View clinical trials related to Atherosclerosis.
Filter by:This is a Phase III, placebo-controlled, double-blind, randomized study in participants with ASCVD and elevated LDL-C despite maximum tolerated dose of LDL-C lowering therapies to evaluate the efficacy, safety, and tolerability of subcutaneous (SC) inclisiran injection(s). The study will be a multicenter study in the United States.
Patients attending stroke prevention clinics and a premature atherosclerosis clinic at University Hospital in London, ON, Canada were recruited to the study. They completed a dietary questionnaire, provided stool samples and had blood drawn to measure plasma levels of metabolites produced by the intestinal bacteria.
Recent studies have shown that the systemic inflammation caused by periodontal disease (PD) can determine important changes in the coronary arteries, favoring atherosclerosis progression and development of acute coronary syndromes (ACS). The aim of ATHERODENT study is to assess the interrelation between PD, inflammation and progression of coronary atherosclerosis in patients with ACS. Material and methods: This case-control observational study will enroll 100 patients (group 1 - ACS and associated PD, and group 2 -ACS and no PD), in whom the following data will be collected: (1) demographic and clinical data, (2) cardiovascular risk factors, (3) full characterization of PD markers, (4) systemic inflammatory biomarkers, (5) imaging biomarkers derived from transthoracic echocardiography, computed tomography, coronary angiography, optical coherence tomography and intravascular ultrasound, and (6) assessment of the presence of specific oral bacteria in samples of coronary plaques collected by coronary atherectomy, which will be performed during percutaneous revascularization interventions, when indicated in selected cases, in the atherectomy sub-study. The follow-up will be performed at 1, 3, 6, 12, 15, 18 and 24 months. The primary endpoint of the study will be represented by the rate of major adverse cardiovascular events (MACE rates) in PD vs non-PD patients and in correlation with: (1) the level of systemic inflammation triggered by PD and/or by ACS at baseline; (2) the vulnerability degree of atheromatous plaques in the coronary tree (culprit and non-culprit lesions); and (3) the presence and burden of oral bacteria in atheromatous plaques. Secondary endpoints will be represented by: (1) the rate of progression of vulnerability degree of non-culprit coronary plaques; (2) the rate of progression of atheromatous burden and calcium scoring of the coronary tree; and (3) the rate of occurrence of left ventricular remodeling and postinfarction heart failure.
The study was designed to test whether short-term treatment with a very low-dose combination of fluvastatin and valsartan could induce improvement of endothelial function, arterial stiffness, vascular inflammation, oxidative stress and expression of protective genes in subjects with moderate cardiovascular risk.
Flaxseed consumption has beneficial effects on cardiovascular risk factors. In addition, the benefit of the Mediterranean-like diet in primary and secondary prevention of cardiovascular diseases has been shown.The purpose of this study is to investigate the effects of flaxseed consumption, alone and in combination with the Mediterranean-like diet, in adjunct to conventional medical treatment, in improving vascular endothelial function, plasma lipid profile and high sensitivity c-reactive protein of coronary artery disease (CAD) patients.
The aim of Multiplaque clinical study is to assess the vulnerability degree of the atheromatous plaques, before and after a myocardial infarction (MI), based on multiomics analysis, associated with invasive and non-invasive data. In this study, a multi-parametric model for risk prediction will be developed, for evaluation of the risk that is associated with the vulnerable coronary plaques in patients that have suffered an acute coronary syndrome. In the study, evaluation of the imaging characteristics of these coronary plaques will be performed with the use of CT, OCT, IVUS and invasive angiography. We will study the correlation between plaque evolution and (1) the degree of vulnerability at baseline, (2) multiomics profile of the patients and (3) clinical evolution during follow-up. Also, new techniques for evaluation of the functional significance of coronary stenoses will be studied and validated, such as calculation of the fractional flow reserve or determination of shear stress in areas that are localized within the near vicinity of the vulnerable coronary plaques.
At a given level of serum cholesterol, patients with T2D have an increased risk of developing atherosclerosis compared with nondiabetic subjects. In a previous study we showed that the interstitial fluid-to-serum gradient of LDL and VLDL cholesterol is reduced in T2D patients compared with healthy controls. This was not found for HDL cholesterol. However, the cholesterol transporting function of HDL particles from interstitial fluid from patients with T2D were lower than in healthy controls. We hypothesize that that the apo B-containing particles in T2D patients are more susceptible to be retained or consumed in the extravascular space. We are to study if skin biopsies from T2D patients contain more cholesterol than biopsies from healthy controls. We hypothesize that samples from T2D patients are richer in cholesterol, which could explain why VLDL and LDL cholesterol are lower in relation to their plasma levels in T2D.
The aim of the study is to compare clinical outcomes between intravascular imaging-guided versus angiography-guided percutaneous coronary intervention (PCI) in complex lesions.
Glucocorticoids (GCs) are a class of endogenous steroid hormones produced by the adrenal glands and controlled by the hypothalamic-pituitary-adrenal axis (HPA). One of the mechanisms of their action is achieved through ligand-receptor attachment to a class of cytosolic steroid hormone receptors termed Glucocorticoid Receptors (GRs). The formed ligand-receptor complex is a transcription factor involved in gene activation of anti-inflammatory products or repression of pro-inflammatory products [1]. Synthetic forms of GCs are a group of anti-inflammatory and immunosuppressive medications (e.g. Prednisone) that are widely used in clinical practice to treat inflammatory diseases (e.g. Rheumatoid Arthritis, Vasculitis, Asthma). The effectiveness of this class of drugs is limited by numerous adverse effects that include, but not limited to, insulin resistance, glucose intolerance, dyslipidemia, and hypertension, all of which are well known risk factors for cardiovascular diseases (CVD) [2,3]. Furthermore, recent research suggest that inflammation has a key role in development of CVD and can predict prognosis [4]. Inflammatory cells have an important role in the development of atherosclerotic lesion in the arteries. Blood monocyte-derived macrophages are involved in this process, and they infiltrate the lesion where they take up various forms of lipids (cholesterol - rich LDL, and oxidized LDL) as well as triglycerides - rich VLDL), followed by the formation of lipid-laden foam cells, the hallmark of early atherogenesis. Inflammatory cells and molecules as well as proteolytic enzymes secreted from inflammatory cells in the atherosclerotic lesion, have a central role in destabilizing the plaque (vulnerable plaque) leading to its rupture, which, in turn, induces thrombosis, and initiating acute coronary events [4,5]. Based on our understanding of the involvement of inflammation in the early development of atherosclerotic lesion, and our experience with the anti-inflammatory effects of synthetic GCs, a hypothesis emerged suggesting this class of drugs as a way to inhibit early atherosclerotic plaque formation, and to attenuate CVDs [6]. Research results in this field are surprising because while glucocorticoids treatment in humans increase the risk of CVDs [6,7,8,9], animal models shows the opposite, atheroprotection was shown in rabbits [10,11,12] and mice [13,14,15]. This paradox may be explained partially by the fact that clinical studies in this field are mainly conducted in patients with predisposing factors to develop CVD, either because of pre-existing traditional risk factors like Diabetes and Hyperlipidemia, or because of the pre-existing medical condition they are being treated for with GCs (e.g. Rheumatoid Arthritis). Mechanism based research to study the effects of GCs on atherogenesis, without confounding factors, is lacking. Only few studies were performed on GCs in healthy subjects but none of them explored their effects on foam cell formation [16,17]. Our study thus aims to further our understanding of the role of specific glucocorticoid, prednisone, in the process of atherogenesis. In order to achieve that we plan to study the following: 1. The effects of five days of treatment with prednisone on serum lipid concentration and oxidative stress. 2. an Ex-vivo study is planned where the serum of healthy human subjects treated with Prednisone, will be introduced to J774A.1 murine macrophage-like cell line, a well-studied macrophage foam cell formation model.
The innate immune system plays a pivotal role in the development and progression of atherosclerosis. Recently, it was reported that monocytes can develop a long-lasting immunological memory after stimulation with various microorganisms, which has been termed 'trained innate immunity'. This memory is induced by epigenetic reprogramming, in particular trimethylation of lysine 4 at histone 3 (H3K4me3). In this study, the investigators aim to investigate the immunophenotype of circulating monocytes in patients with elevated LDL cholesterol levels and the effect of statins on this phenotype.