社区医疗干预对老年下肢动脉硬化闭塞症患者的作用

动脉硬化性闭塞症(ASO)是严重危害人们身体健康的一类疾病,尤其在老年人中发病率较高,多累及下肢,有着很高的致残性和死亡率。该病发病原因复杂,目前尚无明确定论,常是全身动脉硬化的局部表现,是老年人中的常见慢性病。目前药物、介入、手术等治疗手段虽多,但远期效果并不理想,所以全面的社区医疗干预有望在降低发病率、延缓病情发展速度、降低致残率和死亡率方面发挥重要作用。     

糖尿病下肢动脉硬化闭塞症临床分析

糖尿病(DM)动脉硬化闭塞症(ASO)的发病率是非糖尿病的11倍,且周围动脉硬化发展快,程度重,一旦发生,其截肢率是非糖尿病人的40倍[1]。我们通过回顾性分析60例ASO的临床特征,探讨糖尿病与非糖尿病ASO之间的差异及糖尿病动脉硬化闭塞症的治疗方案。临床资料1.一般资料:收集1996年1月～2006年6月我院ASO患者60例(72条肢体),其中DM组32例(40条肢体),非糖尿病组28例(32条肢体)。两组临床资料见表1。2.诊断:本组患者ASO的诊断:(1)有肢体缺血性表现;(2)踝/肱动脉压力指数(ABI)小于0.9;(3)血管造影有明显狭窄;(4)彩超发现有动脉狭窄。72条肢…     

老年住院患者下肢动脉硬化闭塞症与心脑血管疾病的相关性

目的 探讨下肢动脉硬化闭塞症(ASO)与冠心病和脑卒中的相关性。方法 回顾性分析2013年10月至2021年3月在首都医科大学附属北京世纪坛医院血管外科住院的587例老年下肢ASO患者的临床资料。调查住院患者冠心病和脑卒中患病率。分析Fontaine缺血分期、踝肱指数(ABI)与冠心病和脑卒中的相关性。采用SPSS 26.0 统计软件进行数据分析。相关性分析采用Spearman相关分析。结果 587例下肢ASO患者合并冠心病、脑卒中、冠心病和脑卒中患病率分别32.20%(189/587)、13.12%(77/587)及17.21%(101/587)。下肢Fontaine缺血分期与冠心病(r=7.57)及脑卒中(r=3.57)的发生呈正相关(均P<0.01)。Fontaine缺血分期与合并心脑血管疾病种类数呈正相关(r=0.13;P=0.02)。合并冠心病与无冠心病患者[0.30(0.00,0.55)和0.68(0.50,0.80)]、合并脑卒中与无脑卒中患者[0.40(0.15,0.62)和0.60(0.20,0.75)]的ABI数值比较,差异有统计学意义(均P<0.01)。ABI值与合并心脑血管疾病种类数呈负相关性(r=-0.48;P<0.01)。结论 老年下肢动脉硬化闭塞症患者心脑血管疾病发生率高。下肢缺血越重,发生心脑血管疾病风险越高。     

髂、股动脉硬化闭塞症的杂交手术治疗

目的探讨杂交技术治疗髂、股动脉硬化闭塞症的临床疗效。方法回顾性分析该院2009年1月至2013年12月应用杂交技术治疗髂、股动脉硬化闭塞症135例的临床资料。结果围术期无死亡病例。手术成功率95.6%。围术期严重并发症5例(3.7%),大腿截肢2例。踝肱指数(ABI)由术前0.35±0.23增加至术后0.87±0.23(P0.01)。随访3~60个月〔平均(25±7.3)个月〕,术后3个月、6个月、1年及3年的一期通畅率分别为95.9%、89.7%、86.79%和55.2%,二期通畅率分别为100%、98.8%、90.7%和65.8%,术后1年和3年的截肢率分别为4.0%和21.1%。结论杂交技术能够降低手术创伤,扩大手术治疗的适应证,并提高髂、股动脉硬化闭塞症的治疗效果。     

介入治疗老年下肢动脉硬化闭塞症患者112例

动脉硬化闭塞症(ASO)是指动脉粥样硬化引起的慢性动脉闭塞性疾病,以下肢最为常见。本病多见于老年男性,随着生活水平提高,发病率逐年上升。以往,传统的外科转流术是下肢动脉狭窄闭塞症的主要治疗方法〔1〕,疗效确切,远期通畅     

老年血脂异常人群周围动脉硬化闭塞症患病率及相关影响因素

目的分析老年血脂异常人群周围动脉硬化闭塞症(PAOD)患病率和相关因素。方法选取487例老年血脂异常患者作为研究对象,调查PAOD的患病率并分析其相关危险因素。结果 487例老年血脂异常患者中PAOD共85例,患病率为17.5%,按年龄分层:60岁组PAOD患病率为10.2%,70岁组PAOD患病率为15.3%,80岁组PAOD患病率为34.3%,组间比较差异有统计学意义(P<0.05)。经相关分析,年龄与PAOD患病率呈正相关,r=0.965,P<0.05。经多元Logistic回归分析,年龄(OR=2.113,95%CI=1.362².831)、高血压(OR=1.154,95%CI=1.0172.831)、高血压(OR=1.154,95%CI=1.017¹.947)、糖尿病(OR=1.217,95%CI=1.1061.947)、糖尿病(OR=1.217,95%CI=1.106¹.881)和高血压合并糖尿病(OR=1.738,95%CI=1.0091.881)和高血压合并糖尿病(OR=1.738,95%CI=1.009².614)为老年血脂异常人群PAOD的主要危险因素;高HDL(OR=0.472,95%CI=0.1832.614)为老年血脂异常人群PAOD的主要危险因素;高HDL(OR=0.472,95%CI=0.183⁰.771)为老年血脂异常人群PAOD的主要保护因素。结论老年血脂异常患者中PAOD患病率较高,年龄与PAOD患病率呈正相关,年龄、合并疾病和高LDL为PAOD的主要危险因素,高HDL为PAOD的保护因素。     

同型半胱氨酸与老年下肢动脉硬化闭塞的关系

<正>下肢动脉硬化闭塞(PAD)的发病率正逐年增加,70岁以上人群发病率达15%²0%以上。早期可无临床症状或仅轻微不适,渐出现间歇性跛行,严重缺血者可出现静息痛,足背动脉搏动消失等,晚期常导致动脉严重狭窄或闭塞,引起下肢发绀、溃疡甚至坏疽〔120%以上。早期可无临床症状或仅轻微不适,渐出现间歇性跛行,严重缺血者可出现静息痛,足背动脉搏动消失等,晚期常导致动脉严重狭窄或闭塞,引起下肢发绀、溃疡甚至坏疽〔1³〕。目前,大量研究表明同型半胱氨酸(Hcy)浓度是心脑血管疾病的独立危险因素〔4〕,危险度随浓度升高而增加,而其与PAD的关系研究报道较少。本文旨在探讨Hcy     

藻酸双酯钠对下肢动脉硬化闭塞症疗效观察

目的观察藻酸双酯钠(PSS)对下肢动脉硬化闭塞症患者的临床疗效.方法下肢动脉硬化闭塞症患者35例应用PSS100～200mg/d,缓慢静滴,连用10～14d.治疗前后分别观察临床症状、踝/肱指数、下肢动脉狭窄程度(直径)及血流峰速和血糖、血脂及凝血三项等实验室检查.结果治疗后的患者临床症状明显好转,总有效率达91.4%,无出血及其他不良反应.治疗后与治疗前相比血脂明显下降,差异有统计学意义(P＜0.05),血糖有所下降,但差异无统计学意义;凝血三项数据显示有所升高,但差异无统计学意义;动脉狭窄程度及血流峰速、踝/肱指数值差异均无统计学意义.结论PSS可扩张外周血管,降低血管阻力,增加肢体血流量;可明显降低血脂、降低血液粘度;改善微循环、促进侧支循环的形成,是一种较好的微循环障碍改善剂,可安全有效地用于下肢动脉硬化闭塞症的治疗.     

下肢动脉硬化闭塞症患者预后影响因素

下肢动脉硬化闭塞症(ASO)是动脉粥样化的重要肢体表现。1资料与方法1.1研究对象2011年1～10月我院进行手术或介入治疗的ASO 101例,平均年龄(69.64±5.07)岁,其中男68例,女33例。根据采用的术式不同分组手术组患者平均年龄明显低于介入组(P<0.05);两组泛大西洋学会联盟(TASC)分级构成比     

下肢动脉硬化闭塞症的外科治疗进展

下肢动脉硬化闭塞症(ASO)由动脉粥样硬化病变引起,在患者下肢的同一动脉系统中可存在一个或多个节段的动脉严重狭窄或阻塞,是老年人慢性下肢缺血的最常见原因.     

Vascular oxidative stress,nitric oxide and atherosclerosis

In the vascular wall, reactive oxygen species (ROS) are produced by several enzyme systems including NADPH oxidase, xanthine oxidase, uncoupled endothelial nitric oxide synthase (eNOS) and the mitochondrial electron transport chain. On the other hand, the vasculature is protected by antioxidant enzyme systems, including superoxide dismutases, catalase, glutathione peroxidases and paraoxonases, which detoxify ROS. Cardiovascular risk factors such as hypercholesterolemia, hypertension, and diabetes mellitus enhance ROS generation, resulting in oxidative stress. This leads to oxidative modification of lipoproteins and phospholipids, mechanisms that contribute to atherogenesis. In addition, oxidation of tetrahydrobiopterin may cause eNOS uncoupling and thus potentiation of oxidative stress and reduction of eNOS-derived NO, which is a protective principle in the vasculature. This review summarizes the latest advances in the role of ROS-producing enzymes, antioxidative enzymes as well as NO synthases in the initiation and development of atherosclerosis.     

家兔动脉粥样硬化与血小板源内皮型氧化氮合酶表达的相关性

目的 探讨家兔动脉粥样硬化及斑块形成与血小板源内皮型氧化氮合酶(eNOS)表达的关系. 方法 设立模型组、治疗组和非治疗组及对照组,每组家兔6只.模型组、治疗组和非治疗组每天给予胆固醇饮食,至12周建立家兔动脉粥样硬化模型,建模后继续喂养至24周,同时治疗组服用普伐他汀10 mg/d;非治疗组仅给予普通饮食.实验终点剥离家兔主动脉观察大体和组织病理形态,反转录一聚合酶链式反应(RT-PCR)方法 检测血小板源eNOS/mRNA水平. 结果 模型组和非治疗组均可见明显动脉粥样硬化和(或)斑块形成;主动脉最大脂纹或斑块厚度占整个血管壁厚度的百分比,对照组、模型组、治疗组和非治疗组分别是0.04±0.02、0.82±0.16、0.33±0.18和0.77±0.14,治疗组与非治疗组比较,差异有统计学意义(F=33.759,P=0.001).血小板(2～4×108/ml)eNOS mRNA表达在对照组、模型组、治疗组和非治疗组分别是1.02±0.28、0.41±0.27、1.00±0.77、0.40±0.29,治疗组较非治疗组明显增高(F=3.544,P=0.02). 结论 血小板源eNOS表达与动脉粥样硬化及斑块的形成呈负相关;普伐他汀对动脉粥样硬化及斑块的逆转作用可能与血小板源eNOS有关.     

肺心病患者血浆内皮素一氧化氮降钙素基因相关肽的研究

目的 研究缺氧性肺动脉高压产生的机理。方法 经右心导管监测５５例慢性阻塞性肺疾病（ＣＯＰＤ）及慢性肺心病患５５例，依平均肺动脉压（ｍＰＡＰ）≥２．６７ｋＰａ，分为Ａ组（２８例）〈２．６７ｋＰａ分为Ｂ组（２７例）及２２名健康（对照组）观察血流动力学变化，并测定其俩动脉血浆内皮素（ＥＴ－１），一氧化氮（ＮＯ）和降钙素基因相关肽（ＣＧＲＰ）水平，以探讨了ＥＴ－１，ＮＯ，ＣＧＲＰ与肺动脉高压的关系。结     

Chronic ethanol ingestion increases aortic endothelial nitric oxide synthase expression and nitric oxide production in the rat

Background:  Chronic alcohol consumption perturbs cellular function in a variety of organ systems. Previous studies have suggested that moderate alcohol consumption reduces vascular disease, whereas heavier alcohol consumption may worsen it. The mechanisms for these vascular effects of chronic alcohol ingestion continue to be defined and constitute the focus of this study.
Methods:  Male Sprague Dawley rats were fed an isocaloric, Lieber-Decarli liquid diet containing either ethanol (36% calories) or Maltose–Dextrin (substituted for ethanol) for 6 weeks. Telemetric blood pressure measurements were taken before and after ethanol feeding. After the rats were killed, the aortas were analyzed for endothelial nitric oxide (NO) synthase expression and NO production.
Results:  Chronic ethanol ingestion decreased mean arterial pressure and increased aortic NO production as demonstrated by direct ex vivo measurements using iron diethyldithio-carbamic acid as well as analysis of nitrosyl-hemoglobin (NO-Hb) levels. Consistent with these assays of vascular NO production, endothelium-dependent relaxation responses to acetycholine (Ach) were enhanced in ethanol-fed animals. Aortic endothelial nitric oxide synthase expression was also increased by chronic ethanol ingestion.
Conclusions:  These findings demonstrate that a regimen of chronic alcohol ingestion in the rat produced generally salutary effects in the systemic vasculature following a 6-week treatment regimen. These findings extend previous in vitro studies to demonstrate that alcohol has potent effects on vascular endothelial nitric oxide synthase expression, NO production, and vascular function. Consistent with previous reports, these findings confirm that alcohol-induced alterations in the production of reactive nitrogen species play an important role in the pathogenesis of alcohol-mediated tissue effects.     

Therapeutic potential of nitric oxide donors in the prevention and treatment of atherosclerosis.

Well-known risk factors for atherosclerosis include hypercholesterolaemia, hypertension, diabetes, and smoking. These conditions are associated with endothelial dysfunction, which itself is associated with reduced endothelial generation of nitric oxide (NO). This is an overview of the implications of NO generation in atherosclerosis and of the potential therapeutic benefit of drugs which donate NO, such as organic nitrates, nicorandil, and sydnonimines, or those which increase the availability of endogenous NO, such as statins, angiotensin-converting enzyme inhibitors, L-arginine, and tetrahydrobiopterin.     

一氧化氮、一氧化氮合酶与蛛网膜下腔出血后脑血管痉挛

多年以来,脑血管痉挛一直被视为影响蛛网膜下腔出血患者预后的重要因素之一.研究表明,蛛网膜下腔出血后脑血管痉挛与一氧化氮和一氧化氮合酶有关,而调节一氧化氮合成可在脑血管痉挛的治疗中起积极作用.     

血浆一氧化氮及硫化氢水平与冠心病介入治疗前后的临床观察

目的:探讨冠心病患者血浆一氧化氮(NO)和硫化氢(H2S)浓度与冠心病病变的关系。方法:选择经冠状动脉造影诊断的冠心病患者115例,于术前和支架植入后分别测定血浆NO和H2S,分析其与冠状动脉病变的关系。同时选取正常对照组48例,检测入选者的血浆NO及H2S浓度。结果:1.冠心病患者血浆NO和H2S水平明显低于正常人(P<0.01),支架植入后血浆NO和H2S浓度明显升高。2.随着冠状动脉病变支数的增多,血浆NO和H2S浓度逐渐降低;病变血管越多,术后NO和H2S浓度升高的幅度越小。3.合并高血压的冠心病患者,其血浆NO和H2S水平低于血压正常的冠心病患者。结论:冠心病患者血浆NO和H2S水平明显降低,血管重建术对冠状动脉血流再通的过程中有NO和H2S水平的改善。     

一氧化氮在砷中毒中作用的研究

目的探讨砷对机体ＮＯ的影响及ＮＯ在砷中毒发病中的作用。方法采用动物实验和人群调查方法。结果慢性染砷实验中,小鼠血清、肾脏ＮＯ２－／ＮＯ３－含量中、高剂量组显著降低,肝脏、心脏ＮＯ２－／ＮＯ３－含量各剂量组显著降低,且呈剂量—效应关系。全血ＧＳＨ含量低剂量组显著升高,中、高剂量组显著降低,肝脏、心脏ＧＳＨ含量各剂量组均显著下降,肾脏ＧＳＨ含量中、高剂量组显著降低。红细胞、心脏ＳＯＤ活性中、高剂量组显著下降,肝脏ＳＯＤ活性低剂量组显著升高,中、高剂量组显著下降,肾脏各剂量组未见显著差异。人群调查,砷病区病人血中ＮＯ２－／ＮＯ３－、ＧＳＨ含量显著低于非病区健康人,且二者呈正相关,红细胞ＳＯＤ活性未见显著差异。结论砷可导致ＮＯ含量的下降。砷可导致ＧＳＨ含量和ＳＯＤ活性的变化,进而影响ＮＯ合成和代谢     

一氧化氮在糖尿病性肾病中的变化及其临床意义

目的探讨一氧化氮（ＮＯ）在糖尿病性肾病（ＤＮ）中的变化规律及其与肾功能的关系。方法检测５４例糖尿病（ＤＭ）患者血清ＮＯ稳定代谢产物亚硝酸盐（ＮＯ２）与血浆内皮素（内皮缩血管肽，ＥＴ）的水平，并与２０例正常人进行比较。结果正常白蛋白尿和微量白蛋白尿糖尿病患者血清ＮＯ均显著高于正常人和大量白蛋白尿患者（Ｐ＜０．０１），ＮＯ与病程、血清尿素氮、血肌酐、血浆ＥＴ水平呈负相关，与肾小球滤过率呈正相关。结论提示ＤＭ早期高ＮＯ生成与肾小球高滤过有关，晚期低下的ＮＯ水平可能促进ＤＮ发展；ＮＯ与ＥＴ之间可能存在互相制约、动态平衡的关系，平衡紊乱与ＤＮ的发生、发展有关     

Tissue factor and nitric oxide: a controversial relationship!

Tissue factor (TF) is the primary physiological initiator of blood coagulation. TF has a high-affinity for factor (F) VII resulting in the formation of (TF:FVII:FVIIa) bimolecular complex which, in the presence of Ca(2+), increases the enzymatic activity of FVIIa towards its natural substrates, FIX and FX, generating their active forms FIXa and FXa, respectively. This eventually leads to thrombin generation and a fibrin clot formation. Up-regulation of TF in injured blood vessels and atherosclerotic plaque can lead to undesirable vascular thrombosis. Nitric oxide (NO) is a free radical synthesized from L-arginine and molecular oxygen by nitric oxide synthases (NOS). NO participates in diverse physiological and pathophysiological process as an intra or extracellular messenger. A relationship between TF and NO has been proposed. Thus, models of TF regulation by NO has been studied in different cells and experimental animal models, but the results have been conflicting. The premise that NO donors can prevent TF expression in vivo has provided the foundation for a broad field of pharmacotherapeutics in vascular medicine. A new class of drugs combining a statin (inhibitors of coenzyme A reductase) with an NO-donating moiety has been described. The resulting drug, nitrostatin, has been suggested to increase the antithrombotic effects of native statin. However, it is questionable if NO release from these drugs had any significant role on TF inhibition. In summary, care must be taken in drawing conclusions about the relationship between NO and TF. Interpretation of NO studies must take several factors into consideration, including NO bioavailability, its half-life and inactivation, as well as the cell type and experimental model used.