Active clinical trials for "Atherosclerosis"

The study hypothesis is that the bioactive compounds of sea buckthorn berries (Hippophaë rhamnoides), their fractions, and bilberries (Vaccinium myrtillus). have positive effects on lipid and carbohydrate metabolism and will thus reduce the risk of developing metabolic diseases.

The main objective of TANSNIP-PESA is to determine in a population of asymptomatic bank employees with high and low imaging defined cardiovascular disease (CVD) risk the effectiveness of a comprehensive 3-year worksite-based lifestyle intervention consisting of 12 personalized lifestyle counseling sessions, a Fitbit physical activity tracker and a sit-stand Workstation.

Statins are commonly prescribed to lower cardiovascular risk in primary and secondary prevention. Despite their well known efficacy, statin withdrawal is a common event. Even a short term statin withdrawal can have dramatic consequences on atherosclerotic plaque stability, owing to a rebound in cholesterol levels and inflammation. The effects of a short term statin withdrawal on endothelial progenitor cells (EPC) and monocyte/macrophage polarization is unknown. In this study, the investigators will explore the effects of a 5-day statin withdrawal on EPC and monocyte/macrophage polarization, together with other inflammatory biomarkers in type 2 diabetic patients. The investigators hypothesize that statin withdrawal determines a reduction in EPC levels and an inflammatory cell polarization. Patients will be randomized to continue their habitual statin regimen or to withdraw statin. At baseline and 5 days later, blood samples will be collected for experimental measures.

Atherosclerotic plaque uptake of 18F-sodium fluoride (NaF) in positron emission tomography with computed tomography (PET-CT) was recently shown to correlate with clinical instability in patients with CV disease. We hypothesize that rosuvastatin reduces 18F-NaF plaque uptake. Our group will scan coronary, aortic and carotid arteries of high-risk CV subjects with 18F- NaF-PET-CT. Individuals with 18F-NaF-positive plaques will be treated with rosuvastatin for six months, followed by 18F-NaF-PET-CT re-evaluation.

The main purpose of this single-center study is to determine the spectrum and levels of cardiospecific circulating microRNAs in patients with different stages of atherosclerosis according to 640-slice multispiral computed tomography (MSCT).

Atherosclerosis - the main cause of cardiovascular diseases - starts already in childhood. The Tyrolean Early Vascular Ageing-study aims to improve the vascular health of Tyrolean adolescents by a multi-layer intervention program.

The prevailing view in telomere epidemiology is that leukocyte telomere length (LTL) is associated with atherosclerotic cardiovascular disease (ACVD) since it serves as a biomarker of the cumulative burden of inflammation and oxidative stress during adult life. However, our recent results indicate that telomere length (TL) is mainly determined before adulthood, by TL at birth and TL attrition during growth. They also demonstrate that short telomeres precede the clinical manifestation of atherosclerosis. The investigators therefore hypothesize that LT is not a simple marker, but a major determinant of arterial aging. Two mechanistic hypotheses may explain an active role of short telomeres in accelerated arterial aging and development of ACVD. The first is that a short TL at the leukocyte level reflects a short TL in endothelial progenitor cells (EPC). Cell replicative capacity being TL-dependent, short telomeres in the EPC would therefore be responsible for diminished replication capacity and vascular repair potential, thereby increasing the vulnerability for developing age-related arterial diseases. The second hypothesis is that a short LTL reflects short TL in arterial wall cells, leading to an increase in the number of senescent vascular cells. Senescent cells are known to alter their secretion pattern, a phenomenon called senescence-associated secretory phenotype (SASP), and thus contribute to tissue injury by promoting inflammation and tissue remodeling leading to lesion progression. These assumptions cannot be tested by LTL measurements alone. The investigators propose, therefore, a model that makes it possible to examine different elements of TL dynamics in different tissues and cell types: leukocytes, circulating EPCs, in situ EPCs and arterial resident cells (mainly smooth muscle cells) in patients with or without atherosclerosis. Our model is based on the following observations: TL is synchronized (equivalent) across somatic tissues/cells of the newborn: an individual with short telomeres (relative to his pairs) in one tissue should also have short telomeres (relative to his pairs) in other tissues. TL in EPCs (both circulating and in situ) determines the cell proliferative ability and therefore capacity for vessels repair during aging. TL in the cells of the arterial wall determines the number of senescent cells that therefore contribute to tissue injury through their change of phenotype. The general aim of the present project is to examine the mechanistic links between arterial aging and TL in these different cell types.

In the entire world most people die from cardiovascular disease. Death is primarily from myocardial infarction (MI) and stroke which are most often caused by rupture of atherosclerotic plaques. Patients with high-grade, i.e. ≥ 70% carotid artery stenosis are at especially high risk. Magnetic Resonance Imaging (MRI) studies show that two features inside plaques that are associated with the risk of plaque rupture and subsequent cardiovascular events are: lipid rich necrotic core (LRNC) and intraplaque hemorrhage (IPH). MRI studies on carotid artery plaques typically relies on proton-density-weighted fast-spin echo, blood-suppressed T1- and T2-weighted gradient-echo sequences. The end-result is nonquantitative measures, where plaque features are identified due to their relative signal intensity. To address these problems of non-specificity, we developed a quantitative MRI (qMRI) technique based on Dixon sequences. The study intention is to enable in-depth analysis of plaque features and their relation to clinical data. For example there is an insufficient understanding of associations between lipid biomarkers and plaque contents. Our hypothesis is that we can identify quantitative changes in both plaque and lipid biomarkers after one year of optimized cardiovascular risk management (including treatment with lipid lowering drugs), and establish if there is any associations between these features. Because there is a well-established link between systemic inflammation and the presence of atherosclerotic plaques we will also study the relationship between LRNC and IPH as measured by qMRI versus circulating markers of inflammation. Method: Patients with known carotid stenosis are invited for a baseline visit and a 1-year follow up visit. The study visits include clinical assessment, blood tests, patient interview and magnetic resonance imaging of the carotid arteries. All participants are offered optimized cardiovascular risk management through the individual assessment by the study physicians.

The purpose of this study is to compare the effects of homogenized, unhomogenized and skimmed milk on postprandial metabolism in healthy overweight men

The investigators hypothesized that circulating EMP is a useful surrogate marker of early stage of endothelial damage. To determine the effects of chronic smoking on circulating EMP, from healthy volunteers who have habit of chronic smoking, peripheral blood is drawn at the time of flow-mediated dilatation (FMD) examination. Spot urine is also collected. Circulating EMPs are counted using flow-cytometry. After 2-week smoking cessation, the measurements were repeated.