View clinical trials related to Endothelial Dysfunction.
Filter by:Aim The principal objective of this project is: • To evaluate the efficacy of long term (18 months) L-Arginine therapy in preventing or delaying clinical onset of type 2 diabetes mellitus in subjects with impaired glucose tolerance (IGT) and Metabolic Syndrome. Secondary end points are: 1. To define if a long term treatment with L-arginine is able to ameliorate insulin sensitivity and endothelial dysfunction in this population. 2. To find new risk profiles and candidate genes able to define the sub-group of patients at higher risk to develop type 2 diabetes mellitus. Methodology This is a double blind, parallel, one centre study to determine if long term oral L-arginine administration is able to delay or prevent type 2 diabetes mellitus in patients with Metabolic Syndrome. Two hundred and ninety four subjects were recruited at the Cardio-Metabolic and Clinical Trials Unit of the San Raffaele Scientific Institute. One hundred and forty two patients were randomized to enter the study and assigned to two arms: oral L-arginine (6.4 g/die) or placebo, in addition to diet and physical exercise. The treatment were maintained for 18 months. Visits were performed every 3 months for clinical evaluation, blood samples, treatment supply and collection of data on adverse events. Furthermore, patients were contacted every month by telephone to evaluate the accurate continuation of the study and they were instructed to phone to the centre in case of possible adverse events. An OGTT were performed before the enter into the study and at the end of the study period. An additional OGTT were performed at an intermediate visit if fasting glucose levels were more than 126 mg/dl. A diabetic response caused the end-point of the patient. Metabolic, hormonal and endothelial activation and inflammation parameters were measured. Evaluation of endothelium-mediated and non-endothelium-mediated vasodilatation were performed by strain gauche plethysmography evaluating forearm blood at the basal state. in post-ischemic conditions and after nitroglycerine administration. Before the enter into the study, an additional blood sample were drawn for DNA extraction and candidate genes variants evaluation. Before the enter into the study and at the end of the study period, gene expression for inflammation were measured on mRNA extraction on endothelial progenitor cells.
It has been suggested that cardiovascular risk factors either independently or in cluster (metabolic syndrome) increase the risk of both type 2 diabetes (DM2) and cardiovascular diseases (CVD). Consumption of citrus fruits is linked to reduced cardiovascular morbidity and mortality. Hesperidin is a flavanone abundant in citrus fruit with putative vasodilator actions in vitro. While molecular mechanisms of vascular actions of hesperidin begin to be explored, no data on in vivo vascular effect of this flavanone has been ever acquired.
During myocardial infarction, inflammatory response may negatively influence ventricle wall remodeling as well as endothelium-dependent vasomotor function in the coronary and systemic arterial systems. Statins have been consistently proved to attenuate inflammation and improve endothelial function. In this study, we tested the effect of different doses of statin on inflammatory response and endothelium-dependent vasodilation.
The aim of this study is to examine the associations between inflammatory disease activity and endothelial function in rheumatoid arthritis (RA) and spondyloarthritis patients treated with methotrexate and Tumor Necrosis Factor alpha (TNFalpha)inhibitor in combination or methotrexate or TNFalpha-inhibitor alone. Further, to look for improvement in endothelial function, and decrease in bone and cartilage destruction during treatment with the combination therapy of TNFalpha-inhibitor and methotrexate in RA and Psoriatic Arthritis (PSA) patients. Last, examine the TNFalpha inhibitors influence on endothelial function and levels of bone and cartilage markers in patients with Ankylosing Spondylitis (AS).
The purpose of the study is to see how two classes of blood pressure medications,angiotensin-converting enzyme inhibitors (Ace inhibitors) and angiotensin receptor blockers (ARBs), differ in their long term effects on certain chemicals in the body and on the carotid arteries.
We will test the hypothesis that a single dose of Regadenoson will produce equivalent degrees of coronary hyperemia in patients of widely different body size. This will be a prospective, open-label, comparative trial using MRI to measure myocardial perfusion reserve (ratio of myocardial blood flow with vasodilator to myocardial blood flow at rest) during sequential administration of the coronary vasodilators adenosine and regadenoson. Non-invasive MRI measurements of resting myocardial blood flow, and sequential measurements of blood flow during adenosine infusion (weight adjusted dosing) and then blood flow during regadenoson infusion (single, fixed dose. Blood flow measurements will be obtained sequentially and in the same sequence in each subject during a two hour MRI exam. 32 subjects will be recruited for this study. The first 2 will be for testing of the protocol. Inclusion criteria: 2 subjects for initial protocol evaluation, then 30 subjects with body mass index (BMI) between 18 and 40. Exclusions are pregnancy, renal dysfunction and claustrophobia.
Up to 30 patients with lower extremity disease scheduled to undergo diagnostic angiography will undergo baseline bloodwork and IVUS (intravascular ultrasound), followed by dosing with L-arginine to assess changes in endothelial function.
The hypothesis is that GHRP-3 will exert beneficial effects on endothelial function and insulin resistance in older men and women via hormonal (GH, IGF-I, IGFBP-3,-1, insulin) and non-hormonal actions (anti-inflammatory).
Exposure to air pollution has been linked to increased cardiorespiratory morbidity and mortality. The exact component of air pollution that mediates this effect is unknown, but the link is strongest for fine combustion derived particulate matter derived from traffic sources. Recently, it has been demonstrated that inhalation of diesel exhaust impairs vascular vasomotor tone and endogenous fibrinolysis. The mechanism underlying these detrimental vascular is unclear, but is thought to be via oxidative stress and altered bioavailability of endogenous nitric oxide. In these studies we plan to elucidate the role of endogenous nitric oxide (NO) in the adverse vascular responses observed following exposure to diesel exhaust.
Exposure to air pollution has been linked to increased cardiorespiratory morbidity and mortality. The exact component of air pollution that mediates this effect is unknown, but the link is strongest for fine combustion derived particulate matter derived from traffic sources. Recently, it has been demonstrated that inhalation of diesel exhaust impairs vascular vasomotor tone and endogenous fibrinolysis. The mechanism underlying these detrimental vascular is unclear, but is thought to be via oxidative stress and altered bioavailability of endogenous nitric oxide. In these studies we plan to elucidate the role of endogenous nitric oxide synthase isoforms (NO) in the adverse vascular responses observed following exposure to diesel exhaust.