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PubMed2003

Oxidative stress in diabetes-induced endothelial dysfunction involvement of nitric oxide and protein kinase C.

Reactive oxygen species (ROS) formation plays a major role in diabetes-induced endothelial dysfunction, though the molecular mechanism(s) involved and the contribution of nitric oxide (NO) are still unclear. This study using bovine retinal endothelial cells was aimed at assessing (i) the role of oxygen-dependent vs. NO-dependent oxidative stress in the endothelial cell permeability alterations induced by the diabetic milieu and (ii) whether protein kinase C (PKC) activation ultimately mediates these changes. Superoxide, lipid peroxide, and PKC activity were higher under high glucose (HG) vs. normal glucose throughout the 30 d period. Nitrite/nitrate and endothelial NO synthase levels increased at 1 d and decreased thereafter. Changes in monolayer permeability to 125I-BSA induced by 1 or 30 d incubation in HG or exposure to advanced glycosylation endproduct were reduced by treatment with antioxidants or PKC inhibitors, whereas NO blockade prevented only the effect of 1 d HG. HG-induced changes were mimicked by a PKC activator, a superoxide generating system, an NO and superoxide donor, or peroxynitrite (attenuated by PKC inhibition), but not a NO donor. The short-term effect of HG depends on a combined oxidative and nitrosative stress with peroxynitrite formation, whereas the long-term effect is related to ROS generation; in both cases, PKC ultimately mediates permeability changes.

Animals↗

PubMed1998

Influence of puberty on endothelial dysfunction and oxidative stress in young patients with type 1 diabetes.

OBJECTIVE: To examine the influence of puberty on endothelial dysfunction and oxidative stress in children and young people with type 1 diabetes. RESEARCH DESIGN AND METHODS: There were 51 young patients with type 1 diabetes, including 12 prepubertal children, 16 adolescents, and 23 young adults who had no clinical diabetic angiopathy, studied; none had microalbuminuria. The three groups were matched for glycemic control, and systolic and diastolic blood pressures and cholesterol levels were not significantly different between the groups. Endothelium-dependent vasodilatation was assessed by laser Doppler flowmetry after iontophoresis of acetylcholine (ACh) to the skin of the dorsum of the right foot. Soluble E-selectin, intercellular cell adhesion molecule-1 (ICAM-1), von Willebrand factor (vWF), plasma thiol (PSH), red cell glutathione (GSH), and red cell superoxide dismutase (SOD) were measured in blood samples obtained in the early morning. RESULTS: Skin vascular responses to ACh were significantly reduced in the young adult group compared with the prepubertal group (P < 0.05, analysis of variance). The levels of soluble ICAM-1 and E-selectin were significantly higher in the adolescent group compared with the young adult group: 338 (267-415) and 89 (64-106) ng/ml (median [interquartile range]), respectively, versus 255 (222-284) and 58 (54-71) ng/ml (P < 0.01 and P < 0.005, Mann-Whitney U test). SOD levels were significantly higher in the prepubertal group at 250 (238-282) micro/ml, when compared with the adolescent, 217 (171-249) micro/ml (P < 0.04), and young adult, 217 (157-244) micro/ml (P < 0.02), groups. GSH tended to be lower in the adolescent group, 1,192 (1,047-1,367) micromol/l, when compared with the young adults, 1,286 (1,145-1,525) pmol/l, and levels of vWF tended to be higher in the adolescent group, but these failed to reach statistical significance (both P = 0.09). PSH was not different between the three groups. CONCLUSIONS: These results suggest that puberty modulates endothelial function and antioxidant mechanisms in childhood diabetes, which may have implications for therapy and intervention.

Acetylcholine↗

PubMedDate not supplied

[Markers of endothelial dysfunction in patients with iodine induced hyperthyroidism].

INTRODUCTION: It has been reported that hyperthyroidism is associated with an altered endothelial function and increased risk of arterial thromboembolism. The aim of our study was to estimate chosen markers of endothelial dysfunction in iodine-induced thyrotoxicosis (IIT). MATERIALS AND METHODS: The groups studied consisted of 41 hyperthyroid subjects, who had been treated with amiodarone (n = 6) or vitamin preparations supplemented with iodine (n = 35) and 40 persons with normal thyroid function. The following parameters were measured: thyroglobulin antibodies (TG Ab), thyroid peroxidase antibodies (TPO Ab), THS receptor antibodies (TR Ab), soluble adhesion molecules: sVCAM-1 and sICAM-1, von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1), C-reactive protein (CRP), fibrinogen and urine iodine concentration. RESULTS: Patients with IIT had significantly higher levels of sVCAM-1 (p < 0.01), IL-6 (p < 0.005), fibrinogen (p < 0.005) and CRP (p < 0.05) in comparison to healthy subjects, whereas sICAM-1, PAI-1 and vWF concentrations did not differ between the groups studied. The highest sVCAM-1 levels were observed in patients with amiodarone induced thyrotoxicosis, and fibrinogen and CRP--in subjects receiving vitamin preparations. There were significant correlations between sVCAM-1 concentration and the levels of sICAM-1 (r = 0.341; p = 0.029) and PAI-1 (r = 0.347; p = 0.026), as well as with urine iodine concentration (r = 0.448; p = 0.004). IL-6 concentration correlated with vWF (r = 0.456; p = 0.003), TPO Ab (r = 0.328; p = 0.036) and PAI-1 level (r = 0.319; p = 0.042). CONCLUSION: Iodine induced thyrotoxicosis is associated with an increase of sVCAM-1 and IL-6 levels, possibly reflecting inflammatory and destructive processes in the thyroid gland. However, increased procoagulant activity was not found in patients with IIT.

Adult↗

PubMed2001

Vitamin C and quinapril abrogate LVH and endothelial dysfunction in aortic-banded guinea pigs.

Left ventricular hypertrophy (LVH) is a cardiovascular risk factor. A possible role for endothelial dysfunction in this condition was investigated in a Dunkin-Hartley guinea pig aortic-banded pressure overload-induced model of LVH. Aortic banding produced significant elevation of fore- and hindlimb blood pressure (BP), heart-to-body weight ratios, plasma angiotensin II (ANG II), endothelin-1 (ET-1), tumor necrosis factor-alpha (TNF-alpha) levels, and coronary microvascular endothelial cell (CMEC) NAD(P)H-dependent superoxide (O) production, and a significant decrease in basal and stimulated CMEC cGMP levels. Treatment of aortic-banded animals with the angiotensin-converting enzyme inhibitor quinapril and the antioxidant vitamin C, either alone or in combination, did not affect BP but caused a significant inhibition of the increases in the heart-to-body weight ratio, ANG II, ET-1, and TNF-alpha levels, and O production and restored cGMP responses to levels comparable with sham-operated animals. These data suggest that quinapril and vitamin C are capable of inhibiting LVH development due to pressure overload via mechanisms that involve the inhibition of oxidative stress, an improvement in coronary endothelial function, and increased nitric oxide bioavailability.

Animals↗

PubMed2004

Endothelial dysfunction and inflammation after percutaneous coronary intervention.

We studied 30 consecutive patients who underwent coronary stenting with respect to postprocedure endothelial dysfunction and levels of pre- and postprocedure cytokines. Patients with severe impairment of flow-mediated dependent dilation, but not flow- mediated independent dilation, had higher concentrations of C-reactive protein before percutaneous coronary intervention (12.9 +/- 20.2 vs 5.6 +/- 13.0 microg/ml, p = 0.04) and 24 hours after stenting (18.8 +/- 20.8 vs 11.8 +/- 20.0 microg/ml, p = 0.05) than patients without severe abnormities of systemic endothelial function. Thus, endothelium-dependent dilation abnormalities were related to the systemic inflammatory state, whereas endothelium-independent dilation abnormalities were not related to the inflammatory status of the patient.

Aged↗

PubMed1997

beta-Amyloid-induced cerebrovascular endothelial dysfunction.

Cerebrovascular effects of beta-amyloid were investigated using bovine mid-cerebral arteries. beta-amyloid-induced endothelial damage was evidenced by increased vasoconstriction, diminished vasodilation and was evident on electron microscopy. The endothelial dysfunction was mediated by reactive oxygen radicals. Vascular damage by beta-amyloid may be an early event in the development of the pathology of Alzheimer's disease.

Amyloid beta-Peptides↗

PubMed2004

[Angiotensin-converting enzyme gene and the brachial artery endothelial dysfunction in type 2 diabetes without angiopathy].

OBJECTIVE: To investigate the relationship between angiotensin converting enzyme (ACE) gene and endothelial dysfunction. METHODS: One hundred and ten type 2 diabetic patients without angiopathy were selected randomly, and PCR technique was used to determine their ACE genotypes. High resolution ultrasonography was performed to measure the changes in brachial artery diameter at rest, after reactive hyperemia (with increased flow producing an endothelium-dependent dilation) and after sublingual glyceryltrinitrate (GNT, an endothelium-independent dilator). Meanwhile, 50 healthy individuals were selected randomly as controls. RESULTS: In type 2 diabetes mellitus and control groups, the percentages for flow-mediated arterial dilation in patients with DD genotypes were 3.38% and 3.67% respectively, which were significantly lower than those in patients with II genotypes (4.12% and 4.68% respectively, P<0.05). The baseline blood vessel size, baseline blood flow and GNT induced dilation in both groups showed no significant differences among ACE genotypes (P>0.05). By multiple stepwise regression analysis, reduced flow-mediated arterial dilation was associated with age, baseline vessel size, low density lipoprotein cholesterol(LDL-C), Lp(a), D allele, fasting blood glucose (FBG), postparandial blood glucose (PPBG), HbA1c, duration of diabetes in type 2 diabetic patients (P<0.0005). CONCLUSION: ACE DD genotype is related to endothelium-dependent arterial dilation in the early stage of type 2 diabetes mellitus and in healthy individuals.

Adult↗

PubMed2006

Endothelial dysfunction predictor of structural changes of arterial wall in type I diabetes.

AIM: We examined whether alteration in vascular endothelial function exists in non-insulin dependent diabetes mellitus (NIDDM) and whether impaired endothelium-dependent responses in those patients are associated with increased intima-media thickness (IMT), the time sequence of their appearance and the role of individual risk factors in development of structural deterioration of arterial wall. METHODS: Ultrasound technique was used to measure brachial artery flow mediated dilation (FMD) response and carotid IMT in 38 young adults with type I diabetes aged 22-34 years and 35 healthy controls aged 22-36 years. RESULTS: Patients had significantly lower FMD than controls (4.15/2.8/ vs 11.3/3.6/, P<0.0001) and was in all diabetic patients below the mean value of controls. Further, carotid intima-media was in insulin dependent diabetes mellitus (IDDM) patients significantly thicker than in healthy subjects (0.65/0.04 vs 0.56/0.04, P=0.0001) and was related to body mass and body mass index, to the age of patients, the duration of diabetes and several risk variables. In a multivariate model FMD was most significantly and independently associated to IMT. However, significant thickening of intima-media was observed only in patients with progressed deterioration of FMD and it appeared in those subjects with long-lasting disease. IMT was also influenced by urinary albumin excretion and low-density lipoprotein (LDL) cholesterol concentration. CONCLUSIONS: Endothelium dependent FMD response is impaired in IDDM and is associated with increased carotid artery IMT. Significant thickening of intima-media appears in patients with advanced deterioration of FMD that is related to the duration of the disease. These data suggest that advanced endothelial dysfunction in IDDM may predispose to development of morphologic atherosclerotic lesions of arterial wall.

Adult↗

PubMed2003

Postprandial hypertriglyceridemia-induced endothelial dysfunction in healthy subjects is independent of lipid oxidation.

BACKGROUND: To analyze the effects of postprandial hypertriglyceridemia with or without antioxidant supplementation-on endothelial function as related to lipid oxidation in healthy young subjects. METHODS AND RESULTS: Ten healthy male subjects (mean age: 26 years) were examined three times in fasting state (10 hours) following a high-fat meal, a low-fat meal, or a high-fat meal with additional antioxidant vitamin E (800 IU), respectively. Serum triglycerides significantly increased 2 and 4 hours after eating the high-fat meal with or without additional vitamin E. Endothelium-dependent, flow-mediated brachial artery vasodilations (FMD; percentage change in diameter) changed from 13.3+/-1.1% to 6.6+/-1.1% (p<0.05), 7.1+/-0.6% (p<0.05), or 13.2+/-0.8% at 2, 4, or 6 hours after eating a high-fat meal. However, there were no changes of FMD observed following either a low-fat meal or a high-fat meal with additional vitamin E. The flow-dependent vasodilation inversely correlated to postprandial hypertriglyceridemia (r=-0.54, p<0.05). Serum malondialdehydes (MDA; lipid oxidation products) did not significantly change following ingestion of any of the 3 types of meal. CONCLUSIONS: This study suggests that postprandial hypertriglyceridemia-induced endothelial dysfunction is not associated with lipid oxidation and that the protective effects of vitamin E on endothelial function may be due to some alternative, as of yet unknown, mechanism.

Adult↗

PubMed2002

Endothelial dysfunction, angiotensin-converting enzyme inhibitors and calcium antagonists.

The endothelium plays a crucial role in the pathogenesis of cardiovascular disease. Endothelial function is attenuated by the presence of different well known cardiovascular risk factors. Evaluation of endothelial vasodilator function serve as an index integrating the overall stress imposed by cardiovascular risk factors and reinforce the suggestion that endothelial dysfunction is an early marker of cardiovascular disease that precedes clinical manifestations. Angiotensin-converting enzyme inhibitors have been shown to reduce the cardiovascular mortality, an effect that could be the consequence of an improvement in the endothelial function. Recent studies have shown that a calcium antagonist might improve the endothelial function, however, there is controversy about this action and also about the potential mechanisms for the effect of a calcium antagonist in the regulation of endothelial function.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2006

Post-prandial endothelial dysfunction in hypertriglyceridemic subjects: molecular mechanisms and gene expression studies.

OBJECTIVE: Triglyceride-rich lipoproteins (TGRLs) are a cardiovascular risk factor and induce endothelial dysfunction. In the present study, we investigated the effects of post-prandial TGRLs from type IV hyperlipidemic subjects on endothelial activation addressing the effects of the lipoproteins on intracellular pathways and gene expression. METHODS: Thirty fasted hypertriglyceridemic patients were given an oral fat load (OFL) and blood samples were collected before the OFL (T0) and 2, 4, 6 and 8h thereafter. Endothelial function, determined as flow-mediated dilatation of the brachial artery, was assessed at the same time points. TGRLs were isolated at T0 and T4 (PP-TGRL) for in vitro studies. RESULTS: Compared with TGRLs, PP-TGRLs induced to a larger extent phosphorylation of p38 MAPK, CREB and IKB-alpha in human endothelial cells and increased the DNA binding activity of CREB, NFAT and NF-kappaB. Furthermore, PP-TRGLs upregulated the expression of several pro-inflammatory genes including vascular cell adhesion molecule-1 (VCAM-1), PECAM-1, ELAM-1, intercellular adhesion molecule-1 (ICAM-1), P-selectin, MCP-1, interleukin-6 (IL-6), TLR-4, CD40, ADAMTS1 and PAI-1. CONCLUSION: These effects may relate to the severe impairment of endothelial function seen during the post-prandial phase in hypertriglyceridemic patients.

Adult↗

PubMed1998

Endothelial dysfunction and decreased production of nitric oxide in the intrahepatic microcirculation of cirrhotic rats.

Increased intrahepatic resistance in cirrhotic livers is in part caused by increased vascular tone. Several morphological abnormalities have been described in the sinusoidal endothelial cells of cirrhotic livers, but the functional impact of these abnormalities on the intrahepatic vascular tone has not been studied. The aim of this study was to investigate the intrahepatic endothelial function and the role of nitric oxide (NO) with regard to vascular tone in cirrhotic livers. Isolated rat liver perfusions were performed in cirrhotic rats (induced by chronic carbon tetrachloride inhalation) and weight-matched normal controls. After preconstricting the intrahepatic microcirculation with methoxamine (10(-4) mol/L), response to cumulative doses of receptor-mediated endothelial agonist, acetylcholine (10(-7) mol/L-10(-5) mol/L), was obtained. In another series, response to the receptor-independent endothelial agonist, calcium ionophore A23187 (10(-7) mol/L and 3 x 10(-7) mol/L), was obtained in the absence and presence of Nomega-nitro-L-arginine (NNA) and indomethacin. In a third series of rats, nitrate and nitrite production was measured in the perfusate of perfused normal and cirrhotic livers. There was significantly less vasorelaxation in cirrhotic livers as compared with normal livers in response to acetylcholine and calcium ionophore A23187 (P < .0001). The impaired vasorelaxation was a result of a decrease in both NO-mediated and non-NO-mediated components of vasorelaxation. Cirrhotic livers from ascitic rats had significantly less vasorelaxation as compared with livers from nonascitic rats (P < .005). There was significantly less production of nitrates and nitrites in cirrhotic livers (P < .05). The liver microcirculation of cirrhotic livers is characterized by endothelial dysfunction that results in impaired release of endothelial relaxing factors including NO.

Acetylcholine↗

PubMed2001

Endothelial dysfunction induced by oxidized low-density lipoproteins in isolated mouse aorta: a comparison with apolipoprotein-E deficient mice.

We characterized the acute effects of oxidized low-density lipoproteins (oxidized-LDL) on vascular reactivity in isolated aorta from wild-type C57BL/6J mice, and compared these with the chronic alterations in vascular function observed in apolipoprotein-E gene knockout [ApoE(-/-)] mice fed a high-fat diet, which results in hyperlipidemia and atherosclerosis. In the abdominal (but not thoracic) aorta, oxidized-LDL (100 microg/ml) reduced relaxations induced by acetylcholine (10(-9) M-10(-5) M), which are mediated entirely by nitric oxide (NO). The relaxations induced by the NO donor S-nitroso-N-acetylpenicillamine (SNAP, 10(-8) M-10(-4) M), the cyclic GMP analogue 8-bromo cyclic GMP (100 microM) and the nonspecific vasodilator papaverine (100 microM) were not changed by oxidized-LDL. Native LDL had no effect on vasorelaxations. The attenuation of endothelium-dependent relaxations caused by oxidized-LDL mimicked the endothelial dysfunction found in ApoE(-/-) mice. These results are consistent with the suggestion that oxidized-LDL has an important role in the pathogenesis of endothelial NO dysfunction associated with hyperlipidemia and atherosclerosis in these mice.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2004

Endothelial dysfunction in young patients with rheumatoid arthritis and low disease activity.

BACKGROUND: Rheumatoid arthritis (RA) is associated with an increased risk of cardiovascular disease. Endothelial dysfunction represents the earliest stage of atherosclerosis. OBJECTIVE: To evaluate the influence of chronic inflammatory state on endothelial function in patients with RA by measuring endothelial reactivity in young patients with RA with low disease activity and without traditional cardiovascular risk factors. METHODS: Brachial flow mediated vasodilatation (FMV), assessed by non-invasive ultrasound, was evaluated in 32 young to middle aged patients with RA (age </=59 years), with DAS28 </=3.2 and without overt cardiovascular disease, and in 28 age and sex matched controls. RESULTS: Mean (SD) FMV was significantly lower in patients than in controls (3.2 (1.3)% v 5.7 (2.0)%; p<0.001), inversely related to low density lipoprotein cholesterol (r = -0.45, p<0.05) and C reactive protein (CRP), expressed as the value at the moment of ultrasound evaluation (r = -0.44, p<0.05), as the average of CRP levels evaluated at different times during the disease (r = -0.47, p<0.05), or as the average of >/=4 determinations multiplied by the disease duration (r = -0.40, p<0.05). In a multivariate regression model, a lower brachial flow mediated vasodilatation was independently predicted by low density lipoprotein cholesterol (beta = -0.40, p<0.05), average CRP levels multiplied by the disease duration (beta = -0.44, p<0.05), and brachial artery diameter (beta = -0.28, p<0.05). CONCLUSIONS: Young to middle aged patients with RA with low disease activity, free from cardiovascular risk factors and overt cardiovascular disease, have an altered endothelial reactivity that seems to be primarily related to the disease associated chronic inflammatory condition.

Adult↗

PubMed2001

Obesity is independently associated with coronary endothelial dysfunction in patients with normal or mildly diseased coronary arteries.

OBJECTIVES: This study evaluates the impact of obesity on coronary endothelial function in patients with normal or mild coronary artery disease. BACKGROUND: The American Heart Association (AHA) has recently classified obesity as a modifiable risk factor for coronary heart disease. METHODS: A total of 397 consecutive patients with normal or mildly diseased coronary arteries at angiography underwent coronary vascular reactivity evaluation using intracoronary adenosine, acetylcholine and nitroglycerin. Patients were divided into three groups based on the body mass index (BMI): Group 1, patients with a BMI <25 (n = 117, normal weight); Group 2, patients with a BMI 25-30 (n = 149, overweight) and Group 3, patients with a BMI >30 (n = 131, obese). RESULTS: There were no significant differences among the groups in regard to other cardiovascular risk factors, except that overweight but not obese patients were significantly older than normal-weight patients (47 +/- 1 years in Group 1, 53 +/- 1 years in Group 2 and 50 +/- 1 years in Group 3, p < 0.001). The percent change of coronary blood flow to acetylcholine (%delta CBF Ach) was significantly lower in the obese patients than in the normal-weight group (85.2 +/- 12.0% in Group 1, 63.7 +/- 10.0% in Group 2 and 38.1 +/- 9.6% in Group 3, p = 0.009). By multivariate analysis, overweight (odds ratio, 1.55; 95% confidence interval, 1.2-2.0) and obesity (odds ratio, 2.41; 95% confidence interval, 1.5-4.0) status were independently associated with impaired coronary endothelial function. CONCLUSIONS: The study demonstrates that obesity is independently associated with coronary endothelial dysfunction in patients with normal or mildly diseased coronary arteries.

Acetylcholine↗

PubMed1998

Asymmetric dimethylarginine (ADMA): a novel risk factor for endothelial dysfunction: its role in hypercholesterolemia.

BACKGROUND: Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of nitric oxide (NO) synthase. Because endothelial NO elaboration is impaired in hypercholesterolemia, we investigated whether plasma concentrations of ADMA are elevated in young, clinically asymptomatic hypercholesterolemic adults. We further studied whether such elevation of ADMA levels was correlated with impaired endothelium-dependent, NO-mediated vasodilation and urinary nitrate excretion. In a randomized, double-blind, placebo-controlled study, we investigated whether these changes could be reversed with exogenous L-arginine. METHODS AND RESULTS: We measured plasma levels of L-arginine, ADMA, and symmetrical dimethylarginine (SDMA) by high-performance liquid chromatography in 49 hypercholesterolemic (HC) and 31 normocholesterolemic (NC) humans. In 8 HC subjects, endothelium-dependent forearm vasodilation was assessed before and after an intravenous infusion of L-arginine or placebo and compared with 8 NC control subjects. ADMA levels were significantly elevated by >100% (2.17+/-0.15 versus 1.03+/-0.09 micromol/L; P<0.05) in HC subjects compared with NC adults. L-Arginine levels were similar, resulting in a significantly decreased L-arginine/ADMA ratio in HC subjects (27.7+/-2.4 versus 55. 7+/-5.4; P<0.05). In 8 HC subjects, intravenous infusion of L-arginine significantly increased the L-arginine/ADMA ratio and normalized endothelium-dependent vasodilation and urinary nitrate excretion. ADMA levels were inversely correlated with endothelium-mediated vasodilation (R=0.762, P<0.01) and urinary nitrate excretion rates (R=0.534, P<0.01). CONCLUSIONS: We find that ADMA is elevated in young HC individuals. Elevation of ADMA is associated with impaired endothelium-dependent vasodilation and reduced urinary nitrate excretion. This abnormality is reversed by administration of L-arginine. ADMA may be a novel risk factor for endothelial dysfunction in humans.

Arginine↗

PubMed2005

Relationship between endothelial dysfunction, intima media thickness and cardiovascular risk factors in asymptomatic subjects.

AIM: The aim of the study was to evaluate endothelial function and intima media thickness (IMT) in relation to cardiovascular risk factors (RF). METHODS: We enrolled 113 patients, mean age 62 +/- 12 years; patients underwent: anamnesis, physical examination, measurement of body weight and height and blood pressure. Biochemistry variables were also measured: total cholesterol, high- and low-density lipoprotein cholesterol (HDL-C and LDL-C), triglycerides and glycemia. Vascular echography was performed to analyze flow mediated vasodilatation (FMD) at the brachial artery and IMT of the carotid and femoral arteries. RESULTS: Compared with patients without RF, patients with cardiovascular RF showed an impaired FMD (p < 0.05) and higher values of mean carotid IMT (p = 0.03). Age (p < 0.005) and diabetes (p < 0.05) were directly correlated with carotid IMT, while femoral IMT is correlated with age (p < 0.005) and male gender (p < 0.02). Regarding the relationship between endothelial function cardiovascular RF, we showed an inverse linear correlation between systolic blood pressure (p < 0.005), smoking (p < 0.05) and FMD, and concerning biochemical parameters, we founded that total cholesterol (p < 0.05) and LDL-C plasma levels (p < 0.005) were inversely correlated with FMD. Finally, we showed a lower FMD in patients with carotid and femoral IMT in comparison with patients without peripheral atherosclerosis (p = 0.01). CONCLUSIONS: The present data indicate that cardiovascular RF are associated with impaired endothelial function and increased IMT, and that the presence of carotid and femoral IMT is significantly correlated with endothelial dysfunction.

Aged↗

PubMed2003

Predictive value of noninvasively determined endothelial dysfunction for long-term cardiovascular events in patients with peripheral vascular disease.

OBJECTIVES: The goal of this study was to prospectively examine the long-term predictive value of brachial-artery endothelial dysfunction for future cardiovascular events. BACKGROUND: Brachial-artery endothelial function is impaired in individuals with atherosclerosis and coronary risk factors. The prospective relation between endothelial function determined by brachial-artery ultrasound and long-term cardiovascular risk is unknown. METHODS: We examined brachial-artery endothelial function using ultrasound in 199 patients with peripheral arterial disease before elective vascular surgery. Patients were prospectively followed with an average follow-up of 1.2 years after surgery. RESULTS: Thirty-five patients had an event during follow-up, including cardiac death (5 patients), myocardial infarction (17 patients), unstable angina (10 patients), or stroke (3 patients). Preoperative endothelium-dependent flow-mediated dilation (FMD) was significantly lower in patients with an event (4.4 +/- 2.8%) compared with those without an event (7.0 +/- 4.9%, p < 0.001), whereas endothelium-independent vasodilation to nitroglycerin was similar in both groups. In a Cox proportional-hazards model, independent predictors of events included age (p = 0.003), more invasive surgery (surgery other than carotid endarterectomy, p = 0.02), and impaired brachial-artery endothelial function (p = 0.002). Risk was approximately nine-fold higher in patients with FMD <8.1% (lower two tertiles) compared with those in the upper tertile (odds ratio 9.5; 95% confidence interval 2.3 to 40). CONCLUSIONS: Impaired brachial-artery endothelial function independently predicts long-term cardiovascular events in patients with peripheral arterial disease. The findings suggest that noninvasive assessment of endothelial function using brachial-artery FMD may serve as a surrogate end point for cardiovascular risk.

Aged↗