女性甲减患者甲状腺素治疗改善内皮细胞依赖性血管舒张功能

目的　观察甲状腺功能减退症(甲减)患者甲状腺激素补充治疗后内皮依赖性血管舒张功能的变化。方法　选择初诊的女性临床甲减患者33例、亚临床甲减患者25例及正常健康女性25名。采用高分辨血管外超声法检测肱动脉血流介导的内皮依赖性血管舒张功能和硝酸甘油(GNT)介导的非内皮依赖性血管舒张功能。结果　(1)与对照组比较,临床甲减组和亚临床甲减组治疗前TSH、脂蛋白(a)〔L(a)〕、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL C)水平明显升高,血流介导的血管舒张功能降低(均<0. 05)。(2)与治疗前比较,临床甲减组和亚临床甲减组TSH、Lp(a)、LDL C、载脂蛋白B水平明显降低;血流介导的血管舒张功能明显升高(均P<0. 05)。(3)临床甲减组和亚临床甲减组治疗前后TSH、Lp(a)LDL C的变化与血流介导的血管舒张功能呈负相关(均P<0. 05)。结论　甲减患者内皮依赖性血管舒张功能降低,甲状腺激素补充治疗可改善内皮功能。     

桥本甲状腺炎患者血管内皮功能受损与低度炎症反应的关系

目的 探讨低水平的炎症反应在血脂正常的桥本甲状腺炎(HT)患者血管内皮功能受损中的作用.方法 将58例HT患者,分为甲状腺功能正常组(甲功正常组)28例,亚临床甲状腺功能减退组(甲减组)30例,并有28例正常人(对照组)纳入本实验.空腹静脉取血检测甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、促甲状腺素(TSH)、游离甲状腺素(FT4)、游离三碘甲腺原氨酸(FT3)、甲状腺球蛋白抗体(TgAb)、甲状腺过氧化物酶抗体(TPOAb)、一氧化氮(NO)和超敏C-.反应蛋白(hs-CRP).结果 HT患者的甲功正常组、甲减组,分别与对照组比较,NO显著下降(P均＜0.01),而TgAb、TPOAb、hs-CRP则显著升高(P均＜0.01).HT患者中,甲功正常组与甲减组两两比较,NO、TgAb、TPOAb、hs-CRP均没有统计学差异(P均＞0.05).结论 血脂正常的HT患者存在血管内皮功能受损,可能是由于自身免疫异常的长期低水平的炎症反应,参与了HT患者的血管内皮功能损伤.     

冠心病患者肱—踝脉搏波速与血管内皮舒张功能相关

目的探讨冠心病患者肱—踝脉搏波速与内皮依赖性舒张功能的关系。方法选择98例冠心病患者和33例非冠心病对照者,采用高分辨率超声检测肱动脉血流介导的内皮依赖性血管舒张功能;自动脉搏波速度测定仪测定肱—踝脉搏波速。结果冠心病组肱动脉血流介导的内皮依赖性血管舒张功能明显低于对照组(5.4%±2.5%比11.1%±4.4%,P<0.01),冠心病组肱—踝脉搏波速明显高于对照组(1745.3±215.2cm/s比1495.3±202.3cm/s,P<0.01),两组硝酸甘油介导的内皮非依赖性血管舒张功能无明显差异;肱动脉血流介导的内皮依赖性血管舒张功能与肱—踝脉搏波速呈负相关(r=-0.70,P<0.001)。结论冠心病患者血管内皮功能受损和肱—踝脉搏波速增快,提示血管内皮舒张功能的受损伴随冠心病动脉硬化。     

2型糖尿病与甲状腺疾病的关系

目的探讨2型糖尿病(T2DM)与甲状腺疾病的关系。方法选择T2DM患者180例(T2DM组),其中老年组87例、非老年组93例。采用化学发光法检测其血清游离三碘甲状腺素原氨酸、游离甲状腺素、促甲状腺素,微粒子酶免疫法检测人抗甲状腺过氧化物酶抗体(TPO-Ab)、甲状腺球蛋白抗体(TG-Ab);并与160例健康查体者(正常对照组)进行比较。结果 T2DM组甲状腺功能(甲功)异常37例(20.56%),其中甲状腺功能亢进(甲亢)5例、甲状腺功能减退症(甲减)32例;对照组分别为11(6.88%)、5、6例;T2DM组甲功异常率明显高于正常对照组,T2DM老年组甲功异常率(28.74%)明显高于非老年组(12.29%),P均<0.01。T2DM组TPO-Ab异常55例(30.56%),明显高于对照组的19例(11.88%),P<0.01;两组TG-Ab阳性率比较P>0.05。结论 T2DM患者甲功异常率较高,主要表现为甲减、甲状腺自身抗体增高,老年患者尤为明显;提示甲状腺激素可能参与T2DM的发病过程。     

初诊2型糖尿病胰岛素抵抗与血管内皮功能的关系

目的探讨初诊2型糖尿病患者胰岛素抵抗(IR)与血管内皮功能的关系。方法初诊2型糖尿病患者分为IR组34例和非IR组31例,另设非糖尿病对照组30例。采用高分辨率血管外超声法检测肱动脉血管血流介导的内皮依赖性血管舒张功能(EDD)和硝酸甘油介导的内皮非依赖性血管舒张功能(GNT),并运用稳态模式评估方法评价IR。结果IR组和非IR组的EDD较对照组显著降低,分别为6.36%±2.92%、7.70%±3.13%和9.15%±3.46%(P<0.01和P<0.05),IR组又低于非IR组(P<0.05)。EDD在IR组与WHR、HOMA-IR呈负相关(P<0.01),在非IR组与BMI呈正相关(P<0.01),与WHR、HbA1C及TG呈负相关(P<0.05和P<0.01),与IR无明显相关性,而在对照组仅与WHR呈负相关(P<0.05)。结论在以IR为始动因素引发的糖尿病中内皮依赖性舒张功能障碍可能与IR共同参与了糖尿病的发生,而在以胰岛素分泌缺乏为主引发的糖尿病中,内皮功能障碍可能主要继发于高血糖、高血脂或腹型肥胖。     

甲状腺功能异常对糖代谢,胰岛β细胞的影响及与糖尿病的关系

作者检测了82例甲状腺功能异常者的OGTT、OGIRT,观察甲功异常对糖代谢、胰岛β细胞功能的影响及与糖尿病的关系。结果甲减组OGTT与对照组相似,甲亢组血糖略高于正常组,两组OGTT分别与正常组比较,各时相均无显若性差异(P>0.O5)。甲亢、甲减、甲糖与NIDDM组基础胰岛素值与对照组比较无显著性差异(P>O.05),而各组服糖后60分钟胰岛素峰值高于正常,P<0.01。NIDDM及甲糖组胰岛素释放指数(IGI)均低于对照组;甲减、甲亢组IGI反应强烈、迅速,与对照组比较,P相似文献   

脑心通胶囊对冠心病无症状心肌缺血病人血管内皮依赖性舒张功能的影响

目的探讨脑心通胶囊治疗冠心病无症状心肌缺血(SMI)的疗效及其对血管内皮依赖性舒张功能的影响。方法随机将68例冠心病SMI病人分为两组,治疗组35例在常规药物治疗基础上加用脑心通胶囊治疗,对照组33例仅用常规药物治疗。治疗前后进行动态心电图及彩色多普勒超声检测,对缺血及血管内皮依赖性舒张功能的相关指标作对比观察。结果两组治疗12周后S,T段压低伴有症状的次数及其持续时间与无症状的ST段压低及其持续时间均有明显减少及缩短,与治疗前比较有统计学意义(P<0.05或P<0.01),治疗后两组比较也有统计学意义(P<0.05)。治疗组治疗后血管内皮依赖性舒张功能指标明显改善(P<0.01),与对照组比较差异亦有统计学意义(P<0.01)。用药期间病人无严重不良反应。结论脑心通胶囊对冠心病无症状心肌缺血有显著疗效,且能改善血管内皮依赖性舒张功能。     

老年高血压患者血管内皮功能的变化及评价方法

分别测定40例轻、中度老年高血压患者(观察组)和20例健康老年人(对照组)的血浆内皮素-1(ET-1)、NO水平及肱动脉血流介导的血管内皮依赖性舒张功能(EDD)、硝酸甘油介导的非内皮依赖性舒张功能(EID).结果 观察组血浆ET-1明显高于对照组(P<0.01),NO明显低于对照组(P<0.01);观察组EDD明显低于对照组.EDD与ET-1呈负相关,与NO呈正相关(r=-0.5356、0.6829,P均＜0.01).提示血浆内皮素、NO和超声均可反映老年高血压患者血管内皮功能的变化,二种方法各有其优点和不足.     

TSH阻滞抗体对自身免疫性甲状腺炎患者甲状腺功能的影响

大部分成人自发性甲减是由于慢性自身免疫性甲状腺炎所致,后者可以是甲状腺肿大的桥本氏甲状腺炎(HT),也可是萎缩性甲状腺炎(AT)。为了观察TRH阻滞抗体(TSH-BAb)在这两种甲状腺炎中致甲减的病理作用,作者对26名AT及114名HT患者进行了研究。HT患者中27人甲功正常(HT-E),32人为亚临床甲减(HT-SH),55人为明显甲减(HT-M)。对各组病人均测定其甲状腺球蛋白抗体(Tg-Ab),微粒体抗体(M-Ab)和甲状腺过氧化物酶抗体(TPO-Ab)以及TSH-BAb等。 结果,26名AT患者中12人有TSH-BAb,占46%。在55名HT甲减患者中20人可查到TSH-BAb,占36%,而HT-SH组32人中仅有3人占9.4%,HT-E组27人中只有1人占3.7%。统计学证     

L-精氨酸对心力衰竭患者血管内皮功能的影响

目的 :评价L 精氨酸对心力衰竭 (心衰 )患者血管内皮功能的影响。方法 :应用高分辨率超声诊断仪 ,评估 40例心衰患者和 3 0例健康者 (正常对照组 )的内皮依赖性血管舒张功能和非内皮依赖性血管舒张功能 ,并测定血浆一氧化氮、内皮素 1(ET 1)浓度。 40例心衰患者被随机分为 2组 ,每组 2 0例 ,分别予以 2 0 %L 精氨酸注射液 10 0ml(L 精氨酸治疗组 )和 5 %葡萄糖注射液 10 0ml(安慰剂组 ) ,均在 60min内恒速静脉滴注。随即再次评估内皮依赖性血管舒张功能和非内皮依赖性血管舒张功能 ,同时复测血浆一氧化氮和ET 1浓度。结果 :与正常对照组相比 ,心衰患者内皮依赖性血管舒张功能显著受损 (P <0 0 1) ,非内皮依赖性血管舒张功能无明显变化 (P >0 0 5 )。血浆一氧化氮浓度下降 ,ET 1浓度上升 (P均 <0 0 1)。L 精氨酸治疗组内皮依赖性血管舒张功能得到明显改善 (P <0 0 5 ) ,非内皮依赖性血管舒张功能无变化 (P >0 0 5 ) ,血浆一氧化氮浓度升高 ,ET 1浓度下降 (P均 <0 0 5 )。而安慰剂组均无显著变化 (P >0 0 5 )。结论 :L 精氨酸能改善心衰患者血管内皮功能。     

Impairment of endothelium-dependent arterial dilation in Hashimoto's thyroiditis patients with euthyroidism

OBJECTIVE: Recent studies have shown that immune responses contribute to atherosclerosis, and endothelial dysfunction is an important early event in atherogenesis. The aim of this study was to investigate the alteration of endothelial function in Hashimoto's thyroiditis (HT) patients with euthyroidism. METHODS: Study subjects included 28 female HT patients with euthyroidism, 23 female HT patients with hypothyroidism, and 22 healthy women. High-resolution ultrasound was used to measure brachial artery diameter at rest, after reactive hyperaemia and after sublingual glyceryltrinitrate (GTN). RESULTS: Flow-mediated arterial dilation in HT patients with euthyroidism was significantly lower (3.88%) than in controls (4.98%, P = 0.000) and higher than in HT patients with hypothyroidism (3.26%, P < 0.001). Flow-mediated arterial dilation among HT patients with hypothyroidism was significantly lower than that in controls (P = 0.000). GTN-induced arterial dilation, baseline vessel size, and baseline blood flow were not significantly different among the three groups (P > 0.05). On multiple regression analysis, anti-thyroid peroxidase antibody (TPO-Ab), TSH, free T3, low density lipoprotein cholesterol (LDL-C) and lipoprotein (a) [Lp(a)] were found to be significant factors associated with endothelium-dependent arterial dilation. CONCLUSION: Endothelial dysfunction exists in HT patients with euthyroidism. Autoimmune reactivity and an elevated Lp(a) level might be responsible for the endothelial dysfunction.     

Apo e4 allele is associated with endothelium-dependent arterial dilation in women with type 2 diabetes

OBJECTIVE: Previous studies have suggested that the e4 allele of apolipoprotein E (apo E) relates to the endothelium-dependent arterial dilation in men with type 2 diabetes. This study attempted to assess whether apo e4 allele is associated with endothelial dysfunction in women with type 2 diabetes. RESEARCH DESIGN AND METHODS: We selected 144 Chinese Han female type 2 diabetic patients without clinically detectable angiopathy. Polymerase chain reaction/ASO probes were used to determine their mouthwash DNA apo E genotypes, and high-resolution ultrasound was used to measure brachial artery diameter at rest, after reactive hyperemia (with increased flow causing endothelium-dependent dilation) and after sublingual glyceryltrinitrate (GTN, an endothelium-independent dilator). RESULTS: The flow-mediated arterial dilation among the subjects with e4/3 or e4/4 was 3.56+/-0.23%, which was significantly lower than that in subjects with e2/2 or e3/2 (3.97+/-0.36%) (p=0.000). The baseline vessel size, GTN-induced dilation and baseline blood flows were not significantly different among different apo E genotypes. On univariate analysis, reduced flow-mediated arterial dilation was significantly related to total cholesterol, LDL, Lp(a), high blood pressure, older age, family history of premature vascular disease, larger vessel size, duration of diabetes and e4 allele (p<0.05). By multiple stepwise regression analysis, reduced flow-mediated arterial dilation was associated with older age, large vessel size, duration of diabetes, positive family history, LDL, Lp(a) and e4 allele (p<0.01). CONCLUSION: The apo e4 allele is associated with impairment of endothelium-dependent arterial dilation in the relatively early stage of female type 2 diabetes.     

Changes in endothelium-dependent arterial dilation before and after subtotal thyroidectomy in subjects with hyperthyroidism

OBJECTIVE: This case-control study was carried out to assess the alteration of endothelium-dependent arterial dilation before and after subtotal thyroidectomy in subjects with hyperthyroidism. PATIENTS AND METHODS: The study subjects included 12 patients with hyperthyroidism and 39 apparently healthy individuals. We performed a subtotal thyroidectomy on the hyperthyroid patients. The endothelium-dependent arterial dilation was determined with a high-resolution ultrasound method in each patient at the hyperthyroid stage before treatment (stage H), the euthyroid stage induced immediately before surgery (stage E), and the transient hypothyroid stage 1 or 2 months after surgery (stage L). RESULTS: The flow-mediated arterial dilation decreased significantly from H to E and from E to L (P < 0.001). As compared with H, baseline blood flow decreased markedly at stages E and L (P < 0.001). The flow-mediated arterial dilation and baseline blood flow in the control subjects were very close to those at stage E of the hyperthyroid patients. The absolute change in the flow-mediated arterial dilation showed significant negative correlation with the changes in TSH (r =-0.86, P < 0.001), lipoprotein (a) [Lp(a)] (r =-0.77, P < 0.001) and low density lipoprotein (LDL) (r =-0.79, P < 0.001), and significant positive correlation with changes in fT3 (r =+0.88, P < 0.001). The absolute change in the baseline blood flow showed significant positive correlation with the change in fT3 (r =+0.85, P < 0.001) and significant negative correlation with the change in TSH (r =-0.63, P < 0.01). CONCLUSION: The endothelium-dependent arterial dilation increases significantly in untreated hyperthyroid patients, and decreases markedly after a subtotal thyroidectomy. Therefore, we conclude that the endothelium is more responsive to reactive hyperaemia in the hyperthyroid than the euthyroid state.     

糖耐量减低患者联合干预治疗前后内皮依赖性血管舒张功能的变化

目的为了探讨糖耐量减低(IGT)患者联合干预治疗前后内皮功能的变化。方法选择28例IGT患者,和年龄、性别匹配的健康个体25人。IGT患者采用控制饮食、规则的有氧运动及口服二甲双胍联合干预治疗12周。采用高分辨血管外超声法检测肱动脉内皮依赖性血管舒张功能和内皮非依赖性血管舒张功能。结果IGT患者干预治疗前内皮依赖性血管舒张功能为3.50%,明显低于对照组的4.68%(P<0.05)。多元逐步回归分析结果显示,内皮依赖性血管舒张功能与年龄、LDL-C、Lp(a)、HbA1c、FPG及2hPG呈负相关(P<0.001)。经联合干预治疗12周后,内皮依赖性血管舒张功能明显增高,达到4.17%,明显高于IGT患者干预治疗前(P<0.05)。Spearman分析结果显示,治疗前后内皮依赖性血管舒张功能的变化与FBG、2hBG、LDL-C、HbA1c的变化呈负相关(P<0.05)。结论IGT患者内皮依赖性血管舒张功能降低。联合干预治疗可改善血管内皮功能。     

糖耐量受损患者肱动脉内皮依赖性血管舒张功能变化的研究

采用高分辨血管外超声检测糖耐量受损(IGT)患者肱动脉血流介导的内皮依赖性血管舒张功能(EDD)和硝酸甘油介导的内皮非依赖性血管舒张功能(EID)。IGT组EDD明显低于对照组(P<0.05)。EID在两组间无明显差异(P>0.05)。     

Reduction of peripheral flow reserve impairs endothelial function in conduit arteries of patients with essential hypertension

BACKGROUND: A diminished flow reserve in resistance vessels is a hallmark of hypertensive microvascular disease. Hypertension is associated with structural alterations in the microcirculation and a reduced endothelium-dependent dilation in conduit arteries. Both have been demonstrated to predict future cardiovascular events. OBJECTIVE: We hypothesized that a reduced peripheral flow reserve impairs endothelial function in upstream conduit arteries in patients with arterial hypertension. DESIGN: In 43 hypertensive patients (HT) and 38 normotensive controls (NT) endothelial function of the brachial artery was assessed by measurement of flow-mediated dilatation (FMD), using high-resolution ultrasound. Peripheral flow reserve (FR) was determined via measurements of forearm blood flow at rest and during increments of reactive hyperaemia, using venous occlusion plethysmography. RESULTS: FMD was markedly impaired in HT (3.6 +/- 0.3%) as compared with NT (10.2 +/- 0.3%), whereas maximum brachial artery diameter following endothelium-independent dilatation was similar in both groups. In hypertensive patients FR was significantly reduced (HT, 3.2 versus NT, 6.0) during reactive hyperaemia after 5 min of ischaemia. FR was associated with FMD (r = 0.68, P < 0.01). Multiple stepwise regression analysis identified FR as a strong independent variable determining the extent of FMD (r2 = 0.46, P < 0.01). In HT the dose-response curve of FMD upon stepwise increases of FR was shifted significantly to the right. Normalization of FR improved FMD in HT by more than 60%. CONCLUSIONS: In essential hypertension a reduced FR contributes to the endothelial dysfunction of upstream conduit arteries. These findings may have therapeutic and prognostic implications in patients with arterial hypertension.     

Sleep apnea and markers of vascular endothelial function in a large community sample of older adults

Clinical studies have suggested that sleep apnea is associated with impaired brachial artery flow-mediated dilation, a surrogate of endothelial dysfunction. We examined this question among older participants in the baseline examination of the Sleep Heart Health/Cardiovascular Health Study cohort (n = 1,037, age 68 years or older, 56% female). Indices of sleep apnea, derived from 12-channel home polysomnography, were the apnea-hypopnea index (average number of apneas/hypopneas per hour) and the hypoxemia index (percentage of time below 90% O2 saturation). Baseline arterial diameter and percentage of flow-mediated dilation were measured by ultrasound. Sleep apnea measures were associated with baseline diameter and the percentage of flow-mediated dilation, although these associations were weakened after adjustment for other cardiovascular risk factors, particularly body mass index. However, a statistically significant linear association between the hypoxemia index and baseline diameter was observed even after adjustment for body mass index and other confounders (p < 0.01). The associations were stronger among participants who were younger than 80 years and among those who with hypertension. This study adds to the growing body of evidence linking sleep apnea with vascular dysfunction in older subjects. Whether these relationships are entirely independent of obesity is unclear. This association might be one of the mechanisms explaining the relationship between sleep apnea, hypertension, and cardiovascular disease.     

Apolipoprotein e4 allele and endothelium-dependent arterial dilation in Type 2 diabetes mellitus without angiopathy

AIMS/HYPOTHESIS: Several studies have suggested a predisposing role of the e4 allele of apolipoprotein E (ApoE) in the development of atherosclerosis and cardiovascular disease in Type 2 diabetes. Therefore, we hypothesized that the e4 allele is also a risk factor for endothelial dysfunction. We attempted to assess whether Apo e4 allele is associated with endothelial dysfunction in the early stage of Type 2 diabetes. METHODS: We selected 255 Chinese Han Type 2 diabtetic men without angiopathy. PCR or allele-specific oligonucleotide probes were used to analyse ApoE genotypes, and high resolution ultrasound was used to measure brachial artery diameter at rest, after reactive hyperaemia and after sublingual glyceryltrinitrate. RESULTS: The flow-mediated arterial dilation among the subjects with e4/3 or e4/4 was 3.14+/-0.32%, which was lower than that in subjects with e2/2 or e3/2 (4.04+/-0.30%) ( p=0.038). The baseline vessel size, glyceryltrinitrate-induced arterial dilation and baseline flow were not different among different ApoE genotypes. On univariate analysis, reduced flow-mediated arterial dilation was related to total cholesterol, LDL, lipoprotein(a) [Lp(a)], high blood pressure, older age, family history of premature vascular disease, larger vessel size, cigarette smoking, duration of diabetes and e4 allele ( p<0.05). By multiple stepwise regression analysis, reduced flow-mediated arterial dilation was associated with cigarette smoking, LDL, Lp(a), and e4 allele ( p<0.01). CONCLUSION/INTERPRETATION: Apo e4 allele is associated with impairment of endothelium-dependent arterial dilation in the early stage of Type 2 diabetes.     

Non-invasive evaluation of endothelial function in hypertensive elderly patients

Impaired endothelium-dependent vasomotion is a diffuse disease process resulting in abnormal regulation of blood vessel tone and loss of several atheroprotective effects of the normal endothelium. The aim of the present study was to investigate the effects of aging and hypertension on endothelial function. Sixty-six geriatric subjects with ages over 60 (48 hypertensive and 18 healthy) and 40 middle-aged subjects (16 hypertensive and 24 healthy) were included in the study. Systemic vascular endothelial function was evaluated through measuring brachial arterial vasodilation, a physiologic answer to reactive hyperemia occured with increased blood flow in the vessel after transient ischemia (flow-mediated dilation, FMD%), and with carotid artery intima-media thickness (IMT) measurement, using high-resolution ultrasonography. Endothelial independent vasodilation was also measured after administration of sublingual isosorbide dinitrate (isosorbide dinitrate mediated dilation, IDNMD%). FMD% was significantly decreased in elderly and/or hypertensive (HT) patients (geriatric HT: 9.5 +/- 4.7%, geriatric non-HT: 12.7 +/- 5.5%, middle-aged HT: 12.9 +/- 4.3% and middle-aged non-HT: 18.9 +/- 8.1%) (geriatric HT versus geriatric non-HT (P = 0.02), geriatric HT versus middle-aged HT (P = 0.01), geriatric non-HT versus middle-aged non-HT (P = 0.008)). Both FMD% and IDNMD% were inversely correlated with age, baseline vessel diameter and carotid artery intima-media thickness. FMD% was also inversely correlated with diastolic blood pressure. No correlation was found between FMD% and systolic blood pressure, serum cholesterol and triglyceride levels. Endothelium dependent (EDD) and independent dilatation of large arteries decreased with aging even in the healthy elderly, and FMD further declined in HT elderly patients, indicating that age and hypertension independently impair endothelial function. Positive correlations with age and hypertension, and significant inverse correlation with FMD, makes carotid artery IMT a possible indicator of endothelial function.