View clinical trials related to Atherosclerosis of Artery.
Filter by:The aim of the study is to investigate if lesion preparation with a ScoreFlex balloon compared to a standard non-compliant balloon improve vascular healing and minimize lumen reduction after implantation of a Magmaris bioresorbable scaffold.
This is a randomized study comparing Excimer laser and drug coated balloon Versus Excimer laser and plain balloon versus plain balloon and drug coated balloon to Treat femoropopliteal in-stent restenosis
Our group has developed a device called "Velocidad Onda de Pulso Indice Tobillo Brazo (VOPITB)" . In this device the oscillometric method is used for easily and accurately measure the pulse wave velocity PWV in the arms and legs separately, allowing new arterial stiffness indices to be studied (sum, difference, ratio, baPWV and CAVI). The aim of our study will be to validate the PWV measures by VOPITB with other references devices that measures arterial stiffness. Moreover we will perform a clinical study to assess the clinical utility of VOPITB.
This study aimed to evaluate the association between periodontitis and atherosclerosis of the cerebral vasculature in the Chinese population.
Atherosclerosis is a civilization disease, which pathophysiology is based on chronic inflammatory response in the wall of vessels that is caused by increase of pro-inflammatory substances. It is a significant challenge for diagnostics and pharmacology. This disease occurs in over 60% of the population over 70 years old. There are many factors that are responsible for this process including group of the arachidonic acid metabolism products - leukotriens, especially leukotriene E4 (LTE4). The effect of these factors was described as the base of pathology not only cardiovascular diseases but also the base of development of asthma and other allergic diseases. The substance which blocks the activity of these factors - montelukast - is a common method of treatment in asthma. The aim of this project is to investigate the influence of cysteinyl leukotriens receptor antagonists on lower limb arteries reocclusion rate in patients with peripheral artery disease (PAD) after endovascular treatment. During previous years we conducted a prospective study, which helped us evaluating the dynamics of leukotriens and thromboxane levels in patients with PAD, who underwent endovascular treatment - peripheral transluminal angioplasty (PTA). We established for the first time the dependence between the increased level of LTE4 in urine (uLTE4) and restenosis or reocclusion occurrence, which translates to the necessity of further procedures and a decrease in the quality of life. We should ask ourselves a question: Is blocking of cysteinyl leukotriens reaction as proinflammatory and proliferative factors, by the use of receptor CysLT1 antagonists going to decrease the quantity of restenosis and reocclusions after endovascular treatment? Within the project performed in the Angiology Department of Jagiellonian University among the patients suffering from PAD and fulfilling all inclusion criteria, the randomized double-blinded clinical study will be performed. Patients will be assigned to two groups: Treatment Group (which will be receiving cysteinyl leukotriene antagonist (montelukast) in a dose of 10mg/day for 12 months) and Control Group to which placebo will be administered. Among all patients population, at every visit at 1., 3., 6., and 12-month clinical state, ultrasound, hemodynamic parameters, and endothelium imaging will be performed as well as uLTE4 measurements. A comparison of the results between both groups will give us an answer if blocking uLTE4 receptors may become a breakthrough in future atherosclerosis treatment. The mechanisms, which lead to restenosis is still not fully understood, and currently used methods of treatment - antiplatelets, anti-proliferative drugs, and anticoagulants - are not fully effective. Thanks to this research the knowledge about treatment and prevention of atherosclerosis will be increased, which will be connected with future better patient care, especially patients with PAD.
As previously reported (IJC Heart & Vasculature 2017; 17: 11.), our epidemiological analysis showing high incidence of cancers in patients with atherosclerotic cardiovascular diseases as compared with those with non-atherosclerotic cardiovascular diseases may imply a clinical possibility of a role of atherosclerosis in cancer developments. In the present study, to address our hypothesis that cancer developments may come with a strength of atherosclerosis, we traced an incidence of cancers in a total of 8,856 patients with coronary artery diseases (CAD) for a median follow-up of 1,095 days (interquartile range, 719-1,469 days) using the Sakakibara Health Integrative Profile (SHIP) database.
The role of methylase system and Proprotein convertase subtilisin/kexin type 9 (PCSK9) in the accelerated atherosclerotic progression of diabetic patients is unclear. Authors will evaluate methylase activity and PCSK9 in carotid plaques of asymptomatic diabetic and non diabetic patients, as well as the effect of statin added to PCSK9 inhibitors (PCSK9i) therapy vs. statin alone in diabetic plaques. Plaques will be obtained from 43 type 2 diabetic and 30 non diabetic patients undergoing carotid endarterectomy. Diabetic patients will receive statin therapy (n 23) or statin plus PCSK9i (140 mg of evolocumab; n 20) or placebo (n 23) for 4 months before scheduled endarterectomy. Plaques will be analyzed for macrophages (CD68), T-cells (CD3), inflammatory cells (HLADR), methylase activity, nuclear factor (NF)-KB, tumor necrosis factor (TNF)-alpha, nitrotyrosine, matrix metalloproteinase (MMP) and collagen content (immunohistochemistry and enzyme- linked immunosorbent assay. Authors' study hypothesis is that methylase and PCSK9 over-activity will be associated with enhanced inflammatory reaction and NF-KB expression in diabetic plaques. Secondly, the inhibition of methylase activity in atherosclerotic lesions of diabetic patients by metformin plus SLGT2i might be associated with morphological and compositional characteristics of a potential stable plaque phenotype, possibly by down regulating NF-KB-mediated inflammatory pathways.
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.
Cardiovascular disease is a common diagnosed and treated condition in private practices of primary health care. There is growing evidence that atherosclerotic plaques as predictors for stroke and heart attack are more prevalent than expected based on the clinical score in people with low risk for stroke and heart attack . Diagnosing atherosclerotic plaques can help to decide if a lipid lowering therapy should be prescribed even if the clinical risk score is low or on the other hand if they can be observed even in high lipid levels.
The researchers are trying to see whether contrast-enhanced ultrasonography, shear wave elastography, strain imaging, and 3-D volume ultrasonography improves arterial wall visualization and identifies arterial elastic properties among individuals with fibromuscular dysplasia (FMD), atherosclerosis, personal history of spontaneous coronary artery dissections (SCAD), or personal history of segmental arterial mediolysis (SAM) that may be different compared to those without the aforementioned conditions.