Active clinical trials for "Vascular Diseases"

XIENCE V USA is a prospective, multi-center, multi-cohort post-approval study. The objectives of this study are To evaluate XIENCE V EECSS continued safety and effectiveness during commercial use in real world settings, and To support the Food and Drug Administration (FDA) dual antiplatelet therapy (DAPT) initiative. This initiative is designed to evaluate the composite of all death, myocardial infarction (MI) and stroke (MACCE) and the survival of patients that are free from Academic Research Consortium (ARC) definite or probable stent thrombosis (ST) and that have been treated with drug eluting stents (DES) and extended dual antiplatelet therapy.

A cholesterol/lipid profile screening project of high risk patients with hyperlipidaemia (secondary prevention) who already receive cholesterol-lowering therapy. Lipid profile and rate of patients who are treated to target (which is <100mg/dl for patients with high risk and <70mg/dl for patients at very high risk) are screened (hospital-based specialists). The doctors therapy decisions after the screening and possible reasons for these decisions will be documented. Our aim is to evaluate dosing habits, to evaluate how many patients are treated to their LDL-C target and to underline the importance of treating patients to their cholesterol targets.

The purpose of this Randomized Study to evaluate the safety and efficacy of the Excel-II DES compared to the EXCEL DES in the treatment of patients with de novo coronary artery lesions.

The purpose of the study is to compare non-contrast abdominal MR Angiogram (MRA) syngo NATIVE sequence performed on a 3T Verio Siemens magnet to a standard contrast-enhanced MRA performed as part of routine clinical care in patients with normal renal function to determine if the non-contrast NATIVE sequence is a viable alternative to contrast enhanced MRA in patients with renal insufficiency. There are no interventions--this is an observational study.

The purpose of this clinical study is to test whether or not patients treated with HBOT for diabetic foot ulcers will demonstrate measurable changes of the blood vessel function during the course of HBOT treatments. , i.e. an expected increase in the reactive hyperemic index (RHI) measured by the peripheral arterial tonometry (PAT).

The application of sex-gender medicine is strongly recommended by World Health Organization and other international organization. In fact, it is emerging that, although men and women are affected to the same cardiovascular diseases (CVD), however they have different risk factors, disease progression and response to pharmacological and not-pharmacological treatments. Consequentially, the identification of biomarkers and therapeutic approaches taking into account sex gender differences (SGD) is relevant to develop a really evidence-based medicine. With the aim of translate in clinical setting the more recently available basic research evidences on estrogens and androgens balance involvement in modulation of ischemia-reperfusion myocardial damage, the investigators planned to conduct a research study on patients, affected by suspected or known ischemic heart disease (IHD) undergoing angiography and/or percutaneous coronary interventions (PCI), aged more than 18 years of both sex in ratio 1:1. Thus, in this setting, the goals of this proposal are: To assess the sex-gender difference in entity of microvascular reperfusion damage in patients with IHD undergoing urgent or elective PCI; To evaluate estrogen/androgen-dependent and -independent effects in gender-related differences on myocardial ischemia reperfusion damage occurring during PCI; To investigate the differences in terms of platelet biology between men and women affected by IHD undergoing urgent or elective PCI, matched for age and clinical cardiovascular and metabolic characteristics; To verify sex-driven interplay between response to PCI procedure, platelet function, sex hormones and entity of reperfusion and myocardial damage, as well as, the impact on clinical outcomes during a 1-year follow up. This research study wants to explore and consequently elucidate biological mechanisms responsible for sex-based differences in vivo human models of ischemia reperfusion myocardial damage. Moreover, the investigators expected to clarify the impact of biological variables evaluated on clinical outcomes after reperfusion therapeutic intervention.

Heart transplantation (HT) is a lifesaving procedure for patients with end-stage heart failure and provides a better survival and quality of life if compared to medical treatment. HT is subject to alloimmune response, which, if left uncontrolled, is capable of jeopardizing long-term cardiac function. Advances in immunosuppression have enhanced the survival of HT patients. Nearly 2500 HT per year have been performed in the US during the last 10 years and despite significant improvements, long-term survival rates remain poor. More than 20% of patients do not survive more than 3 years, and those who survive are afflicted by long-term complications of alloimmunity and chronic immunosuppression. Life expectancy of patients who lose cardiac allografts is dramatically poor due to the absence of any therapeutic tool apart from re-transplantation, which is plagued by poor outcomes. The identification of novel therapeutic targets is thus mandatory. ATP/P2X7R signaling in T cells is highly relevant for cardiac allograft survival. ATP is a small molecule present at high concentrations inside cells; it is released as extracellular ATP (eATP) following cell damage or death where it acts as a danger signal. ATP is sensed by the P2X receptors (seven receptors named P2X1-7), mainly expressed by T lymphocytes. We have recently demonstrated that the ATP/P2X7R axis has a key role in cardiac allograft survival in humans and mice. Cardiac allograft vasculopathy (CAV) is a major limiting factor for HT survival; indeed CAV occurs in 50% of HT recipients by 5 years after transplantation and invariably results in allograft failure. CAV is clearly of immunological origin, as syngeneic murine grafts do not develop it. Once CAV occurs, the most definitive treatment is re-transplantation, but survival remains poor. We hypothesize that a single nucleotide polymorphysm (SNP) loss-of-function P2X7R mutation (p.Glu496Ala / c.1513A>C, rs3751143) generates a compensatory upregulation of the other purinergic receptors (P2XsR), thus creating a state of hypersensitivity to eATP. This eATP hypersensitivity results in an abnormal generation of Th1/Th17 cells, that leads to CAV and early cardiac allograft loss. Our study will answer a fundamental question: What is the effect of the P2X7R loss-of-function mutation on the immune system? Our goal is to generate the first targeted-therapy for a selected group of cardiac transplant recipients.

The relationship of the natural history of atherosclerosis between different vascular beds has not been well characterized. Determination and comparison of the relative rates of progression and extents of atherosclerosis in the coronary and carotid arterial trees may have major impacts on clinical research and clinical practice. Correlation between findings in the carotid and coronary circulations is an important scientific and clinical topic to address. Results from a well design study incorporating imaging technologies that currently represent the gold standards for the assessment of coronary and carotid artery plaque burden, will have potentially impact on clinical research and clinical practice.

OBJECTIVES: Vascular Disease is the leading cause of complications and death in patients with diabetes. Risk markers and underlying mechanisms have not been fully elucidated, and may differ from those in non-diabetic individuals. The unifying theme for the Program Project is that hyperglycemia and insulin resistance alter a number of biological processes which interact in vicious cycles to accelerate atherogenesis and are consequently major underlying risk factors for vascular disease. The overall objectives are to define these unique processes and to elucidate underlying biochemical, metabolic, and genetic determinants of vascular disease complications in diabetes. RESEARCH PLAN: Over the past 4 years, we have collaborated with the DCCT/EDIC Study Group, and have made novel observations regarding vascular disease pathogenesis in Type 1 Diabetes. This work has focused our studies on specific pathogenic processes. We will now study a Type 2 Diabetes cohort from the VA Cooperative Study, "Glycemic Control and the Complications of Diabetes, Type 2", with high vascular disease event rates. These collaborations provide a unique opportunity to address the pathogenesis of accelerated atherogenesis in the two main types of diabetes, and will greatly augment the scientific knowledge that will be gained in the conduct of these world-class prospective trials. METHODS: The Program Project has 4 projects and 3 cores. Project 1 will assess lipoproteins, glycoxidative stress, and inflammation as risk factors in studies involving Type 2 Diabetes patients and cultured cell systems. Based on preliminary data from our initial studies Type 1 patients, changes in the NMR lipoprotein subclass profile will be emphasized. Project 2 will elucidate interactions between inflammation, modifications of lipoproteins, and autoimmunity in vascular disease risk. These novel concepts are also based upon exciting preliminary data pertaining to LDL-antibody complexes. Project 3 will pursue interesting preliminary data and define the role of the kallikrein-kinin system in vascular disease complications, with effects on mitogenesis and matrix production. Project 4 will assess the role of the Insulin Resistance Syndrome and novel factors secreted from adipocytes in the pathophysiology of biochemical risk factors and cardiovascular complications. Cores include an Administrative Core, a Biostatistics and Epidemiology Core which will link with the trials data coordinating centers, and Molecular and Statistical Genetics Core. Investigators will work in close collaboration with the VA Executive Committee, Study Centers, the Hines Coordinating Center, and some of the other ancillary studies. All data analysis involving clinical outcomes will be performed at the Hines Coordinating Center. There is true synergism among the projects at both scientific and logistical levels. The Program Project design allows for interactions among multidisciplinary investigators studying the same cohort, which will define how multiple pathological processes interact at the level of the arterial wall to promote atherosclerosis.

To examine the epidemiology of renal disease and its relationship to cardiovascular disease.