原发性高血压患者微量白蛋白尿与无症状性脑血管损害的研究

目的探讨原发性高血压(EH)患者微量白蛋白尿(MAU)与无症状性脑血管损害及颈动脉粥样硬化的关系。方法根据24h尿蛋白滤过率(UAER)测定结果,将162例EH患者分为正常白蛋白尿(NAU)组101例和MAU组61例。应用高频多普勒超声检测颈动脉内膜中层厚度(IMT)及颈动脉粥样硬化斑块;头颅MRI评价腔隙性脑梗死。采用logistic回归分析颈动脉IMT增厚和腔隙性脑梗死相关的危险因素。结果162例EH患者中MAU的阳性率为37.7%;与NAU组比较,MAU组颈动脉IMT明显增厚[(1.00±0.26)mmvs(0.86±0.20)mm,P<0.01],腔隙性脑梗死的发生率明显增高(62.3%vs44.6%,P<0.05);MAU与颈动脉IMT增厚及腔隙性脑梗死的发生独立相关(OR=2.639,95%CI:1.240～5.615,P<0.05及OR=2.369,95%CI:1.156～4.856,P<0.05)。结论MAU是高血压患者发生腔隙性脑梗死和颈动脉IMT增厚的一个预测指标,可作为判断无症状性脑血管损害及颈动脉粥样硬化的早期指标。     

原发性高血压患者微量白蛋白尿与亚临床动脉粥样硬化的相关性

目的:探讨原发性高血压(EH)患者尿微量白蛋白(UMA)水平与颈总动脉粥样硬化及踝臂指数(ABI)的相关性。方法:收集2014年4月至2015年8月我院收治的215例EH患者。根据24hUMA水平,患者被分为正常UMA组(116例)和微量白蛋白尿(MAU)组(99例)。测量比较两组一般资料、UMA水平、颈动脉内膜中层厚度(CIMT)、颈动脉管腔内径、斑块发生率以及ABI。分析EH合并MAU患者UMA水平与CIMT、ABI的相关性。结果:两组年龄、性别、血压、空腹血糖、血脂、血肌酐水平均无显著差异(P均0.05)。与正常UMA组比较,MAU组UMA水平[20.25(15.75,25.75)mg/d比86.50(56.50,104.50)mg/d]、CIMT[(1.20±1.09)mm比(1.76±0.81)mm]、斑块发生率(55.17%比75.76%)显著升高,ABI[(1.12±0.11)比(0.97±0.11)]显著降低,P均0.01。直线相关分析显示,EH合并MAU患者UMA水平与CIMT呈显著正相关(r=0.551,P=0.001),与ABI呈显著负相关(r=-0.266,P=0.008)。结论:EH合并MAU患者微量白蛋白尿水平和颈动脉内膜中层厚度显著正相关,与踝臂指数显著负相关,提示微量白蛋白尿不仅和高血压肾脏病变有关,也是亚临床期动脉粥样硬化的早期标志。     

2型糖尿病患者尿微量白蛋白与颈动脉内膜中层厚度的关系

目的观察糖尿病患者尿微量白蛋白与颈动脉内膜中层厚度的相关性，并探讨其临床意义。方法2型糖尿病患者98例（T2DM组），糖尿病合并颈动脉内膜中层增厚患者（T2DM＋IMT组）55例，正常对照组64例，分别测定空腹血糖、血脂、尿微量白蛋白，并统计微量白蛋白尿的阳性例数及阳性率。结果T2DM组、T2DM＋IMT组空腹血糖、血脂、尿微量白蛋白水平及阳性率高于正常对照组（P〈0．05），T2DM＋1MT组尿微量白蛋白水平及阳性率高于单纯T2DM组（P〈0．05），尿微量白蛋白水平与颈动脉内膜中层厚度呈正相关（r=0．22，P〈0．05）。结论T2DM患者尿微量白蛋白与颈动脉内膜中层厚度密切相关。     

2型糖尿病患者微量白蛋白尿水平与颈动脉内膜中层厚度的相关性

目的 研究2型糖尿病微量白蛋白尿水平与颈总动脉内膜中层厚度(CIMT)的关系.方法 选取2型糖尿病患者129例,根据24h 尿白蛋白排泄率分为尿蛋白正常组75例(24 h尿白蛋白＜30 mg/24 h),微量蛋白尿组54例(24h尿白蛋白30～300 mg/24 h),并根据微量白蛋白水平将后者为3个亚组.观察尿蛋白正常组与微量蛋白尿组及微量蛋白尿组内3个亚组间颈总动脉内膜中层厚度(CIMT)及斑块情况的关系.结果 两组CIMT比较有显著差异(P＜0.05),各亚组间CIMT值有显著性差异(P＜0.05);各组间有斑块人数占该组人数百分比的差异有统计学意义(P＜0.05);两组空腹血糖、餐后2h血糖、糖化血红蛋白、TC、糖尿病病史及血压、高血压病史比较差异有统计学意义(P＜0.05);两组年龄、体质量指数、TG、HDL-C、LDL-C水平比较差异无统计学意义(P＞ 0.05);Logistic多元回归分析发现,糖尿病病程、高血压、空腹血糖是尿微量白蛋白排泄的危险因素.结论 糖尿病患者颈动脉内膜-中层厚度与尿微量白蛋白排泄有明显相关性.     

微量白蛋白尿与脑梗死面积的关系探讨

目的探讨脑梗死患者微量白蛋白尿水平变化与脑梗死面积之间的关系。方法用比浊法测尿微量白蛋白值,比较大梗死组、中梗死组、腔隙性梗死组及对照组微量白蛋白尿的阳性率及尿微量白蛋白水平。结果微量白蛋白尿阳性率大梗死组62.4%、中梗死组58.9%、腔隙性梗死组54.5%,对照组32.6%。尿微量白蛋白水平大梗死组(22.56±14.28mg/L)、中梗死组(16.82±11.78mg/L)、腔隙性梗死组(11.76±10.28mg/L)、对照组(7.12±10.12mg/L)。3个脑梗死组与对照组比较差异均有统计学意义(P<0.05),大梗死组、中梗死组与腔隙性组比较有统计学意义(P<0.05)。结论脑梗死患者呈现微量白蛋白尿高发率;尿微量白蛋白水平越高,梗死面积越大。可为临床预后的预测因子。     

小血管病变所致急性腔隙性脑梗死与尿微量白蛋白的相关性研究

目的探讨小血管病变所致的急性腔隙性脑梗死与尿微量白蛋白的相关性。方法回顾性分析2012年11月—2014年4月在中国医科大学附属盛京医院神经内科住院的急性腔隙性脑梗死患者136例的临床资料,并根据颈动脉彩色多普勒超声及头部MR血管成像将其分为小血管病变(CSVD)组(72例)和大血管病变(CLVD)组(64例)。观察并比较两组患者尿微量白蛋白水平。应用SAS 9.1软件进行统计学分析,采用多因素Logistic回归分析方法确定小血管病变所致的急性腔隙性脑梗死的独立危险因素。结果 CSVD组尿微量白蛋白浓度[(22±13)mg/L]明显低于CLVD组[(29±14)mg/L],差异有统计学意义(P0.05);CSVD组与CLVD组患者尿微量白蛋白水平增高情况差异有统计学意义(P0.01),其中CSVD组尿微量白蛋白浓度为10~30mg/L(轻度增高)患者的比例[56.9%(41/72)]较CLVD组[26.6%(17/64)]有增高趋势。Logistic回归分析结果显示,尿微量白蛋白轻度增高与小血管病变所致急性腔隙性脑梗死相关(OR=3.130,95%CI:1.481~6.618,P0.01)。结论尿微量白蛋白轻度增高是小血管病变所致急性腔隙性脑梗死的独立危险因素。     

糖尿病患者认知功能障碍相关危险因素分析

目的研究2型糖尿病患者认知功能障碍的相关危险因素。方法使用蒙特利尔量表(Mo CA)对100例糖尿病患者进行评分后分为认知功能正常组40例,认知功能障碍组60例。比较两组间年龄、性别、腹围、体质指数(BMI)、糖尿病病程、糖化血红蛋白(Hb A1c)、胰岛素抵抗指数(IR)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)、血清肌酐(Cr)、尿微量白蛋白水平(U-MA1)、颈动脉内膜中层厚度(IMT)的差异,并将评分与上述因素做直线相关及逐步回归分析。结果两组间糖尿病病程、胰岛素抵抗指数、微量白蛋白水平差异有统计学意义(均P0.05),Mo CA值与年龄、病程、胰岛素抵抗指数、尿微量白蛋白、颈动脉内膜中层厚度呈负相关(均P0.05)。逐步多元回归分析结果示糖尿病病程、颈动脉内膜中层厚度、尿微量白蛋白水平、胰岛素抵抗指数为独立危险因素(均P0.05)。结论糖尿病患者认知功能障碍与糖尿病病程、胰岛素抵抗指数、尿微量白蛋白水平、大血管病变程度相关。     

新疆维吾尔族、汉族原发性高血压患者动脉僵硬度与尿微量白蛋白及血浆醛固酮水平的相关性

目的探讨新疆维吾尔族、汉族原发性高血压患者动脉僵硬度与尿微量白蛋白、血浆醛固酮水平的关系。方法收集2008-08-2011-04住院的原发性高血压患者共411例,其中男225例,女186例,维吾尔族123例,汉族288例,年龄(46.4±10.7)岁。对维吾尔族、汉族患者进行24h尿微量白蛋白、臂踝动脉脉搏波传导速度(baPWV)、颈动脉内膜中层厚度测定。根据baPWV水平分为正常组(baPWV≤1400cm/s,n=183)和异常组(baPWV>1400cm/s,n=228)。结果维吾尔族、汉族异常组患者24h尿微量白蛋白[维吾尔(29.23±18.44)比(14.18±4.73)mg/24h;汉(24.82±25.43)比(13.69±6.74)mg/24h,P<0.05],颈动脉内膜中层厚度[维吾尔(0.12±0.04)比(0.09±0.03)cm;汉(0.10±0.03)比(0.09±0.02)cm,P<0.05],血浆醛固酮(立位)水平[维吾尔(0.20±0.18)比(0.09±0.02)μg/L;汉(0.18±0.19)比(0.08±0.02)μg/L,P<0.05]高于正常组。经多因素Logistic回归分析显示:维吾尔族、汉族24h尿微量白蛋白,血浆醛固酮(立位)水平,颈动脉内膜中层厚度与baPWV相关(P<0.05)。结论 24h尿微量白蛋白、颈动脉内膜中层厚度及血浆醛固酮(立位)水平为维吾尔族、汉族高血压患者动脉僵硬度共同的危险因素。     

老年高血压合并糖尿病患者颈动脉粥样硬化的观察

目的 观察老年高血压患者合并2型糖尿病时对颈动脉内膜中层厚度的影响及血脂水平的变化,探讨此类患者颈动脉粥样硬化的特点.方法 将120例患者分为高血压组（EH组,60例）、高血压合并糖尿病组（EH＋DM组,60例）,并按性别年龄匹配对照组.采用高分辨率超声采集患者颈动脉内膜中层厚度数据并收集患者其他一般情况数据.结果 EH＋DM组及EH组患者血浆甘油三酯水平均明显升高,EH＋DM组低密度脂蛋白胆固醇明显增高,颈动脉内膜中层厚度及斑块发生率均明显高于EH组.结论 高血压患者一旦合并糖尿病,相对于单纯高血压患者,其血脂异常及动脉粥样硬化的危险均增加,更易形成斑块.     

老年脑梗死患者血清中性粒细胞明胶酶脂质运载蛋白及凝集素样氧化型低密度脂蛋白受体-1水平的表达及临床意义

目的分析老年颈内动脉粥样硬化脑梗死患者血清中性粒细胞明胶酶脂质运载蛋白(NGAL)、凝集素样氧化型低密度脂蛋白受体-1(sLox-1)表达及颈动脉内膜改变,探讨其临床意义。方法收集2012年3月至2013年9月在湖南省老年医院神经内科确诊为动脉粥样硬化脑梗死患者70例为A组,颈内动脉粥样硬化患者72例为B组,两组按随机分组法再分为常规治疗组和强化治疗组两个亚组,分别在0周、12周、24周时采用酶联免疫吸附法测定患者血清NGAL、sLox-1水平,并同时测定患者的颈动脉内膜中层厚度和斑块面积,数据结果采用SPSS 17.0软件进行统计分析。结果脑梗死组患者血清中NGAL和sLox-1的表达水平、颈动脉内膜中层厚度及斑块面积均高于动脉硬化组(P0.05),阿托伐他汀治疗24周后强化亚组下降明显(P0.05),且颈动脉内膜中层厚度及斑块面积较前降低(P0.05)。结论血清NGAL及sLox-1参与动脉粥样硬化性脑梗死的发生机制,强化调脂治疗后其表达水平下调。     

Ultrastructural changes in renal arterioles and juxtaglomerular cells in hypertension

The ultrastructural appearance of socalled arteriolar hyalinosis was qualitatively indistinguishable in renal biopsies from patients with essential hypertension with or without diabetes mellitus, renovascular hypertension (the unimpaired member), hypertension associated with progressive systemic sclerosis and gout, normotensive aging (greater than 50 years), persons without renal disease, and a high percentage of adolescent normotensive diabetic individuals. These findings provide further evidence identifying the hypertension observed in patients with gout and progressive systemic sclerosis with that of the essential type.     

高血压患者血清瘦素、抵抗素水平与颈动脉内膜-中层厚度的关系

目的:探讨原发性高血压患者血清瘦素、抵抗素水平的变化及与颈动脉粥样硬化的相关关系.方法:入选80例原发性高血压患者(病例组),另选32例健康对照者.采用酶联免疫吸附法检测血清瘦素、抵抗素水平;采用彩色超声诊断仪测定颈动脉内膜-中层厚度(IMT).结果:病例组的瘦素(t=-2.530,P=0.013)和抵抗素水平(t=-2.077,P=0.041)均高于对照组.病例组的颈动脉IMT(t=-3.115,P=0.003)和颈动脉最大IMT(t=-3.271,P=0.002)均大于对照组.Pearson相关分析示,高血压患者血清瘦素与IMT(r=0.311,P=0.012)和最大IMT(r=0.308,P=0.013)呈显著正相关;血清抵抗素与IMT(r=0.335,P=0.006)和最大IMT(r=0.284,P=0.022)呈显著正相关.结论:原发性高血压患者的血清瘦素、抵抗素水平显著升高,且它们和颈动脉IMT存在相关性.     

Effects of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral blood flow, and the blood-brain barrier.

Acute hypertension was induced in 19 anesthetized cats by the intravenous administration of angiotensin. The caliber of pial arteries was measured by a television image-splitting technique and local cerebral blood flow by the hydrogen clearance technique. As the blood pressure was increased, pail arterioles constricted and cerebral blood flow remained relatively constant, showing that autoregulation of cerebral blood flow was intact. At mean arterial pressures of more than 170 mm Hg arteriolar dilation appeared. In smaller arterioles (initial diameter less than 100 mum) a segmental dilation (the "sausage'string" phenomenon) frequently preceded uniform dilation. This arteriolar dilation was associated with a marked increase in local cerebral blood flow indicating that the upper level of autoregulation had been breached. In no cat was vasospasm or a decrease in blood flow observed during induced hypertension. Hypertension also caused dysfunction of the bloodbrain barrier since, in 17 out of 19 of the cats examined, there was extravasation of protein-bound Evans blue into brain tissue. In only one of the 19 cats subjected to neuropathological analysis was ischemic brain damage identified and this was restricted to minimal ischemic cell change. The results indicate that severe, induced hypertension in cats produces cerebral arteriolar dilation, an increase of cerebral blood flow, and dysfunction of the blood-brain barrier. These observations may be of importance in understanding the pathogenesis of hypertensive encephalopathy.     

Dependence of morphological changes of the carotid arteries on essential hypertension and accompanying risk factors.

BACKGROUND: Aims: to evaluate morphological changes (intima-media thickness, IMT) of the carotid arteries in patients being treated for essential hypertension (EH), and to discover whether this abnormality can be detected in normotensive offspring of subjects with EH (familial trait, FT); and to investigate the interrelationship between IMT and accompanying risk factors. METHODS: Experimental design: cross-sectional study. Setting: angiology department, university teaching hospital. Subjects: the study encompassed 172 subjects, of whom 46 were treated hypertonics aged 40-55 (49) years, and 44 age matched, normotensive volunteers as controls. We also investigated 41 normotensives with FT for essential hypertension aged 20-30 (25) years and 41 age- and sex-matched controls without FT. Interventions: the hypertensive subjects were being treated either with long-acting calcium-channel antagonists or ACE-inhibitors. Measures: using high resolution ultrasound, IMT of the carotid bifurcation and of the common carotid artery was measured. RESULTS: In the hypertensives, the mean IMT was greater than that in the controls (0.92 (0.10) mm vs 0.72 (0.07) mm; p<0.00005). The IMT was independently related to accompanying risk factors: a positive family history of hypertension, age of the patient, duration of EH and the level of systolic/diastolic blood pressure (BP), body mass index and total/LDL-cholesterol. In subjects with FT, IMT was also greater compared to the control group (0.60 (0.05) mm vs 0.55 (0.04) mm; p<0.00005). IMT was not related to BP values. CONCLUSIONS: In treated essential patients with the EH, the IMT was increased. Individuals with FT also had greater IMT in the absence of elevated BP. The IMT in hypertensives was related to accompanying risk factors, which could be pathogenetic determinants of EH and/or its complications.     

Renal pathology of essential hypertension.

Microscopic analysis of over 2,000 renal biopsies taken at surgical sympathectomy operations has been correlated with blood pressures in essential hypertension. Statistically significant relationships exist between the average diastolic pressure and the degree of afferent renal arteriolar thickening and narrowing. Postoperative prognosis was favorable with all but the most severe and diffuse arteriolar sclerosis, and vascular fibrinoid necrosis did not affect survival. Juxtaglomerular cell hyperplasia and inferred renin hypersecretion were significantly involved in the kidney biopsies of essential hypertension. Diabetic juxtaglomerular cell atrophy and sclerosis reduced this component of hypertension. After age 80, kidneys at autopsy showed no evident relation between arteriolar lesions and hypertension.     

Increased intima-media thickness of the common carotid artery in primary aldosteronism in comparison with essential hypertension

BACKGROUND: Aldosterone contributes to the accumulation of collagen fibers and extracellular matrix in arterial wall. The aim of this study was to compare intima-media thickness (IMT) of the common carotid artery and carotid bifurcation in patients with primary aldosteronism, essential hypertension and healthy controls. METHODS: Carotid ultrasound studies were carried out in 33 patients aged 42-72 years with primary aldosteronism, 52 patients with essential hypertension and in 33 normotensive controls. RESULTS: The patients with primary aldosteronism had significantly higher IMT of the common carotid artery than patients with essential hypertension and controls (0.987 +/- 0.152 mm; 0.892 +/- 0.154 mm versus 0.812 +/- 0.124 mm; P < 0.001; P < 0.05). There was also significantly higher IMT of the common carotid in patients with essential hypertension compared to control group (0.892 +/- 0.154 mm versus 0.812 +/- 0.124 mm; P < 0.01). The differences between both hypertensive groups remained statistically significant after adjustment for age and 24-h systolic blood pressure (P = 0.001). The differences of the IMT in the carotid bifurcation were statistically significant only between patients with primary aldosteronism and controls (1.157 +/- 0.243 mm versus 0.994 +/- 0.199 mm; P <0.05). CONCLUSION: Patients with primary aldosteronism have increased common carotid IMT compared to the patients with essential hypertension. This finding could be caused by the deleterious effects of aldosterone excess on the fibrosis and thickening of the arterial wall, mainly in the straight segments of vessels.     

老年原发性高血压患者颈动脉内膜中层厚度与心血管危险因素相关性分析

目的分析老年原发性高血压患者预动脉内膜中层厚度（IMT）与心血管危险因素的相关性方法对82例老年原发性高血压患者行颔动脉超声测定IMT,同时检测患者血压乐、血三酰甘油（TG）、总胆固醇（TC）、高密度胆固醇（HDL—C）、低密度胆同醇（LDL—C）、空腹糖（FBG）及超敏C反应蛋白（hsCRP）。按照颈动脉IMT厚度分为IMT增厚组和IMT正常组,并对两组年龄、病程、血压值及生化指标等进行比较分析结果IMT增厚组较IMT正常组年龄较大,高血压病程较长,收缩压（SBP）、TC、LDL—C、FBG、hsCRP较高,HDL—C较低;随着IMT的增厚,高LDL—C、高FBG、高hsCRP的检出率增加。结论老年原发性高血压患者预动脉IMT与心血管危险因素聚集有显著的相关性。     

Vascular remodeling of the carotid artery in patients with untreated essential hypertension increases with age.

We examined whether hypertrophy of the carotid artery in patients with untreated essential hypertension is associated with compensatory carotid artery enlargement as these patients age. Carotid ultrasonography was evaluated in 163 patients with untreated essential hypertension (74 males and 89 females) and in 76 normotensive subjects. Intima-media end-diastolic thickness (IMT) and outer vessel diameter (VD) were measured, and relative wall thickness (IMT/R, R=VD/2) and vascular mass (VM) were calculated. Determinants of vascular hypertrophy in patients with untreated essential hypertension were also investigated. VD, VM, and IMT were significantly correlated with age in both the normotensive and hypertensive groups. Additionally, IMT was significantly correlated with VD in both groups. There was no correlation between increasing age and IMT/R in either group. IMT, VD and VM were significantly higher in the hypertensive group >50 years than in age-matched normotensive controls. However, IMT/R was significantly higher in the 50-59 years hypertensive group than in normotensive controls of the same age group. In addition to age, VM was related to systolic blood pressure, pulse pressure, fasting blood sugar, IMT, VD, and IMT/R in the hypertensive group. Multivariate regression analysis in the hypertensive group indicated that IMT/R was the strongest predictor of carotid vascular mass. Age and pulse pressure were also independently related to vascular mass. These results indicate that, as patients with untreated hypertension age, carotid arteries undergo remodeling. This should add further impetus to the implementation of appropriate hypertension treatment for such patients.     

Association between carotid hemodynamics and asymptomatic white and gray matter lesions in patients with essential hypertension.

The aim of this study was to clarify the magnitude of common carotid artery (CCA) structural and hemodynamic parameters on brain white and gray matter lesions in patients with essential hypertension (EHT). The study subjects were 49 EHT patients without a history of previous myocardial infarction, atrial fibrillation, diabetes mellitus, impaired glucose tolerance, chronic renal failure, symptomatic cerebrovascular events, or asymptomatic carotid artery stenosis. All patients underwent brain MRI and ultrasound imaging of the CCA. MRI findings were evaluated by periventricular hyperintensity (PVH), deep and subcortical white matter hyperintensity (DSWMH), and état criblé according to the Japanese Brain dock Guidelines of 2003. Intima media thickness (IMT), and mean diastolic (Vd) and systolic (Vs) velocities were evaluated by carotid ultrasound. The Vd/Vs ratio was further calculated as a relative diastolic flow velocity. The mean IMT and max IMT were positively associated with PVH, DSWMH, and état criblé (mean IMT: rho=0.473, 0.465, 0.494, p=0.0007, 0.0014, 0.0008, respectively; max IMT: rho=0.558, 0.443, 0.514, p=0.0001, 0.0024, 0.0004, respectively). Vd/Vs was negatively associated with état criblé (rho=-0.418, p=0.0038). Carotid structure and hemodynamics are potentially related to asymptomatic lesions in the cerebrum, and might be predictors of future cerebral vascular events in patients with EHT.     

Insulin resistance/compensatory hyperinsulinemia predict carotid intimal medial thickness in patients with essential hypertension

BACKGROUND AND AIM: Approximately 50% of subjects with essential hypertension (EH) are insulin resistant, and this defect in insulin action could contribute to increased cardiovascular disease (CVD) risk in these patients. To test this hypothesis, we attempted to see if there was a link between insulin resistance (IR) and carotid intimal medial thickness (IMT), an early index of CVD, in patients with essential hypertension. METHODS AND RESULTS: Ultrasound quantification of carotid IMT was performed in 79 hypertensive patients, and 63 patients (31 m and 32 f), defined as being free of plaque (IMT < 1.3 mm), were further subdivided into normal (<1.0 mm) and thickened (1-1.3 mm) IMT groups. Subjects in the thickened IMT group were older and had significantly (p < 0.05) higher plasma concentrations of fasting insulin, nitric oxide (NO(x)) and intercellular adhesion molecule 1 (ICAM-1). However, the two groups were not significantly different in terms of blood pressure, overall or regional obesity, fasting lipid levels, uric acid, concentrations of other cellular adhesion molecules or levels of C-reactive protein. There were significant (p < 0.05) correlations in the whole population between IMT and age, fasting insulin and NO(x), and multiple regression analysis identified fasting insulin as an independent predictor of IMT. CONCLUSIONS: The presence of increased IMT is significantly related to several metabolic and endothelial abnormalities associated with IR/hyperinsulinemia, and fasting insulin independently predicts the thickness of the intima-media layer. These results support the view that CVD risk is greatest in those patients with essential hypertension who are also IR/hyperinsulinemic.