Short- and long-term influence of diet and simvastatin on brachial artery endothelial function

BACKGROUND: Endothelium-dependent dilation (EDD) has often been studied in patients with hypercholesterolemia without overt coronary atherosclerosis where an improvement after statin treatment has been documented within few weeks. The aim of the study was to assess the short-term effect of diet as well as short- and long-term effect of simvastatin on EDD in patients with hypercholesterolemia and ischemic heart disease. METHODS: In 43 male patients with hypercholesterolemia and ischemic heart disease, EDD of the brachial artery was measured at baseline, after 3 months on a lipid-lowering diet, and after another 1, 3 and 12 months on simvastatin at 40 mg/day. RESULTS: Three months changes in EDD were neither influenced by diet nor short-term simvastatin therapy (4.9% vs. 4.9% vs. 4.8%, p=ns). Twelve months simvastatin treatment, however, significantly improved EDD by 32.7% (4.9% vs. 6.5%, p=0.007). By regression analysis an individual adjusted increase in EDD during the simvastatin treatment period was seen (coefficient 0.132 a month, p=0.002). A significant reduction in total cholesterol of 31.0% (6.1+/-0.8 vs. 4.2+/-0.7, p<0.001) and LDL cholesterol of 42.6% (4.0+/-0.8 vs. 2.2+/-0.6, p<0.001) was observed. CONCLUSION: EDD is improved after long-term simvastatin therapy; however, neither did 3 months diet or 3 months simvastatin therapy has influence on the EDD.     

Elevation of the soluble thrombomodulin levels is associated with inflammation after percutaneous coronary interventions

BACKGROUND: Thrombomodulin (TM) is an endothelial cell surface thrombin-binding protein with anticoagulation ability by thrombin-mediated activation of protein C. An increase of plasma soluble TM level is reported to be associated with severity and worse outcome of coronary artery disease. HYPOTHESIS: This prospective study investigated the relation of the elevated levels of plasma soluble TM and inflammatory and myonecrotic markers in patients undergoing percutaneous coronary intervention (PCI). METHODS: Plasma levels of soluble TM, C-reactive protein (CRP), and creatine kinase and its MB isoenzyme were measured before and after PCI in 100 patients undergoing PCIs. RESULTS: Peak TM levels after PCIs were significantly higher than baseline (3.39 +/- 1.63 vs. 2.90 +/- 1.57 ng/ml, p < 0.001). The peak TM levels after PCIs correlated significantly with the peak CRP and MB levels, and the maximal inflation duration (r = 0.423, p < 0.001; r = 0.212, p = 0.034; r = 0.307, p= 0.002, respectively). CONCLUSIONS: Soluble TM levels increase significantly after PCI. The elevation of the soluble TM after PCI shows better correlation with inflammation than myocardial injury, indicating an endothelial origin. Measurement of soluble TM could be useful and calls for further studies on the prognostic effects of this marker in this clinical condition.     

Endothelial dysfunction in patients with asthma: the role of polymorphisms of ACE and endothelial NOS genes.

OBJECTIVES: Polymorphisms of the angiotensin converting enzyme (ACE) and endothelial nitric oxide (eNOS) genes have been implicated in asthma pathogenesis. Angiotensin II and NO have important roles in maintaining vascular tone. In this study, the relationship between endothelial dysfunction and ACE and eNOS gene polymorphisms was investigated in patients with asthma. METHODS: This cross-sectional, controlled study was conducted at the Yedikule Chest Disease Hospital and Cardiology Center in a University Hospital. Forty-nine patients with asthma (18 male, 31 female; mean age: 33+/-12 years) and 49 age- and sex-matched healthy controls (20 male, 29 female; mean age: 30+/-8 years) were included. Pulmonary function tests and flow-mediated dilatation of the brachial artery [endothelium dependent dilatation (EDD)] were examined by high-resolution ultrasonography. The ACE and eNOS genotypes were determined by PCR. RESULTS: Asthma patients showed lower EDD (12+/-6% vs. 22+/-6%, p<0.001) as compared to controls. The EDD was correlated with both predicted value of FEV1 (r=0.31, p=0.04) and predicted value of FVC (r=0.37, p=0.013). Conversely, EDD values in patients with moderate asthma were significantly lower than those in patients with mild asthma (10.1+/-5.2% vs. 14.1+/-5.7%, p=0.017). However, the ACE and eNOS genotype distribution was not significantly different between controls and asthma groups. Furthermore, EDD was not associated with both gene polymorphism of ACE and eNOS. CONCLUSION: Patients with asthma have decreased vasodilatatory response to shear stress (EDD). Decreased EDD is correlated with the severity of asthma, but not with the distribution of ACE and eNOS genotypes.     

Impaired endothelial function in systemic lupus erythematosus

Systemic lupus erythematosus (SLE) patients suffer from excess cardiac deaths due to accelerated atherosclerosis. Endothelial dysfunction is a marker of early atherosclerosis. We tested the hypothesis that SLE patients have impaired endothelial function and assessed the relationship between endothelial function and clinical outcome over the subsequent five years. Thirty-six female SLE patients were compared with 22 healthy age and sex matched controls. Endothelial dependent vasodilatation (EDD) was assessed at the brachial artery in response to shear stress. Endothelium-independent dilatation induced by glyceryl trinitrate was also measured. Patients were followed for up to five years and the development of damage in the cardiovascular and other systems recorded. SLE patients showed significantly impaired endothelial function (median EDD 5.6%, IQR 3.1-7.2%) compared with healthy controls (median EDD 8.0%, IQR 6.3-9.3%; P = 0.001). Endothelium independent dilatation did not differ between the two groups. Endothelial function was significantly worse in postmenopausal compared with premenopausal women (median EDD 6.6%, IQR 3.9-7.8% versus 3.1%, IQR 2.6-5.1%; P = 0.016). Total cholesterol was inversely correlated with endothelial function in SLE patients (Spearman correlation r = -0.422, P = 0.025). There was no relationship between endothelial function and the development of damage in any organ system, including the cardiovascular system during patient follow-up. Patients with SLE have impaired endothelial Lupus (2007) 16, 84-88.     

Effect of insulin therapy on endothelium-dependent dilation in type 2 diabetes mellitus

Endothelial dysfunction is an early marker of atherosclerosis occurring in patients with type 2 diabetes mellitus. Endothelium-dependent dilation (EDD) has been shown to improve by combined therapy of insulin and metformin. Studies on endothelium-independent vasodilatory capacity, however, have had controversial results. We sought to investigate the vascular reactivity--EDD and endothelium-independent dilation--and their changes induced by the addition of insulin therapy to patients with type 2 diabetes mellitus pretreated with diet and oral hypoglycemic drugs. We therefore performed vascular studies in 21 poorly controlled type 2 diabetic patients and 11 nondiabetic control subjects by using high resolution ultrasound of the brachial artery. After 3 months of additional insulin therapy, vascular and laboratory measurements including C-reactive protein and parameters of glucose and lipoprotein metabolism were repeated. At baseline, EDD was significantly impaired in diabetic patients compared with controls (2.7 +/- 2.2% vs 7.0 +/- 1.8%, p <0.001), whereas endothelium-independent dilation was normal in both groups. After insulin therapy, EDD increased from 2.7 +/- 2.2% to 5.0 +/- 2.8% (p <0.001) in diabetic patients. All other vascular parameters did not change over the treatment period. The absolute change in EDD showed a significant negative correlation with the change in hemoglobin A(1c) (r = -0.67, p <0.001) and with fasting blood glucose (r = -0.84, p <0.001) levels. In contrast, there was no correlation between EDD and the observed changes in lipid and C-reactive protein levels. Our findings demonstrate that insulin therapy has beneficial effects on vascular function, resulting in enhanced EDD, most probably due to an improved glycemic control as the underlying mechanism.     

A randomized trial comparing the effect of casein with that of soy protein containing varying amounts of isoflavones on plasma concentrations of lipids and lipoproteins.

CONTEXT: Isolated soy protein reduces plasma concentrations of total and low-density lipoprotein (LDL) cholesterol. OBJECTIVE: To identify the agent(s) responsible for the cholesterol-lowering effect of soy in mildly hypercholesterolemic volunteers: isoflavones isolated together with soy protein or soy protein itself. DESIGN: Double-blind randomized parallel trial. SETTING: Single-center study. PARTICIPANTS: A total of 156 healthy men and women with LDL cholesterol levels between 3.62 mmol/L (140 mg/dL) and 5.17 mmol/L (200 mg/dL) after instruction in a National Cholesterol Education Program Step I diet and recruited by advertisement from the community. INTERVENTION: One of 5 daily diets (25 g of casein [for isoflavone-free comparison] or 25 g of isolated soy protein containing 3, 27, 37, or 62 mg of isoflavones). MAIN OUTCOME MEASURES: Change and percent change from baseline in plasma concentrations of triglycerides and total, LDL, and high-density lipoprotein cholesterol after 9 weeks. RESULTS: Compared with casein, isolated soy protein with 62 mg of isoflavones lowered total and LDL cholesterol levels by 4% (P = .04) and 6% (P = .01), respectively. In patients with LDL cholesterol levels in the top half of the population studied (>4.24 mmol/L [>164 mg/dL]), comparable reductions were 9% (P<.001) and 10% (P = 001), respectively; in this group, isolated soy protein with 37 mg of isoflavones reduced total (P = .007) and LDL (P = .02) cholesterol levels by 8%, and there was a dose-response effect of increasing amounts of isoflavones on total and LDL cholesterol levels. Plasma concentrations of triglycerides and high-density lipoprotein cholesterol were unaffected. Ethanol-extracted isolated soy protein containing 3 mg of isoflavones did not significantly reduce plasma concentrations of total or LDL cholesterol. CONCLUSIONS: Naturally occurring isoflavones isolated with soy protein reduce the plasma concentrations of total and LDL cholesterol without affecting concentrations of triglycerides or high-density lipoprotein cholesterol in mildly hypercholesterolemic volunteers consuming a National Cholesterol Education Program Step I diet. Ethanol-extracted isolated soy protein did not significantly reduce plasma concentrations of total or LDL cholesterol.     

Endothelial dysfunction in Turkish patients with non-alcoholic fatty liver disease

Background: The components of the metabolic syndrome are closely related with endothelial dysfunction, which is a pathophysiological issue of cardiovascular diseases. Non‐alcoholic fatty liver disease (NAFLD) is considered as one of the components of the metabolic syndrome. The aim of this study was to evaluate the endothelial‐dependent dilatation (EDD) and endothelial‐independent dilatation (EID) of the brachial artery in NAFLD. Methods: Fifteen non‐alcoholic steatohepatitis (NASH), 17 patients with simple steatosis and 16 healthy subjects formed the study group. Non‐alcoholic fatty liver disease group was composed of patients admitted to the gastroenterology outpatient clinic because of increased liver enzymes. Endothelial functions of the brachial artery were evaluated by vascular ultrasound. EDD was assessed by establishing reactive hyperaemia, and EID was determined by using sublingual nitrate. Results: No statistical difference for the basal diameter of brachial artery was found between the groups (P = 0.49). The values for EDD and EID were significantly different across all three groups (P < 0.0001 and P < 0.0001, respectively). EDD and EID were significantly lower in NASH compared with simple steatosis (P = 0.01 and P < 0.01, respectively). However, there was no statistical significance for EDD and EID in simple steatosis groups compared with controls (P = 0.58 and P = 0.98, respectively). Conclusions: Our study showed that patients with NASH had significantly worse endothelial dysfunction compared with patients with simple steatosis and healthy subjects. The treatment strategies with ameliorative effects for endothelial dysfunction might be effective for delaying the development of cardiovascular complications in NAFLD.     

Effect of rosuvastatin on plasma levels of asymmetric dimethylarginine in patients with hypercholesterolemia

Elevated plasma levels of asymmetric dimethylarginine (ADMA) have been associated with attenuated endothelium-dependent vasodilation in hypercholesterolemic patients. However, whether lowering of plasma cholesterol concentration by hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) can reduce plasma ADMA levels is still not clear. This study was a multicenter, randomized, double-blind, placebo-controlled design including 46 patients with elevated low-density lipoprotein cholesterol levels. Patients were randomized into 2 groups: rosuvastatin 10 mg/day and placebo for 6 weeks. Plasma levels of ADMA, 8-isoprostane (as a marker of oxidative stress), homocysteine, and high-sensitivity C-reactive protein were measured at baseline and 6 weeks later. Endothelial function assessed by flow-mediated vasodilation of the brachial artery was performed in 11 patients in the rosuvastatin group and in 12 in the placebo group. Baseline characteristics of both groups were similar, and the plasma ADMA levels were significantly correlated with 8-isoprostane (r = 0.388, p = 0.008). After 6 weeks of treatment, plasma ADMA levels were significantly reduced in the rosuvastatin group (from 0.60 +/- 0.19 to 0.49 +/- 0.10 micromol/L, p <0.001). Increases in flow-mediated vasodilation were positively correlated with reductions in plasma levels of ADMA (p = 0.017) and low-density lipoprotein cholesterol (p <0.001). Thus, our findings suggest that treatment with rosuvastatin in patients with hypercholesterolemia may lead to a significant reduction in plasma ADMA levels, which appear to be related to the improvement in endothelial function by rosuvastatin.     

Low serum bilirubin levels are independently and inversely related to impaired flow-mediated vasodilation and increased carotid intima-media thickness in both men and women

BACKGROUND: Elevated levels of low-density lipoprotein (LDL) cholesterol and its oxidative modification have been described to be involved in the process of atherogenesis. Bilirubin, an antioxidant, prevents oxidative modification of LDL and therefore may protect from atherosclerosis and coronary heart disease (CHD). Impaired brachial artery flow-mediated dilatation (FMD), which means endothelial dysfunction (ED) and carotid intima-media thickness (IMT) are predictors for the development and progression of atherosclerosis. In the present study, FMD and IMT were studied in healthy subjects with lower and higher serum bilirubin concentrations in physiological ranges. METHODS: Ninety-one healthy subjects between 25 and 45 years of age (47 with lower and 44 with higher serum bilirubin concentrations) were included in this study. Carotid IMT and brachial artery flow-mediated dilatation was measured by means of high-resolution vascular ultrasound. FMD was assessed by establishing reactive hyperemia and endothelium-independent dilatation (EID) was determined by using sublingual isosorbide dinitrate. RESULTS: EDD in subjects with lower serum bilirubin concentrations was significantly worse than in those with higher serum bilirubin concentrations (11.6+/-4.4% versus 7.2+/-4.7%, respectively, p<0.0001). EID measurements were not significantly different between the groups (16+/-5.1% versus 16.8+/-7%, respectively). In addition, carotid IMT was significantly greater in subjects with lower serum bilirubin concentrations (0.5+/-0.13 mm versus 0.42+/-0.07 mm, p<0.0001). Furthermore, FMD in women with lower serum bilirubin concentrations was significantly lower than in women with higher serum bilirubin concentrations (11.5+/-4.9% and 17.5+/-4.7%, respectively, p<0.001). Accordingly, men with lower serum bilirubin concentrations had significantly lower FMD as compared to hyperbilirubinemic ones (11.7+/-3.6% versus 16.7+/-4.8%, respectively, p=0.009). Conversely, carotid IMT was significantly greater in both women and men with lower serum bilirubin concentrations compared to the subjects with elevated serum bilirubin concentrations (0.51+/-0.08 versus 0.41+/-0.08, p<0.001; 0.55+/-0.12 versus 0.40+/-0.07, p=0.002, in women and men, respectively). CONCLUSION: The healthy subjects with lower serum bilirubin concentrations show significant ED and increased carotid IMT, which are predictors for atherosclerosis.     

Arterial Reactivity Is Enhanced in Genetic Males Taking High Dose Estrogens

Objectives. We sought to assess whether high dose estrogen treatment is associated with enhanced arterial reactivity in genetic males.

Background. Although estrogens have been shown to enhance arterial reactivity in women, and are thereby thought to confer cardiovascular benefit, the vascular effects of long-term estrogen therapy in genetic males is unknown.

Methods. We studied the arterial physiology of 30 genetic males—15 male to female transsexuals receiving long-term high dose estrogen therapy and 15 healthy male control subjects matched for age, smoking history and vessel size. Using external vascular ultrasound, brachial artery diameter was measured at rest, after flow increase (causing endothelium-dependent dilation [EDD]) and after nitroglycerin (GTN), an endothelium-independent dilator. Blood pressure, cholesterol and testosterone levels were also measured in each subject.

Results. Total testosterone and free testosterone index levels were lower in the transsexuals compared with the control subjects (p < 0.001). In contrast, EDD was significantly higher in the transsexuals than in the control males (mean [±SD] 7.1 ± 3.1% vs. 3.2 ± 2.8%, p = 0.001), as was the GTN response (21.2 ± 6.7% vs. 14.6 ± 3.3%, p = 0.002). Total and high density lipoprotein cholesterol, blood pressure levels and baseline vessel size were similar in the two groups. On multivariate analysis, enhanced EDD was associated independently with estrogen therapy (p = 0.02) and with low total cholesterol (p = 0.04). An enhanced GTN response was also significantly associated with estrogen therapy (p = 0.03).

Conclusions. Long-term treatment with high dose estrogens is associated with enhanced arterial reactivity in genetic males, which may be due to the effects of estrogen excess or androgen deprivation, or both.

(J Am Coll Cardiol 1997;29:1432–6)     

Asymmetric dimethylarginine determines the improvement of endothelium-dependent vasodilation by simvastatin: Effect of combination with oral L-arginine.

OBJECTIVES: We hypothesized that the level of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of endothelial nitric oxide (NO) synthase (eNOS), might determine the endothelial effects of statins. BACKGROUND: Endothelial NO synthase is up-regulated by statins. However, statins failed to improve endothelial function in some studies. Asymmetric dimethylarginine inhibits eNOS by a mechanism that is reversible by L-arginine. METHODS: Ninety-eight clinically asymptomatic elderly subjects had their plasma ADMA levels screened. Those in the highest (high ADMA, n = 15) and lowest quartiles of the ADMA distribution (low ADMA, n = 13) were eligible to receive, in a randomized order, simvastatin (40 mg/day), L-arginine (3 g/day), or a combination of both, each for 3 weeks. Endothelium-dependent vasodilation (EDD) was assessed by brachial artery ultrasound. RESULTS: Simvastatin had no effect on EDD in subjects with high ADMA (6.2 +/- 1.2% vs. 6.1 +/- 0.9%), whereas simvastatin plus L-arginine significantly improved EDD (9.8 +/- 1.5% vs. 5.3 +/- 0.8%; p < 0.01). In subjects with low ADMA, simvastatin improved endothelial function when given alone (9.5 +/- 3.2% vs. 6.1 +/- 3.8%; p < 0.001) or in combination with L-arginine (9.0 +/- 3.1% vs. 6.3 +/- 3.3%; p = 0.001). L-arginine alone improved endothelial function in both groups. Endothelium-independent vasodilation was not affected. CONCLUSIONS: Simvastatin does not enhance endothelial function in subjects with elevated ADMA, whereas it does so in patients with low ADMA. Combination of simvastatin with oral L-arginine improves endothelial function in subjects with high ADMA, but has no additional effect in subjects with low ADMA. As NO-mediated effects may play a major role in the therapeutic effects of statins, ADMA concentration is an important factor that influences the "pleiotropic" effects of simvastatin.     

Endothelial function in hypercholesterolemic subjects: Effects of plant stanol and sterol esters

We investigated the effects of stanol (STAEST) and sterol esters (STEEST) on endothelial function in hypercholesterolemic subjects. In addition, associations of variables of cholesterol metabolism with endothelial function were investigated. In a double-blind randomized cross-over study (n=39) with age-matched parallel control group (n=37) the subjects consumed STAEST or STEEST spread (total plant sterols and stanols 1.93-1.98g/day) for 10 weeks each. Controls consumed the spread without sterols or stanols for 20 weeks. At baseline, brachial artery diameter was positively correlated with serum triglycerides (r=0.375, p=0.001) and glucose (r=0.420, p<0.001) and with cholesterol synthesis marker ratios to cholesterol (e.g. desmosterol r=0.540, p<0.001) and negatively with HDL cholesterol (r=-0.309, p=0.008) and absorption marker ratios (e.g. campesterol r=-0.332, p=0.004). During the intervention, LDL cholesterol was reduced by 6-9% from baseline with STAEST and STEEST spreads (p<0.05), and by 9-12%, respectively, from controls (p<0.05). Flow-mediated dilatation did not change during the investigation. Brachial artery diameter was unchanged in controls and during STAEST periods, but it was reduced during STEEST by 2.2% (p=0.012) from STAEST. In conclusion, variables of cholesterol metabolism are associated with brachial artery diameter at baseline. STEEST diminishes brachial artery diameter, but its clinical relevance remains unclear.     

Relationship between plasma soluble thrombomodulin levels and insulin resistance syndrome in type 2 diabetes: a comparison with von Willebrand factor.

Endothelial dysfunction plays a pivotal role in the initial stage of atherosclerosis. Insulin resistance is associated with accelerated atherosclerosis, especially coronary heart disease. To elucidate the relationship between endothelial dysfunction and insulin resistance or insulin resistance syndrome in patients with type 2 diabetes, we investigated the correlation between plasma soluble thrombomodulin (TM) and von Willebrand factor (vWF), measures of endothelial dysfunction, and the degree of insulin resistance evaluated by homeostasis assessment models of insulin resistance (HOMA-IR), or variables of insulin resistance syndrome. We studied 53 patients with type 2 diabetes, 23 treated with diet alone and 30 treated with sulfonylureas, who had normal renal function. The plasma soluble TM concentrations were highly correlated with HOMA-IR (r=0.64, p<0.0001), the plasma insulin (r=0.72, p<0.0001), the systolic blood pressure (r=0.45, p=0.0005), and the plasma fibrinogen (r=0.43, p=0.0018), while they were inversely correlated with the serum HDL cholesterol concentrations (r=-0.27, p=0.0344). The plasma vWF concentrations were positively correlated with HOMA-IR (r=0.35, p=0.0151) and the plasma fibrinogen (r=0.32, p=0.0203), but not with the plasma insulin, the systolic blood pressure or the HDL cholesterol concentrations. Furthermore, plasma TM, but not vWF, was positively correlated with total number of variables of insulin resistance syndrome (r=0.45, p=0.0005). These results indicate that endothelial dysfunction may be associated with the pathogenesis of insulin resistance syndrome as well as insulin resistance, and that the plasma TM might reflect endothelial damage better than the plasma vWF in the state of insulin resistance in patients with type 2 diabetes.     

通心络胶囊对原发性高血压病病人内皮功能的影响

目的探讨通心络胶囊对原发性高血压病病人内皮功能的影响。方法选取高血压病病人72例,随机分为常规治疗组(36例)及通心络组(36例),两组用药疗程均为8周。实验前后分别测定血清一氧化氮(NO)、内皮素(ET)及血清脂蛋白,并采用超声测量肱动脉血流介导的舒张反应(EDD)。结果两组治疗后血清NO,EDD较治疗前明显升高,血清ET浓度下降(P<0.05)。与常规治疗组相比,通心络组NO,EDD治疗后升高更显著(P<0.05)。结论常规降压治疗基础上应用通心络胶囊可进一步改善高血压病病人的内皮舒张功能。     

Interrelationship between noninvasive predictors of atherosclerosis: transthoracic coronary flow reserve, flow-mediated dilation, carotid intima-media thickness, aortic stiffness, aortic distensibility, elastic modulus, and brachial artery diameter

BACKGROUND: In this study, we searched for a correlation between transthoracic coronary flow reserve (CFR) and well-established surrogates of coronary atherosclerosis. METHODS: The study was conducted on 136 healthy subjects (mean age: 39.9 +/- 7.3 years) who were free of coronary risk factors. Transthoracic echocardiography was used to measure the aortic stiffness index (AoSI), aortic distensibility (AoD), and aortic elastic modulus (AoEM). High-resolution ultrasound was used to measure brachial artery endothelium-dependent and independent vasomotion and carotid intima-media thickness (IMT). In addition, transthoracic second harmonic Doppler echocardiography was used to measure CFR. RESULTS: All of the parameters significantly correlated with each other except brachial endothelium-independent dilation. CFR correlated significantly with brachial endothelium-dependent dilation (EDD) (r = 0.302, P < 0.01), carotid IMT (r =-0.388, P < 0.01), brachial artery diameter (r = 0.340, P < 0.01), AoD (r = 0.275, P < 0.01), AoS (r =-0.299, P < 0.01), and AoEM (r =-0.30,7 P < 0.01). Carotid IMT correlated significantly with brachial EDD and modestly with brachial artery diameter, AoD, AoS, and AoEM.In multivariate analysis, carotid IMT (beta=-0.323, P < 0.0001) and brachial artery diameter (beta = -0.259, P = 0.001) were significant independent predictors of CFR. The left ventricular mass index (beta= 0.371, P < 0.0001), brachial EDD (beta = -0.232, P = 0.002), and CFR (beta = -0.228, P = 0.003) were significant predictors for IMT. CONCLUSION: Transthoracic CFR correlated significantly with well-established noninvasive predictors of atherosclerosis, and we suggest that it can be used as a surrogate for coronary atherosclerosis.     

The effect of soy nut on serum total antioxidant,endothelial function and cardiovascular risk factors in patients with type 2 diabetes

BackgroundType 2 diabetes has a high spread and growing process. Using appropriate food diets is among therapeutic approaches has been applied for diabetic patients. Soya utilization has shown effective results in controlling metabolic abnormalities of these patients. The aim of this study is to investigate the effects of soy nut on glycemic conditions, blood pressure, lipid profile, antioxidant effects and vascular endothelial function of these patients.Methods70 patients with type 2 diabetes were randomly divided into two groups of the test (35 people) and control (35 people). The patients in the intervention group were subjected to 60 g soy nut diet as a part of daily protein for 8 weeks and the control group under the usual diet of diabetes. The fasting glucose, blood pressure, lipid profile, brachial blood flow, the level of serum E-Selectin and total antioxidant capacity in control and test group were assessed before and after diet.ResultsConsuming 60 g soy nut for 8 weeks significantly decreased the fasting blood glucose (P = 0.03), total serum cholesterol (P < 0.01), LDL-c (P = 0.01), and E-Selectin (P < 0.01) and increased the capacity of serum total antioxidants (P < 0.01), brachial blood flow (P < 0.01) but didn't have any significant effect on systolic/diastolic blood pressure, HDL-c, and TG.ConclusionSoy nut utilization in the patients with type-2 diabetes can significantly improve the glycemic condition, increase brachial blood flow, decrease E-selectin (improvement of endothelial function), increase serum total antioxidants and lipid profile but has no significant effect on blood pressure and HDL-c.     

波动性高血糖对血管内皮功能的影响

目的观察波动性高血糖对血管内皮功能的影响,探讨其致动脉粥样硬化的机制。方法选择新诊断的2型糖尿病患者72例,根据动态血糖监测结果分持续性高血糖组33例和波动性高血糖组39例,检测患者的肱动脉内皮依赖性舒张功能(EDD)及颈动脉内膜中层厚度(IMT)、血脂、空腹血糖、空腹胰岛素、餐后2 h血糖(2hPG)及餐后2 h胰岛素(2hINS)、高敏C反应蛋白(hs-CRP)、血管性假血友病因子(vWF)及尿微量白蛋白(MAU)。结果与持续性高血糖组比较,波动性高血糖组的2hPG、2hINS、hs-CRP、vWF、MAU及IMT明显升高(P<0.05,P<0.01),肱动脉EDD明显降低[(6.61±0.79)%vs(5.21±0.88)%,P<0.01]。结论波动性高血糖较持续性高血糖对血管内皮功能危害更大,可能与餐后高血糖、胰岛素抵抗和炎性因子增多有关。     

Plasma viscosity in female patients with hypothyroidism: effects of oxidative stress and cholesterol

Hypothyroidism is associated with atherosclerotic events, however, the mechanism is unclear. We investigated the effects of oxidative stress and cholesterol on plasma viscosity in female patients with hypothyroidism (n = 20; mean age: 45.5 +/- 5.5 years) at baseline and after L-thyroxine replacement therapy (average daily dose being 0.1 to 0.15 mg). Two blood samples were taken after 2.3 +/- 1.2 months. In hypothyroid state plasma viscosity and thiobarbituric acid reactive substance (TBARS; marker of oxidative stress were significantly higher (p < 0.001 and p < 0.001), and plasma protein thiol (antioxidants) levels were significantly lower (p < 0.001) than in the healthy state (female; n = 15). After L-thyroxine replacement therapy, patients reached to euthyroid state. In this state, the levels of plasma viscosity and TBARS were decreased (p < 0.001 and p < 0.001), and protein thiol levels were significantly elevated (p < 0.001). There was a significant correlation between plasma cholesterol and viscosity (r = 0.64, p < 0.001), as well as plasma protein thiol (r = -0.59, p < 0.001) in the patients. The correlation between viscosity and TBARS was weak (r = 0.29, p < 0.01). Therefore hypothyroidism may be associated with atherosclerotic process by different mechanisms.     

老年高血压昼夜节律与左心功能及血管内皮功能的关系

目的探讨老年高血压血压昼夜节律与左室肥厚(LVH)、肱动脉扩张性、循环中一氧化氮(NO)、内皮素(ET)的关系。方法选择400例老年高血压患者,最后符合入选本研究的293例。根据动态血压(ABPM)将其分为血压昼夜节律正常组及血压昼夜节律消失组。用高分辨率超声测心脏结构,肱动脉内皮功能。用放射免疫法测定血浆ET,用镀铜镉还原法测定血浆NO,进行统计分析。结果血压昼夜节律消失组室间隔厚度(IVSd)、左室质量指数(LVMI)、相对室壁厚度、ET均增高,而E/A有下降趋势,肱动脉内皮依赖性扩张(FMD)及药物依赖性扩张(GTN-ID)均减弱。NO,NO/ET明显下降,夜间血压下降率与FMD、GTN-ID、NO、NO/ET呈显著正相关,而与ET、IVSd、左室后壁厚度、LVMI呈显著负相关。结论老年EH患者血压昼夜节律消失可促进或加重LVH、削弱血管扩张性及NO和ET合成释放失衡。     

Effects of rosiglitazone on endothelial function, C-reactive protein, and components of the metabolic syndrome in nondiabetic patients with the metabolic syndrome

Fifty nondiabetic patients who met a modified National Cholesterol Education Program definition for the metabolic syndrome were randomized to receive either rosiglitazone (4 mg/day; n = 25) or placebo (n = 25) for 8 weeks. Compared with those receiving placebo, patients in the rosiglitazone group achieved significant reductions in fasting plasma insulin levels (-40%), homeostasis model assessment indexes (-45%), systolic and diastolic blood pressures, and high-sensitivity C-reactive protein levels (-31%). There were no changes in fasting plasma glucose with either treatment. Although rosiglitazone treatment greatly increased plasma levels of low-density lipoprotein cholesterol (18%) and apolipoprotein B (16%), it significantly improved both endothelium-dependent flow-mediated vasodilation (p <0.001) and endothelium-independent nitroglycerin-induced vasodilation (p = 0.01) of the right brachial artery.