)岁,病程(5.14±1.02)年明显短于研究组的(7.82±3.15)年,糖化血红蛋白水平(10.80±1.70)%低于研究组的(11.60±2.50)%,合并高脂血症占比60.00%、合并高尿酸血症占比24.00%均低于研究组的82.00%、40.00%,差异均有统计学意义(P<0.05);对照组男性、吸烟、肥胖占比低于研究组,但差异无统计学意义(P>0.05)。根据Logistic回归分析显示,年龄、病程、糖化血红蛋白、合并高脂血症、合并高尿酸血症是2型糖尿病合并高血压患者引发外周动脉粥样硬化的危险因素(P<0.05)。结论年龄、病程、糖化血红蛋白合并高脂血症、合并高尿酸血症是2型糖尿病合并高血压患者引发外周动脉粥样硬化的危险因素,应尽早给予患者降压、调脂、降糖等对症支持治疗,转变患者的生活方式,从而降低外周动脉粥样硬化发生的风险性。 展开更多
关键词 2型糖尿病 高血压 外周动脉粥样硬化
在线阅读 下载PDF
二维超声成像技术对外周血管动脉粥样硬化的诊断价值研究 被引量:1
3
作者 张美玲 《中国实用医药》 2021年第1期94-96,共3页
目的探讨二维超声成像技术对外周血管动脉粥样硬化的诊断价值。方法54例外周血管动脉粥样硬化患者,均实施二维超声成像技术进行检查。观察患者的影像学表现、斑块形成部位、斑块类型和基础疾病情况。结果54例患者中,内膜面粗糙占比83.33... 目的探讨二维超声成像技术对外周血管动脉粥样硬化的诊断价值。方法54例外周血管动脉粥样硬化患者,均实施二维超声成像技术进行检查。观察患者的影像学表现、斑块形成部位、斑块类型和基础疾病情况。结果54例患者中,内膜面粗糙占比83.33%(45/54),增厚占比为33.33%(18/54);颈动脉内膜粗糙占比为44.44%(24/54),增厚占比为11.11%(6/54)。斑块形成部位共64处,其中左侧34处(53.13%),右侧为30处(46.88%)。斑块形成部位中,颈总动脉球部位占比最多,占48.15%(26/54),分叉部位占比24.07%(13/54),颈内动脉起始部位占比16.67%(9/54),颈总动脉部位占11.11%(6/54)。软斑和硬斑所占比例较大,其中软斑占比为44.44%(24/54),硬斑占比为40.74%(22/54),混合斑占比为7.41%(4/54),扁平斑占比为7.41%(4/54)。54例患者中,16例(29.63%)脑梗死,11例(20.37%)冠心病,3例(5.56%)脑萎缩,2例(3.70%)糖尿病。结论外周血管动脉粥样硬化的超声诊断主要表现为斑块的形成、粗糙的内膜面,以软斑和硬斑之间的比例最高,因此,二维超声成像技术在外周血管粥样硬化的诊断中具有非常显著的应用价值,在临床中具有推广意义。 展开更多
关键词 二维超声成像技术 外周血管动脉粥样硬化 诊断
在线阅读 下载PDF
Systemic inflammatory response following acute myocardial infarction 被引量:37
4
作者 Lu FANG Xiao-Lei Moorea +1 位作者 Anthony M Dart Le-Min WANG 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2015年第3期305-312,共8页
Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response... Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Iuflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction (AMI), Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes (such as death, recurrent myocardial in- farction, and heart failure) in patients with AMI. 展开更多
关键词 Acute myocardial infarction Inflammatory markers Leukocytes Systemic inflammatory response
在线阅读 下载PDF
Cilostazol inhibits plasmacytoid dendritic cell activation and antigen presentation 被引量:1
5
作者 Fei SUN Zhao YIN +4 位作者 Hai-Sheng YU Quan-Xing SHI Bei ZHAO Li-Guo ZHANG Shou-Li WANG 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2015年第4期388-393,共6页
Background Cilostazol, an anti-platelet drug for treating coronary heart disease, has been reported to modulate immune cell functions Plasmacytoid dendritic cells (pDCs) have been found to participate in the progres... Background Cilostazol, an anti-platelet drug for treating coronary heart disease, has been reported to modulate immune cell functions Plasmacytoid dendritic cells (pDCs) have been found to participate in the progression of atherosclerosis mainly through interferon ct (IFN-ct) production. Whether cilostazol influences pDCs activation is still not clear. In this study, we aimed to investigate the effects of cilostazol on cell activation and antigen presentation ofpDCs in vitro in this study. Methods Peripheral blood mononuclear cells isolated by Ficoll cen- trifugation and pDCs sorted by flow cytometry were used in this study. After pretreated with cilostazol for 2 h, cells were stimulated with CpG-A, R848 or virus for 6 h or 20 h, or stimulated with CpG-B for 48 h and then co-cultured with naive T cell for five days. Cytokines in supernatant and intracellular cytokines were analyzed by ELISA or flow cytometry respectively. Results Our data indicated that cilostazol could inhibit IFN-α and tumor necrosis factor α (TNF-α) production from pDCs in a dose-dependent manner. In addition, the ability of priming na ve T cells of pDCs was also impaired by cilostazol. The inhibitory effect was not due to cell killing since the viability of pDCs did not change upon cilostazol treatment. Conclusion Cilostazol inhibits pDCs cell activation and antigen presentation in vitro, which may explain how cilostazol protects against atherosclerosis. 展开更多
关键词 Antigen presentation CILOSTAZOL Interferon α Plasmacytoid dendritic cell Tumor necrosis factor α
在线阅读 下载PDF
上一页 1 下一页 到第
使用帮助 返回顶部