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Results for “Endothelial function”

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At least 289 records · Page 16Linked to original sources

PubMed2004

Effect of endogenous estrogen on endothelial function in women with coronary heart disease and its mechanism.

BACKGROUND: Estrogen promotes and modulates vascular endothelial function, which may be protective against development of atherosclerosis. Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, has been reported to be associated with the impairment of vascular endothelial function. Recent studies suggested estrogen replacement therapy lowers plasma concentrations of ADMA in healthy postmenopausal women. However, the relation between endogenous estrogen and ADMA and their effect on endothelial function in patients with coronary heart disease (CHD) remains unclear. METHODS: Flow-mediated dilatation (FMD) and nitroglycerin-induced dilatation (NID) of the brachial arteries were detected by using high-resolution ultrasound in 33 women with CHD and 17 healthy controls. Plasma estradiol, ADMA, and lipid concentrations were also measured in all subjects. RESULTS: In comparison with control group, FMD and NID were significantly decreased in the CHD group (1.73 +/- 1.26% vs. 5.37 +/- 3.20%, p < 0.001 and 12.38 +/- 6.70% vs. 20.79 +/- 7.57%, p < 0.01, respectively). Plasma estradiol concentrations in the CHD group were lower than in controls (27.80 +/- 12.28 vs. 43.83 +/- 14.30 pg/ml, p < 0.01), whereas ADMA concentrations in the CHD group were higher than in controls (3.39 +/- 1.07 vs. 1.31 +/- 0.69 micromol/l, p < 0.001). Pearson correlation analysis determined that plasma estradiol concentrations were associated with FMD, NID, age, systolic pressure, diastolic pressure and ADMA (r = 0.610, p < 0.01; r = 0.392, p < 0.01; r = -0.589, p < 0.01; r= -0.364, p < 0.01; r = -0.350, p < 0.05; r = -0.553, p < 0.01; respectively). Multiple linear stepwise regression analysis revealed that plasma estradiol concentrations was independently positively correlated with FMD (p < 0.005) and negatively correlated with ADMA (p < 0.05). CONCLUSIONS: Both FMD and NID are impaired in women with CHD. The decrease of endogenous estrogen concentrations and the increase of ADMA concentrations may involve the endothelial dysfunction in women with CHD.

Brachial Artery↗

PubMed2005

Inflammation, complement activation and endothelial function in stable and unstable coronary artery disease.

BACKGROUND: Endothelial dysfunction plays an important role in the pathogenesis of coronary artery disease (CAD). Apart from traditional risk factors complement activation and inflammation may trigger and sustain endothelial dysfunction. We sought to assess the association between endothelial function, high sensitivity C-reactive protein (hs-CRP) and markers of complement activation in patients with either stable or unstable coronary artery disease. METHODS: We prospectively recruited 78 patients, 35 patients with stable angina pectoris (SAP) and 43 patients with unstable angina pectoris (UAP). Endothelial function was assessed as brachial artery reactivity (BAR). Hs-CRP, C3a, C5a and C1-Inhibitor (C1 inh.) were measured enzymatically. RESULTS: Patients with UAP showed higher median levels of hs-CRP and C3a compared to patients with SAP, while BAR was not significantly different between patient groups. In UAP patients, hs-CRP was significantly correlated with cholesterol (r=0.27, p<0.02), C3a (r=0.32, p<0.001) and C1 INH.(r=0.41, p<0.003), but not with flow mediated dilatation (r=0.09, P=0.41). Hs-CRP and C1 INH.were found to be independent predictors of UAP in a backward stepwise logistic regression model. CONCLUSIONS: We conclude that both hs-CRP, a marker of inflammation and C3a, a marker of complement activation are elevated in patients with UAP, but not in patients with SAP.

Aged↗

PubMed2005

Relation of plasma glucose and endothelial function in a population-based multiethnic sample of subjects without diabetes mellitus.

To determine whether endothelial dysfunction precedes the clinical diagnosis of diabetes mellitus, we investigated the relation of endothelial flow-mediated dilation (FMD) with fasting plasma glucose among a multiethnic population-based cohort of 579 nondiabetic subjects without previous myocardial infarction or stroke enrolled in the Northern Manhattan Study (age 66 +/- 9 years; 41% men, 16% white, 15% black, and 68% Hispanic). Impaired fasting glucose or prediabetic status, defined as a fasting glucose level of 100 to 125 mg/dl, was present in 95 subjects (16%). Endothelial function was determined using FMD during reactive hyperemia. Multiple linear regression analyses were used to assess the relation between plasma glucose and endothelial function after adjustment for potential confounders. FMD was significantly lower (4.9 +/- 3.8% vs 6.1 +/- 3.7%, p = 0.003) in those with impaired fasting glucose than in subjects with normal fasting glucose. Prediabetic status was significantly associated with impaired FMD (odds ratio 1.9, 95% confidence interval 1.1 to 3.1, p = 0.02). After adjustment for age, gender, body mass index, and hypertensive status, a higher fasting glucose was significantly associated with a lower FMD (beta = -0.024 +/- 0.012, p = 0.04) in a continuous linear relation. Thus, for each 10-mg/dl increase in plasma glucose, a 0.24% decrease occurred in FMD. Impaired FMD was present among prediabetics. An elevated fasting plasma glucose level is associated with impaired endothelial function among nondiabetics. These results further support the role of hyperglycemia in the pathogenesis of vascular dysfunction at different stages of diabetes development and the role of impaired fasting glucose as a risk factor for macrovascular disease.

Black or African American↗

PubMedDate not supplied

[Endothelial function in clinical practice].

Endothelial dysfunction is the essential occurrence in an early phasis of atherogenic process, pointing at the first functional disturbances of cardiovascular system at endothelial level. By the assessment of endothelial dysfunction, subjects with the increased risk for cardiovascular incidents in preclinical phasis, can be selected. Non-invasive assessment of endothelial function with ultrasound test is the new non-invasive measurement that has enabled the assessment, observation and the repeated tests without any limit or risk for the patient, and all in a frame of primary and secondary prevention of cardiovascular diseases.

Arteriosclerosis↗

PubMed2005

Polymorphonuclear leukocytes may impair endothelial function: results of crossover randomized study of lipid-lowering therapies.

OBJECTIVES: To examine whether polymorphonuclear leukocytes (PMNs) in hypercholesterolemia (HC) are activated to generate large amount of superoxide in vivo and hence impair endothelial function and, if so, whether statins, which possess anti-inflammatory properties, may restore PMN-mediated endothelial dysfunction. METHODS AND RESULTS: At baseline, subjects with HC showed impaired endothelial function (P<0.001), estimated by flow-mediated vasodilation of the brachial artery, and increased susceptibility of low-density lipoprotein (LDL) to oxidation (P<0.0001) compared with control subjects. PMNs obtained from HC produced greater amount of superoxide (P<0.0001), showed higher adhesiveness to cultured endothelial cells (HUVECs) (P<0.0001), and impaired endothelial nitric oxide synthase (eNOS) Ser1177 phosphorylation of HUVECs compared with controls (P<0.001). Crossover administration of fluvastatin or colestimide for 3 months lowered LDL to the same levels (P<0.001 for both). Endothelial function was restored (P<0.0001). LDL oxidation (P<0.0001) and superoxide release from PMNs (P<0.0001) were diminished only in fluvastatin but not in colestimide arm. Fluvastatin attenuated PMN adhesion to HUVECs (P<0.0001) and restored eNOS Ser1177 phosphorylation of HUVECs (P<0.001). CONCLUSIONS: Statins may improve endothelial function at least in part by inactivating neutrophils independently of LDL reduction. Our results raise a novel concept that polymorphonuclear leukocytes may attack endothelia and play a pivotal role in the pathogenesis of atherosclerosis.

Anticholesteremic Agents↗

PubMed2004

Cytomegalovirus infection in heart transplant recipients is associated with impaired endothelial function.

BACKGROUND: Cardiac allograft vasculopathy (CAV) is initiated by allograft endothelial injury. We hypothesized that a major mechanism by which cytomegalovirus (CMV) could contribute to CAV is by dysregulation of the endothelial vasomotor response. METHODS: Coronary endothelial vasomotor function was determined in 183 consecutive patients (24+/-33 months after transplantation), and was correlated with recipient and donor CMV serological status before transplantation and with documented CMV infection episodes (CMVpp65Ag+). Serial endothelial function measurements were performed in a subgroup of 53 transplant recipients (1 month and 12 months after transplantation). The composite endpoint of cardiovascular related events and death during a follow-up of 66+/-41 months was analyzed based on the CMV serological status before transplantation. RESULTS: The medium event-free time for CMV-negative recipients of CMV-positive hearts was 8.1 years compared with 13.3 years for the other groups (P<0.05). Distal epicardial but not microvascular endothelial function was significantly impaired in CMV seronegative recipients of seropositive donor hearts (n=48) compared with all other groups (P<0.01 versus seronegative recipient/seronegative donor; P<0.05 versus seropositive recipient/seronegative donor; P<0.05 versus seropositive recipient/seropositive donor). Distal epicardial endothelial dysfunction was more pronounced in heart transplant recipients with a history of documented CMV infection compared with patients without any documented CMV infection (P<0.01). In a longitudinal subgroup analysis, distal epicardial and microcirculatory endothelial vasomotor response deteriorated significantly in recipients with documented CMV infection (P<0.05 versus baseline) but not in patients without previous CMV infection. CONCLUSIONS: Documented CMV infection episodes in heart transplant recipients are associated with impaired coronary endothelial function. CMV-negative recipients of CMV-positive donor hearts have an impaired distal epicardial endothelial function and an increased incidence of cardiovascular-related events and death during follow-up. CMV infection may contribute to allograft failure by accelerating coronary endothelial dysfunction.

Adult↗

PubMed1995

Effect of aging and chronic angiotensin I converting enzyme inhibition on the endothelial function of the mesenteric arterial bed of the rat.

Endothelial function was studied in perfused mesenteric arterial bed preparations removed from 6, 12, 24, or 30 month-old, male, normotensive rats. Half of the animals were treated with a hypotensive dose of an angiotensin I converting enzyme (ACE) inhibitor (perindopril, 1 mg/kg/day, p.o.) from 6 months onwards. Disruption of endothelium produced a fall in baseline perfusion pressure in all animals except 30-month old controls, suggesting that the maintenance of baseline tone by endothelial vasoconstrictor(s) is impaired with age. Physiologic antagonism of norepinephrine-induced vasoconstriction by the muscarinic agonist carbachol was impaired in 30-month old controls. Norepinephrine-induced vasoconstriction increased following disruption of endothelium, suggesting that norepinephrine-induced release of endothelium-derived relaxing factor attenuates vasoconstriction. This mechanism was impaired in 30-month old controls. Chronic ACE inhibition postponed the age-related decrease in vasodilator and vasoconstrictor endothelial functions, either directly or indirectly via the hypotensive action of such treatment.

Aging↗

PubMed2006

Endothelial function in HIV-infected patients with low or mild cardiovascular risk.

BACKGROUND: Highly active antiretroviral therapy for HIV-infected patients is associated with metabolic side effects, which could cause an increased cardiovascular risk in these patients. Non-invasive study of endothelial function by brachial artery ultrasound can detect subclinical atherosclerosis. Several studies have assessed endothelial function in HIV-infected patients with associated cardiovascular risk factors. OBJECTIVES: The aim of this study is to determine endothelial function in HIV-infected patients under antiretroviral therapy with low or mild coronary risk and lipid levels within the normal range. METHODS: Transversal study including 28 HIV-infected adults (15 receiving antiretroviral therapy and 13 naive) with low or mild cardiovascular risk and 12 healthy controls. Subjects with diabetes mellitus, hypertension, cardiovascular disease, obesity, high cholesterol or high triglyceride levels were excluded. Endothelial function was determined with flow-mediated dilation (FMD) of the brachial artery by ultrasound study. RESULTS: Treated HIV-infected patients had significantly lower FMD (5.93 +/- 3.56) than healthy controls (10.64 +/- 3.08, P = 0.008). Naive patients had an intermediate FMD, but this was not statistically significant. CONCLUSIONS: HIV-infected patients receiving antiretroviral therapy who have low or mild cardiovascular risk and lipid levels within the normal range have endothelial dysfunction compared with healthy controls.

Adult↗

PubMed1999

Relationship of the C242T p22phox gene polymorphism to angiographic coronary artery disease and endothelial function.

Patients with coronary artery disease (CAD) have impaired endothelial function in part due to an increase in vascular oxidant stress. p22phox, an essential component of the NADPH oxidase, is thought to play a critical role in the generation of superoxide anions in the vessel wall. The C242T polymorphism, located in the potential heme-binding site of the p22phox gene, has recently been reported to confer a protective effect on CAD risk in a Japanese study population. In a U.S. population of 252 patients (83% Caucasian) undergoing angiography for diagnosis of CAD, we investigated whether the C242T polymorphism was associated with the presence of CAD. In a subset of 142 patients, we studied whether the polymorphism manifests its potential protective effects through alteration of vascular endothelial function by measuring coronary epicardial and microvascular responses to intracoronary acetylcholine and sodium nitroprusside. Prevalence of the C242T allele was not different in 149 patients with CAD compared to 103 patients with angiographically normal coronary arteries (65.1% vs. 54.4%, P = 0.11). The C242T allele frequency in our population was nearly fourfold higher than reported previously in a Japanese population. There were also no significant differences in coronary epicardial or microvascular responses to acetylcholine or sodium nitroprusside between groups of patients with or without the C242T allele. In a U.S. population, the C242T polymorphism does not appear to confer protection from endothelial dysfunction or CAD. Am. J. Med. Genet. 86:57-61, 1999. Published 1999 Wiley-Liss, Inc.

Acetylcholine↗

PubMed2006

Endothelial function in patients with obstructive sleep apnea syndrome but without hypertension.

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) influences endothelial function and causes hypertension. OBJECTIVES: Our aim was to evaluate the role of endothelial dysfunction in the pathogenesis of hypertension in OSAS. METHODS: Twenty-three patients with OSAS but without hypertension and 15 healthy normotensive subjects were investigated. The presence or absence of OSAS was evaluated with a sleep study. Endothelial function was investigated with brachial artery ultrasound examination. RESULTS: Baseline characteristics were equivalent between the two groups. Minimal oxygen saturation and apnea-hypopnea indexes in the OSAS and control groups were 62.9 +/- 16.5 versus 94.9 +/- 1.1% (p < 0.0001) and 53.1 +/- 20.3 versus 3.8 +/- 0.9 (p < 0.0001), respectively. There was not statistically significant difference between basal brachial artery diameters measured in the morning and in the evening in all groups. Flow-mediated dilation (FMD) values measured in the morning were lower than those measured in the evening in both OSAS patients and the control group: FMD of OSAS patients was 6.04 +/- 3.18% in the morning and 10.38 +/- 4.23% in the evening hours (p = 0.001), and FMD of control subjects was 10.9 +/- 2.6% in the morning and 13.9 +/- 2.32 in the evening hours (p = 0.002). Differences in FMD values measured both in the morning and evening hours in OSAS patients were lower compared with those in control subjects (p < 0.0001 in the morning hours and p = 0.003 in the evening hours). CONCLUSIONS: We detected a prominent diurnal deterioration in endothelial function in normotensive OSAS patients compared with healthy subjects. This deterioration may occur due to ongoing hypoxemia during the night and it may be a possible cause of hypertension and atherosclerotic cardiovascular diseases in patients with OSAS.

Brachial Artery↗

PubMed2000

Coenzyme Q improves LDL resistance to ex vivo oxidation but does not enhance endothelial function in hypercholesterolemic young adults.

Oxidative modification of low-density lipoprotein (LDL) may cause arterial endothelial dysfunction in hyperlipidemic subjects. Antioxidants can protect LDL from oxidation and therefore improve endothelial function. Dietary supplementation with coenzyme Q (CoQ(10)) raises its level within LDL, which may subsequently become more resistant to oxidation. Therefore, the aim of this study was to assess whether oral supplementation of CoQ(10) (50 mg three times daily) is effective in reducing ex vivo LDL oxidizability and in improving vascular endothelial function. Twelve nonsmoking healthy adults with hypercholesterolemia (age 34+/-10 years, nine women and three men, total cholesterol 7.4+/-1.1 mmol/l) and endothelial dysfunction (below population mean) at baseline were randomized to receive CoQ(10) or matching placebo in a double-blind crossover study (active/placebo phase 4 weeks, washout 4 weeks). Flow-mediated (FMD, endothelium-dependent) and nitrate-mediated (NMD, smooth muscle-dependent) arterial dilatation were measured by high-resolution ultrasound. CoQ(10) treatment increased plasma CoQ(10) levels from 1.1 +/-0.5 to 5.0+/-2.8 micromol/l (p =.009) but had no significant effect on FMD (4.3+/-2.4 to 5.1+/-3.6 %, p =.99), NMD (21.6+/-6.1 to 20.7+/-7.8 %, p = .38) or serum LDL-cholesterol levels (p = .51). Four subjects were selected randomly for detailed analysis of LDL oxidizability using aqueous peroxyl radicals as the oxidant. In this subgroup, CoQ(10) supplementation significantly increased the time for CoQ(10)H(2) depletion upon oxidant exposure of LDL by 41+/-19 min (p = .04) and decreased the extent of lipid hydroperoxide accumulation after 2 hours by 50+/-37 micromol/l (p =.04). We conclude that dietary supplementation with CoQ(10) decreases ex-vivo LDL oxidizability but has no significant effect on arterial endothelial function in patients with moderate hypercholesterolemia.

Adolescent↗

PubMed2003

Vitamin C improves resistance but not conduit artery endothelial function in patients with chronic renal failure.

BACKGROUND: Chronic renal failure is associated with impaired endothelium-dependent vasodilation and accelerated atherogenesis. To examine whether endogenous reactive oxygen species (ROS) modify endothelial function in renal failure, we evaluated the effect of the antioxidant vitamin C on endothelium-dependent responses in both the conduit and resistance vasculature of subjects with severe renal impairment. METHODS: Endothelial function of the forearm resistance vasculature was assessed using plethysmography to measure the dilator response to intra-arterial acetylcholine (Ach) (25 to 100 nmol/min). Endothelial function of radial and brachial arteries was assessed using vascular ultrasound to measure the dilator response to flow during reactive hyperemia [flow-mediated dilatation (FMD)]. Studies were performed before and after administration of vitamin C by intra-arterial infusion (25 mg/min) in 33 predialysis patients or by intravenous infusion (3 g) in 17 hemodialysis patients. RESULTS: Parenteral administration of vitamin C resulted in a 100-fold increase (intra-arterial studies) and a 4.5-fold increase (intravenous studies) in serum antioxidant activity. Vitamin C administration increased the dilator response to ACh in resistance vessels (P = 0.01), but did not alter the dilator response to flow in conduit vessels of either dialysis (P = 0.3) or predialysis subjects (P = 0.8). In the presence of the nitric oxide (NO) synthase inhibitor NGmonomethyl-L-arginine (L-NMMA), there was no effect of vitamin C on resistance vessel endothelial function. In all cases the dilator response to the endothelium-independent dilators was unaffected by vitamin C. CONCLUSION: Acute administration of vitamin C reduces oxidant stress in renal failure and improves NO-mediated resistance vessel dilatation.

Adult↗

PubMed2000

The postprandial effect of components of the Mediterranean diet on endothelial function.

OBJECTIVES: This study investigated the postprandial effect of components of the Mediterranean diet on endothelial function, which may be an atherogenic factor. BACKGROUND: The Mediterranean diet, containing olive oil, pasta, fruits, vegetables, fish, and wine, is associated with an unexpectedly low rate of cardiovascular events. The Lyon Diet Heart Study found that a Mediterranean diet, which substituted omega-3-fatty-acid-enriched canola oil for the traditionally consumed omega-9 fatty-acid-rich olive oil, reduced cardiovascular events. METHODS: We fed 10 healthy, normolipidemic subjects five meals containing 900 kcal and 50 g fat. Three meals contained different fat sources: olive oil, canola oil, and salmon. Two olive oil meals also contained antioxidant vitamins (C and E) or foods (balsamic vinegar and salad). We measured serum lipoproteins and glucose and brachial artery flow-mediated vasodilation (FMD), an index of endothelial function, before and 3 h after each meal. RESULTS: All five meals significantly raised serum triglycerides, but did not change other lipoproteins or glucose 3 h postprandially. The olive oil meal reduced FMD 31% (14.3 +/- 4.2% to 9.9 +/- 4.5%, p = 0.008). An inverse correlation was observed between postprandial changes in serum triglycerides and FMD (r = -0.47, p < 0.05). The remaining four meals did not significantly reduce FMD. CONCLUSIONS: In terms of their postprandial effect on endothelial function, the beneficial components of the Mediterranean and Lyon Diet Heart Study diets appear to be antioxidant-rich foods, including vegetables, fruits, and their derivatives such as vinegar, and omega-3-rich fish and canola oils.

Adult↗

PubMed1999

Cholesterol reduction rapidly improves endothelial function after acute coronary syndromes. The RECIFE (reduction of cholesterol in ischemia and function of the endothelium) trial.

BACKGROUND: Cholesterol lowering reduces coronary events. One mechanism could be improvement of endothelial function. In line with this hypothesis, this study investigates whether cholesterol reduction can result in rapid improvement of endothelial function after acute coronary syndromes. METHODS AND RESULTS: Patients with acute myocardial infarction or unstable angina and total cholesterol levels at admission >/=5.2 mmol/L or LDL >/=3.4 mmol/L were randomized to placebo (n=30) or pravastatin 40 mg daily (n=30) for 6 weeks. Brachial ultrasound was used to measure endothelium-dependent flow-mediated dilatation (FMD) and response to endothelium-independent nitroglycerin. Changes in the levels of markers of platelet activation, coagulation factors, and plasma endothelin levels were also assessed. Total and LDL cholesterol levels were similar at admission and before randomization in both groups. With pravastatin, but not with placebo, they decreased by 23% (P<0.05) and 33% (P<0.01), respectively. FMD was unchanged with placebo, 5.43+/-0.74% (mean+/-SEM) to 5.84+/-0.81%, but increased with pravastatin, 4.93+/-0.81% to 7.0+/-0.79% (P=0.02), representing a 42% relative increase. Responses to nitroglycerin were similar during the time course of the study in the 2 groups. Markers of platelet activity, coagulation factors, and endothelin levels were not affected by pravastatin. CONCLUSIONS: Cholesterol reduction with pravastatin initiated early after acute coronary syndromes rapidly improves endothelial function after 6 weeks of therapy.

Anticholesteremic Agents↗

PubMed1994

HBPRCA Astra Award. Therapeutic restoration of endothelial function in hypercholesterolaemic subjects: effect of fish oils.

1. Endothelial dysfunction, evidenced as an impaired response to acetylcholine, is well documented in hypercholesterolaemic subjects. We examined the ability of dietary supplementation with fish oils to restore endothelial function in forearm resistance vessels in these patients and compared this with restoration by lipid-lowering therapy. 2. Responses of forearm blood flow to acetylcholine (4.6, 9.25, 18.5 and 37 micrograms/min) and sodium nitroprusside (200, 400, 800 and 1600 ng/min) were obtained using forearm venous occlusion plethysmography in nine hypercholesterolaemic and seven age-matched control subjects. The dose-response curve to acetylcholine was significantly blunted in hypercholesterolaemic subjects when compared with controls (P < 0.001). Responses to sodium nitroprusside were not different between the two groups (P = 0.37). 3. Lipid-lowering therapy decreased total plasma cholesterol levels by 33% and significantly augmented the responses to acetylcholine (P = 0.001) but not to sodium nitroprusside in the hypercholesterolaemic subjects. 4. Dietary supplementation with fish oils had no effect on either total or low density lipoprotein-cholesterol but significantly augmented the responses to acetylcholine (P = 0.011) in hypercholesterolaemic subjects. Responses to sodium nitroprusside were not altered (P = 0.94). 5. This study shows that endothelium-dependent relaxation is impaired in subjects with high cholesterol levels and that this impairment can be reversed by lowering low density lipoproteins (LDL) cholesterol levels. In addition, we demonstrate that restoration of endothelial function can occur without changes in LDL levels, by dietary supplementation with fish oils.

Acetylcholine↗

PubMed2002

Hormone replacement effects on endothelial function measured in the forearm resistance artery in normocholesterolemic and hypercholesterolemic postmenopausal women.

We investigated whether forearm resistance artery endothelial function differed between hypercholesterolemic postmenopausal women (n = 41) and normocholesterolemic postmenopausal women (n = 37), both generally and in terms of effects of long-term hormone replacement therapy (HRT) on endothelial function. Both menopause and hypercholesterolemia are associated with endothelial dysfunction and increased coronary risk. Forearm blood flow (FBF) during reactive hyperemia and after sublingual nitroglycerin (NTG) administration was measured by strain-gauge plethysmography. Treated women received conjugated equine estrogen (0.625 mg) plus medroxyprogesterone acetate (2.5 mg) daily for 6 months. Nitrite/nitrate, angiotensin-converting enzyme, and lipids were measured in serum. FBF during reactive hyperemia as well as serum nitrite/nitrate concentrations were significantly lower in hypercholesterolemic than normocholesterolemic subjects. Increases in the FBF induced by NTG were similar in the two groups. HRT significantly increased estradiol, high-density lipoprotein cholesterol, and serum nitrite/nitrate, while decreasing circulating angiotensin-converting enzyme activity in both groups. Reduction in total and low-density lipoprotein cholesterol was seen only in hypercholesterolemic subjects. After 6 months of HRT, maximal FBF response during reactive hyperemia increased in both groups. Augmentation of this response was greater in hypercholesterolemic than in normocholesterolemic subjects (maximal FBF, 55.4 +/- 11.2 vs. 25.9 +/- 11.5%; P < 0.05). Changes in the FBF with NTG were not altered by HRT in either group. Long-term HRT augments endothelial function in forearm resistance artery. This beneficial effect is greater in patients with hypercholesterolemia.

Arteries↗

PubMed2004

Short-term treatment with rosiglitazone improves glucose tolerance, insulin sensitivity and endothelial function in renal transplant recipients.

BACKGROUND: Insulin resistance (IR) contributes to the development of glucose intolerance (post-transplant diabetes mellitus or impaired glucose tolerance) following renal transplantation. Furthermore, endothelial dysfunction (ED) is associated with IR. Glucose intolerance, IR and ED are all independent risk factors for cardiovascular disease. Therefore, treatment with insulin sensitizers may benefit glucose-intolerant renal transplant recipients. The main objectives of the present study were to investigate the effect of 4 weeks' treatment with the PPAR-gamma agonist rosiglitazone on insulin sensitivity, plasma glucose and endothelial function in renal transplant recipients with glucose intolerance. Safety parameters were also addressed. METHODS: A total of 10 glucose-intolerant renal transplant recipients were treated with rosiglitazone (initially 4 mg/day increasing to 8 mg/day after 1 week). A hyperinsulinaemic euglycaemic glucose clamp, an oral glucose tolerance test and endothelial function assessment with laser Doppler flowmetry were performed both at baseline and at follow-up. RESULTS: Treatment with rosiglitazone was followed by a significantly improved mean glucose disposal rate (from 6.5 to 9.1 g/kg/min; P = 0.02) and a significant decline in fasting and 2 h plasma glucose (from 6.4 to 5.8 mmol/l, P = 0.01 and from 14.2 to 10.6 mmol/l, P = 0.03, respectively). Furthermore, a significant improvement in endothelial function was demonstrated (AUC(ACh); from 389 to 832 AU x min, P = 0.04). No serious adverse events or hypoglycaemic episodes were observed. CONCLUSIONS: Four weeks' treatment with rosiglitazone was associated with increased insulin sensitivity, lowered fasting and 2 h plasma glucose and improved endothelial function in renal transplant recipients with glucose intolerance. The drug was well tolerated and may be a good alternative for treating these patients.

Blood Glucose↗

PubMed2004

Oral folic acid enhances endothelial function in patients with hypercholesterolaemia receiving statins.

BACKGROUND: Folic acid therapy has been shown to improve endothelial function in patients with familial hypercholesterolaemia via a possible antioxidant mechanism. Data on the possible role of folic acid in hypercholesterolaemic patients receiving statins are lacking. In the present study we tested the hypothesis that folic acid supplementation improves endothelial function in patients with hypercholesterolaemia and treatment with statins. METHODS: Thirty-four hypercholesterolaemic patients receiving statins participated in the study; all subjects underwent measurement of endothelium-dependent, flow-mediated dilatation of the brachial artery and subsequently randomized to receive 5 mg of the folic acid (n=17) or placebo (n=17) for 4 weeks. Flow-mediated dilatation of the brachial artery was repeated at the end of the 4-week period. RESULTS: Folic acid and placebo groups were comparable regarding age, sex, smoking, hypertension, coronary artery disease, obesity, family history and blood lipids. Folic acid administration resulted in an improvement of flow-mediated dilatation (4.7+/-3.2% to 7.1+/-3.1%, P=0.02), whereas there was no improvement after placebo administration (5.7+/-3.8% to 5.6+/-2.2%, ns). No significant change in nitrate-induced, endothelium- independent dilatation was observed after folic acid or placebo (ns). CONCLUSIONS: Oral administration of folic acid (5 mg) for 4 weeks improves endothelial function in patients with hypercholesterolaemia treated with statins, with possible beneficial effects on the prognosis of these patients.

Administration, Oral↗