SEARCH · PubMed Health

Results for “Endothelial function”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources

PubMed2005

A review of methods currently used for assessment of in vivo endothelial function.

An intact vascular endothelium is critical to the maintenance of normal arterial tone and coagulation status. Endothelial injury leading to dysfunction is thought to be a precursor to most if not all vascular disease, and has been implicated as a critical event in atherosclerosis. At present there are several methods available for detection of in vivo endothelial function, and the aim of this study was to critically review these methods. Five distinct methods were identified and studied in detail. These methods are diverse and each assesses a different vascular bed. Importantly there is no uniformity among investigators over choice of method and protocol, making it difficult to compare in vivo enothelial dysfunction between groups. These issues need to be addressed in large scale comparative analyses so that investigators can agree a common approach to endothelial function assessment.

Brachial Artery↗

PubMed2004

Relation between C reactive protein concentrations and coronary microvascular endothelial function.

OBJECTIVE: To determine how C reactive protein (CRP), a sensitive marker of inflammation, is related to coronary endothelial function. DESIGN: Changes in quantitative coronary angiographic findings and Doppler flow velocity measurements in response to locally infused acetylcholine were assessed. SETTING: Tertiary cardiology centre. PATIENTS: 46 patients with angiographically normal coronary arteries were divided into groups with normal (< or = 3 mg/l) or increased (> 3 mg/l) CRP concentrations. INTERVENTIONS: Acetylcholine (3 and 30 microg/min) was infused into the left coronary ostium for two minutes. MAIN OUTCOME MEASURES: Percentage change in diameter of epicardial coronary arteries and coronary blood flow (CBF) in response to acetylcholine; and correlations between these parameters and serum CRP concentrations. RESULTS: 15 patients had increased CRP concentrations. The change in coronary artery diameter induced by acetylcholine infusion was similar between the groups but the increase in CBF induced by acetylcholine was smaller in patients with increased CRP concentrations (54.9% v 139.4% with acetylcholine 30 microg/min, p = 0.0030). Multivariate analysis identified increased CRP concentration as independently associated with attenuated CBF response to acetylcholine at 30 microg/min (p = 0.0078, R2 = 0.434). CONCLUSIONS: These findings suggest that inflammation appears to be associated with impaired coronary endothelial function in resistance but not conduit vessels. The data suggest a close relation between chronic vascular inflammation and endothelial dysfunction in atherosclerosis.

Acetylcholine↗

PubMed2006

Adiponectin is associated with improvement of endothelial function after rosiglitazone treatment in non-diabetic individuals with metabolic syndrome.

OBJECTIVE: The risks of metabolic syndrome (MetSyn) rely on the interaction between insulin resistance, metabolic abnormalities, inflammation and vascular dysfunction. Insulin sensitizers counteract some of these abnormalities. The objective of this study was to evaluate the effects of rosiglitazone (ROSI) on vascular reactivity, adipokines and inflammatory markers in a group of non-diabetic subjects with MetSyn. METHODS AND RESULTS: Thirty subjects with NCEP-ATPIII criteria for MetSyn and eight healthy subjects were studied at baseline and 18 subjects with MetSyn were treated with ROSI 8 mg/day for 24 weeks. Venous occlusion plethysmography exams before and during intra-arterial infusions of acetylcholine and sodium nitroprusside were performed to assess endothelial-dependent and independent vasodilation. Forearm blood flow (FBF) and vascular resistance (VR) responses were analyzed. Treatment with ROSI improved endothelial function (235% increment in FBF; p<0.01 and 56% decrement in VR; p=0.01), adiponectin (7.3[3.6-17.9] versus 37.9[19.3-42.4]; p<0.01), HOMA-IR (3.5+/-1.2 versus 2.7+/-1.6; p<0.05), C-reactive protein (CRP) (1.05[0.57-2.07] versus 0.3[0.2-0.8]; p<0.01) and fibrinogen (3.1+/-0.73 versus 2.62+/-0.64; p<0.05) levels. The difference between groups on endothelial-dependent vasodilation, adiponectin and CRP levels disappeared after treatment and the improvement of endothelial function was associated with the increment of adiponectin levels. CONCLUSION: ROSI treatment restored endothelial function in MetSyn subjects, probably through an adiponectin-mediated process.

Acetylcholine↗

PubMed2004

Fluvastatin reduces oxidative stress, decreases serum monocyte chemotactic protein-1 level and improves endothelial function in patients with hypercholesterolemia.

BACKGROUND AND PURPOSE: Statins may have anti-inflammatory properties and exert endothelial protection independently of their lipid-lowering effect. However, data are scarce concerning the co-existence of these lipid-lowering-independent effects in humans. METHODS: Forty three patients with hypercholesterolemia were randomly assigned in a 2:1 ratio to receive either fluvastatin 80 mg/day (n = 30) or placebo (n = 13) for 12 weeks. Plasma levels of monocyte chemotactic protein-1 (MCP-1), thiobarbituric acid reactive substances (TBARS)--an index of oxidative stress, and flow-mediated vasodilatation (FMD)--an index of endothelial function, were measured before and after statin therapy. RESULTS: Fluvastatin significantly reduced the serum level of total cholesterol (201.8 +/- 25.2 vs 271.6 +/- 24.7 mg/dL; p < 0.001), low-density lipoprotein cholesterol (129.4 +/- 5.1 vs 190.2 +/- 19 mg/dL; p < 0.001), MCP-1 (190.3 +/- 40 vs 217.6 +/- 61 pg/mL; p = 0.001), and TBARS (3.7 +/- 1.3 vs 5.2 +/- 1.4 nmol/mL; p < 0.001). FMD was significantly increased, from 3.7 +/- 2.5% to 5.9 +/- 2.9% (p < 0.001) in the fluvastatin group. The reduction of serum MCP-1 or TBARS level was not correlated with the improvement of either plasma cholesterol level or FMD. No significant changes of these markers were observed in the placebo group. CONCLUSIONS: Fluvastatin reduced oxidative stress and inflammatory marker levels, and improved endothelial function, in addition to its lipid-lowering effect. These observations provide a clinical rationale for the co-existence of complex and multiple vascular protective mechanisms of statins.

Aged↗

PubMed2005

The long-term effects of tibolone on aortic stiffness and endothelial function.

OBJECTIVE: To investigate the effect of 10 years of treatment with tibolone on aortic stiffness and endothelial function. DESIGN: Cross-sectional study of women currently participating in an open-label, non-randomized study of the long-term efficacy of tibolone. A total of 113 recently postmenopausal women were recruited in 1988. Fifty-eight agreed to take tibolone 2.5 mg daily and 55 were followed during the study as matched controls (who chose not to take any form of hormone replacement therapy (HRT) for the duration of the study). The groups were matched for age, weight and time since last menstrual period. SETTING: A Central London Teaching Hospital. SUBJECTS: After 10 years, 60 women remained in the study, 32 in the tibolone group and 28 in the control group. All of these women were invited to participate in this pilot study and attend the Menopause Research Unit. Fourteen women from each group agreed to attend. The main outcome measures were aortic stiffness, measured by pulse wave velocity, and endothelial function, as assessed by flow-mediated dilatation of the brachial artery. RESULTS: Pulse wave velocity was significantly lower in the tibolone group (10.4 +/- 1.2) than in the control group (11.6 +/- 1.2), p = 0.042. The flow-mediated dilatations were similar in both groups. CONCLUSION: In this study, long-term use of tibolone over 10 years has a beneficial effect on aortic stiffness. The differences seen in brachial artery vasoreactivity failed to reach statistical significance. Whether this is a true indication of the effects of long-term tibolone on brachial artery vasoreactivity will only be determined by performing a larger, placebo-controlled, randomized study.

Aorta↗

PubMed2002

In vivo early and mid-term flow-mediated endothelial function of the radial artery used as a coronary bypass graft.

OBJECTIVES: We sought to evaluate the in vivo endothelial function of the radial artery (RA) used as a coronary graft. BACKGROUND: The RA is becoming a recognized alternative coronary bypass conduit. In vivo endothelial function is a possible predictor of long-term performance. METHODS: Sixty consecutive patients underwent coronary artery bypass graft surgery (CABG); all received RA and left internal mammary artery (LIMA) grafts. Three weeks after CABG, 36 patients underwent angiography under basal conditions, during pacing and after intragraft injection of glyceryl trinitrate (GTN). Angiography was repeated at six months in 20 patients. RESULTS: The estimated mean difference of 66 segments of the radial graft on the first QCA study was 0.170 mm (95% confidence interval [CI] 0.101 to 0.258, p < 0.001) between baseline and pacing, and 0.310 mm (CI 0.225 to 0.401, p < 0.001) between baseline and GTN. At six months, the differences between baseline and pacing and baseline and GTN were 0.112 mm (CI 0.062 to 0.162, p < 0.001) and 0.274 (CI 0.192 to 0.353, p < 0.001), respectively. The difference between baseline values at three weeks and six months was 0.416 mm (CI 0.236 to 0.603, p < 0.001). In the LIMA segments, the difference between baseline and pacing and baseline and GTN were 0.206 mm (CI 0.136 to 0.278, p < 0.001) and 0.304 mm (CI 0.213 to 0.396, p < 0.001), respectively. At six months, the differences between baseline and pacing and baseline and GTN were 0.098 mm (CI 0.014 to 0.173, p < 0.001) and 0.218 mm (CI 0.130 to 0.298, p < 0.001). The difference between baseline values at three weeks and six months was 0.061 mm (CI 0.064 to 0.176, p > 0.05). CONCLUSIONS: In vivo flow-mediated dilation of the RA is comparable to that of pedicled LIMA. The increased dilation both at baseline and after pacing at six months represents a time-related improvement in the vasomotor function of the RA, which could have implications for its performance as a coronary conduit.

Aged↗

PubMed2000

Estriol (E3) replacement improves endothelial function and bone mineral density in very elderly women.

We investigated the effects of estriol (E3) on endothelial function and bone mineral density (BMD) in very elderly women. Twenty-four very elderly women (80 +/- 3.5 years old) were administered CaCl2 with or without estriol treatment (2 mg/day) for 30 weeks (hormone replacement treatment [HRT] group vs control group). Endothelium-dependent flow-mediated dilatation (FMD), endothelium-independent dilatation by nitroglycerin of the brachial artery, and BMD were assessed. Levels of plasma lipids and apoproteins were not changed; however, both plasma E3 and E2 were substantially increased (E2, 4.6 to 31.3 +/- 8.1; E3, <5 to 45.3 +/- 7.9 pg/mL) by HRT. The FMD value was also increased by HRT, as were the plasma nitrite/nitrate and cGMP values. The response to nitroglycerin was not changed. The BMD was increased by HRT, but decreased in the control group. There were significant differences between the HRT group and control group after 30 weeks' treatment in the levels of osteocalcin, P1CP, and urinary deoxypiridinoridine. E3 significantly improved BMD by inhibiting bone resorption. Endothelial function was improved in line with the antiatherosclerotic effects. E3 might be effective for use in HRT in elderly patients.

Aged↗

PubMed2003

Raloxifene and endothelial function in healthy postmenopausal women.

OBJECTIVE: The purpose of this study was to determine the effects of raloxifene on endothelial function in healthy, postmenopausal women. STUDY DESIGN: This was a randomized, double-blind, placebo-controlled crossover trial. Subjects (n = 19; mean age, 61 years) underwent endothelial function testing at baseline and after treatment with placebo or raloxifene (60 mg per day for 6 weeks). RESULTS: Brachial artery diameter change (flow-mediated dilation) increased 5.0% with placebo and 8.56% with raloxifene (SE = 1.83, P =.03) in response to a hyperemic stimulus; an adjustment of this response for a variation in stimulus intensity resulted in greater discrimination (P =.009). The ratio of area under the curve response to area under the curve reference with the use of laser Doppler measures was 1.18 for placebo and 1.28 for raloxifene (P =.05). Flow-mediated dilation and area under the curve ratio correlated significantly (r = 0.33, P =.04). CONCLUSION: Treatment with raloxifene enhanced endothelial-mediated dilation in brachial arteries and digital vessels in healthy, postmenopausal women. A potential mechanism for a cardioprotective effect of raloxifene is suggested and warrants further study.

Brachial Artery↗

PubMed2003

A comparison of low-dose and standard-dose oral estrogen on forearm endothelial function in early postmenopausal women.

We investigated the effects of low-dose estrogen plus progestin on endothelial function. Postmenopausal women received daily doses of conjugated equine estrogen (CEE, 0.625 mg) plus medroxyprogesterone acetate (MPA, 2.5 mg) (standard-dose group, n = 18), CEE (0.3 mg) plus MPA (2.5 mg) (low-dose group, n = 18), or no treatment (control group, n = 15) for 3 months. Serum concentrations of lipids and malondialdehyde (MDA)-modified low-density lipoprotein (LDL) were measured. Forearm blood flow (FBF) during reactive hyperemia and after sublingual nitroglycerin administration was measured by strain-gauge plethysmography. Decreases in serum concentrations of LDL cholesterol and MDA-modified LDL and increases in high-density lipoprotein cholesterol and nitrite/nitrate were observed in both treatment groups. After 3 months of treatment, similar increases in the maximal FBF response during reactive hyperemia were observed in both treatment groups (standard-dose group, from 35.8 +/- 3.0 to 47.5 +/- 2.8 ml/min per 100 ml tissue; and low-dose group, from 35.2 +/- 2.2 to 46.8 +/- 3.4 ml/min per 100 ml tissue, P < 0.01). FBF levels in the control group were unchanged. Treatment did not affect nitroglycerin-induced dilation. The incidences of vaginal bleeding and breast tenderness were lower with the low-dose group than with the standard-dose group. Low-dose CEE plus MPA augments endothelial function in forearm resistance arteries and decreased MDA-modified LDL levels similarly to standard doses of CEE plus MPA, with fewer side effects.

Administration, Oral↗

PubMed2004

Non-invasive assessment of endothelial function by brachial artery flow mediated vasodilatation and its association with coronary artery disease: an Indian perspective.

Endothelial dysfunction is the final common pathway through which various coronary risk factors culminate into atherosclerosis and subsequent coronary artery disease (CAD). Endothelial function can be reliably assessed by flow mediated vasodilatation (FMD) in the brachial artery using high-resolution ultrasonography and has been shown to be an excellent surrogate marker for the presence of CAD. Two hundred and forty-one individuals comprising of 101 patients with CAD (angiographically proven, or with history of documented myocardial infarction) and 140 individuals without CAD were included in the study. All subjects underwent clinical evaluation, fasting lipid profile, treadmill test and FMD assessment. Selected individuals underwent coronary angiography too. Brachial artery diameter and Doppler indices (systolic and diastolic velocity time integrals) were recorded using high resolution ultrasonography at baseline, immediately after and at one minute after release of cuff (occlusion time 5 minutes). FMD was calculated as percentage increase in brachial artery diameter at one minute. FMD index was calculated as the ratio of FMD and percentage increase in flow during reactive hyperaemia. Mean FMD was significantly higher in non-CAD group (8.71+/-4.77%) than in CAD group (3.77+/-2.03%; p < 0.0001). The FMD index was also significantly higher in the non-CAD group (0.031 ) than in CAD group (0.021; p=0.0117). On multiple regression analysis, FMD index was found to be significantly associated with presence of CAD (p=0.0015), independent of conventional cardiovascular risk factors. Endothelial function as assessed by FMD is significantly depressed in patients with established CAD and this association is independent of presence of conventional cardiovascular risk factors.

Blood Flow Velocity↗

PubMed2004

The effects of atorvastatin on endothelial function in diabetic patients and subjects at risk for type 2 diabetes.

We have investigated the effect of atorvastatin on the endothelial function of patients with diabetes and subjects at risk for type 2 diabetes in a 12-wk, prospective, randomized, placebo-controlled, double-blind clinical trial. The flow- mediated dilation (FMD; endothelium dependent) and nitroglycerin-induced dilation (endothelium independent) in the brachial artery and the vascular reactivity at the forearm skin were measured. FMD improved in the atorvastatin-treated, at-risk subjects [median (25-75 percentile), 7.2% (2.9-9.6%) at exit visit vs. 6.6% (2.9-9.5%) at baseline; P < 0.05]. A similar improvement of FMD was found in atorvastatin-treated diabetic patients [median (25-75 percentile), 5.6 (3.9-7.9) at exit visit vs. 4.2 (3.2-7.2) at baseline; P = 0.07]. No changes were observed in nitroglycerin-induced dilation and the microcirculation reactivity measurements in either group. In the at-risk group, there was a decrease in the C-reactive protein [median (25-75 percentile), 0.12 mg/dl (0.07-0.27 mg/dl) at exit visit vs. 0.24 mg/dl (0.07-0.35 mg/dl) at baseline; P < 0.05] and TNF alpha [median (25-75 percentile), 2.6 pg/ml (1.8-4.1 pg/ml) at exit visit vs. 4.4 pg/ml (3.6-6.0 pg/ml) at baseline; P < 0.05] in the atorvastatin-treated patients, whereas in the diabetes group, a decrease in endothelin-1 (mean +/- SD, 0.97 +/- 0.29 pg/ml at exit visit vs. 1.19 +/- 0.42 pg/ml at baseline; P < 0.05) and plasminogen activator inhibitor-1 [median (25-75 percentile), 18 ng/ml (9-24 ng/ml) at exit visit vs. 27 ng/ml (7-41 ng/ml) at baseline; P < 0.05] were observed. We conclude that atorvastatin improves endothelial function and decreases levels of markers of endothelial activation and inflammation.

Adult↗

PubMed2026

Endothelial function in relation to low-level chronic residential air pollution in a general population: a cohort study.

BACKGROUND: Given the recently updated clean-air targets, this population study assessed endothelial function at low exposure to particulate matter with an aerodynamic diameter of ≤10 µm (PM10) and ≤2.5 µm (PM2.5), nitrogen dioxide (NO2) and black carbon (BC). METHODS: In 453 Flemish participants (47.7% women; mean age, 52.8 years), endothelial function was assessed by finger photoplethysmography after 5 min of ischaemia. The outcome measures were the maximal ischaemic-to-control ratio (Rmax) and the maximal difference (Dmax) in pulse amplitude between the test and control fingers. The air pollutants were related to Rmax and Dmax using mixed models accounting for coresidence, to cardiovascular endpoints by proportional hazards regression, and to residential address by high-resolution spatiotemporal interpolation. RESULTS: From 2010 to 2015, PM10, PM2.5, NO2 and BC decreased (p < 0.0001) with 6-year levels averaging 15.9, 12.8, 14.3 and 1.04 µg/m3. Irrespective of adjustment for risk factors, Dmax was inversely correlated with PM2.5, while associations of Rmax with PM2.5 and associations of both Dmax and Rmax with other pollutants were weaker (p values <0.10), but consistently inverse. Association sizes of Rmax and Dmax with PM10 and PM2.5 weakened over 6 years, paralleling the decreasing air pollutants (p ≤ 0.044). In adjusted analyses, the risk of a composite cardiovascular endpoint decreased (p ≤ 0.043) with higher Rmax and Dmax with hazard ratios ranging from 0.31 to 0.49. Finally, in the geographical analysis, endothelial dysfunction followed the spatial gradients in PM2.5. CONCLUSIONS: Long-term low-level air pollution is associated with subclinical endothelial dysfunction, the initial and critical step leading to adverse cardiovascular outcomes.

Humans↗

PubMed2004

Assessment of endothelial function in complex regional pain syndrome type I using iontophoresis and laser Doppler imaging.

OBJECTIVES: To assess microvascular endothelial function in patients with complex regional pain syndrome type I (CRPS) compared with healthy controls, as measured by iontophoresis of vasoactive chemicals and laser Doppler imaging. METHODS: Microvascular blood flow was stimulated locally in affected and contralateral limbs of patients with CRPS (n = 17) and in control subjects (n = 16) using iontophoresis of the endothelial-dependent vasodilator acetylcholine (ACh) and the endothelial-independent vasodilator sodium nitroprusside (NaNP). Changes in blood flow were measured using laser Doppler imaging. Comparisons were made between right and left limbs and between patients and controls. RESULTS: No significant differences in blood flow [expressed as a median percentage increase from baseline (interquartile range)] were detected between affected and contralateral limbs in patients with CRPS for ACh [affected 237 (95-344); unaffected 251 (152-273)] or for NaNP [affected 102 (49-300); unaffected 190 (53-218)]. In addition, there were no significant differences between patients and healthy controls [controls, ACh 216 (119-316); controls, NaNP: 122 (48-249)]. CONCLUSIONS: In this pilot study, CRPS was not associated with impairment of microvascular endothelial function. This may be a true result or may reflect the diversity of the CRPS disease process.

Acetylcholine↗

PubMed2006

Effects of tea and tea flavonoids on endothelial function and blood pressure: a brief review.

1. The consumption of tea worldwide is second only to water. Thus, any physiological effects of tea could have a significant impact on population health. 2. Tea is the major contributor to total flavonoid intake in many populations. Flavonoids in tea have been shown to have a range of activities and effects that could contribute to improved health. Tea intake and the intake of flavonoids found in tea have been associated with reduced risk of cardiovascular disease in several cross-sectional and prospective population studies. A variety of possible mechanisms have been investigated. The focus of the present review is on the mounting evidence that tea flavonoids can improve endothelial function and lower blood pressure. 3. In vitro studies using isolated vessels have shown that tea flavonoids possess vasodilator activity. Results of human intervention trials have shown that increased flavonoid intake from tea, as well as other dietary sources, can improve endothelial function. Emerging data also suggest that the degree of benefit may be related to flavonoid metabolism. 4. The effects of tea flavonoids on blood pressure are less consistent. Results of animal studies and population studies are consistent with a blood pressure-lowering effect of tea. However, short-term intervention trials, mainly in normotensive individuals, have not demonstrated any blood pressure reduction with tea. 5. Overall, the available data suggest that the effects of tea flavonoids on endothelial function and, perhaps, blood pressure may be responsible, at least in part, for any benefits of drinking tea on the risk of cardiovascular disease.

Animals↗

PubMed2003

Endothelial nitric oxide synthase gene polymorphism, homocysteine, cholesterol and vascular endothelial function.

Nitric oxide-dependent vasodilation is impaired early in the pathogenesis of vascular disease. Both the 4ab polymorphism of endothelial nitric oxide synthase (eNOS) and elevated plasma homocysteine are putatively associated with coronary artery disease (CAD). Few studies have investigated the influence of either on endothelial function in normal subjects. We aimed to examine any effect of three eNOS gene polymorphisms and plasma levels of homocysteine, folate and lipids on vascular endothelial function in normal healthy subjects. Community subjects (n=60) were selected for their eNOS genotype. Largely NOz.-dependent, flow-mediated dilation (FMD) of the brachial artery and the response to glyceryl trinitrate (GTN) were measured. Neither FMD nor response to GTN in 4a allele carriers was significantly different from that of 4b homozygotes, (7.1+/-0.5 S.E.M. vs. 7.1+/-0.6%) and (18.9+/-1.2 vs. 18.9+/-0.9%), respectively. Responses were also independent of the other polymorphisms. FMD was significantly correlated with HDL-cholesterol (P=0.02). After accounting for serum folate, there was a significant inverse correlation between FMD and plasma homocysteine (P=0.03). In these normal community subjects, plasma homocysteine and HDL-cholesterol were predictors of FMD despite subjects being recruited without regard to these variables and despite normal plasma levels.

Adult↗

PubMed2005

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.

Adult↗

PubMed2002

Influence of methylenetetrahydrofolate reductase genotype, exercise and other risk factors on endothelial function in healthy individuals.

Cardiovascular disease has a multifactorial aetiology that is influenced by both genetic and environmental factors. Endothelial dysfunction is a key event in the pathogenesis of vascular disease that occurs before structural vascular changes or clinical symptoms are evident. Conventional risk factors, for example hypertension and diabetes mellitus, are associated with endothelial dysfunction, but the influence of other putative risk factors is not clear. The methylenetetrahydrofolate reductase (MTHFR) C677T genotype, a common polymorphism that induces hyperhomocysteinaemia, has been proposed as being a genetic risk factor for cardiovascular disease. A total of 126 healthy adults recruited by MTHFR C677T genotype (42 of each genotype, i.e. CC, CT and TT) underwent assessment of endothelial function. Brachial artery endothelium-dependent flow-mediated dilatation (FMD) was measured using high-resolution ultrasonic vessel "wall-tracking". Using multiple regression analysis, MTHFR genotype and 21 other subject and subject-lifestyle variables were investigated as potential predictors of endothelial function. FMD was influenced positively by frequency of aerobic exercise and by hormone replacement therapy, and negatively by increases in systolic blood pressure. MTHFR C677T genotype and the associated variation in plasma homocysteine levels did not influence FMD. Additionally, other factors, including plasma cholesterol and self-supplementation with either antioxidant vitamins or cod liver oil, showed no significant relationship with FMD, although these findings are compromised by the narrow range studied for cholesterol and the small number of subjects taking supplements. These observations have implications for risk factor management in the primary prevention of cardiovascular disease in healthy individuals.

Adolescent↗

PubMed2005

Endothelial function is impaired in patients with primary antiphospholipid syndrome.

INTRODUCTION: The aim of this study was to evaluate endothelial function in patients with primary antiphospholipid syndrome (PAPS). PATIENTS AND METHODS: Flow mediated (FMD) and glyceryl trinitrate (GTN) induced dilation of the right brachial artery were studied in 25 patients with PAPS and 25 controls matched by age, sex and conventional risk factors for atherosclerosis. Fibrinogen, D-dimer, adhesion molecules, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) antigens and activities were measured. RESULTS: Mean (SD) FMD was significantly lower in PAPS than in controls (8+/-5% vs. 15+/-6%, P<0.001); GTN-induced dilation did not differ between the groups. There was a correlation between the baseline diameter of the brachial artery and duration of the disease (-0.56, P<0.05) and between GTN induced dilation and duration of the disease (0.51, P<0.05). Concentrations of vascular cell adhesion molecule-1 (P<0.001), intracellular adhesion molecule-1 (P<0.001) and fibrinogen (P<0.05) were higher in patients than in controls but no differences were observed for D-dimer, t-PA and PAI-1 antigens and activities. There was correlation between concentration of vascular cell adhesion molecule-1 and FMD (-0.35, P<0.05) and between intracellular adhesion molecule-1 and FMD (-0.41, P<0.05). CONCLUSIONS: This study shows that endothelial function is impaired in patients with primary APS, possibly contributing to accelerated atherosclerosis and thromboembolic complications in these patients.

Administration, Oral↗