View clinical trials related to Plaque, Atherosclerotic.
Filter by:Patients treated at the Hôpital Nord de Marseille for at least one smoking-related pathology (atheroma, chronic bronchitis, non-progressive cancer > 5 years) or with eligibility criteria for lung cancer screening (inclusion criteria in the NLST or NELSON studies or American recommendations) Interventional study with minimal risks and constraints, with evaluation of lung cancer prevalence; immunological, blood inflammatory and microbiota profile Determine the maximum clinical, radiological, and biological phenotyping completeness rate following the implementation of a new lung cancer screening care pathway with multidimensional clinical, radiological, and biological phenotyping capabilities
Lipid accumulation, with mostly emphasized role of low-density lipoprotein cholesterol (LDL-C), is the pathogenetic cornerstone of atherosclerotic cardiovascular disease. Standard hypolipidemic therapy, based on statins and ezetimibe, does not always decrease LDL-C levels enough to achieve therapeutic goals. A novel and promising direction is inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9) in hepatocytes, subsequently reducing LDL-C receptor degradation and increasing intracellular LDL-C uptake. Aim of this study is to evaluate the effect of optimal hypolipidemic pharmacotherapy, including PCSK9 inhibitors and inclisiran, on plasma lipid profile and qualitative features of atherosclerotic plaques in very-high cardiovascular risk patients. This study enrolls patients with an established atherosclerotic cardiovascular disease, receiving PCSK9 inhibitors or inclisiran as add-on treatment to statins in maximally tolerated dose and/or ezetimibe. Effect of hypolipidemic pharmacotherapy is evaluated by analysis of plasma lipid profile parameter changes and qualitative features of atherosclerotic plaques using Near-Infrared Spectroscopy Intravascular Ultrasound Imaging (NIRS-IVUS) method. Results of the study would be sufficient for complementing evidence regarding therapeutic strategy in very-high cardiovascular risk patients.
To predict coronary atherosclerosis progression in patients with acute coronary syndrome by the use of intracoronary imaging methods. To investigate the ability of NIRS to detect vulnerable plaque characterized by the presence of OCT-defined TCFA To study the influence of gene polymorphisms (in genes playing role in vessel dilatation) on the progression of coronary atherosclerosis and clinical outcomes
Background: Fat and calcium can build up as plaque in artery walls. The Agatston score measures plaque using computed tomography (CT) that does not use an injected contrast agent. Plaque in the arteries of the pelvis and abdomen is linked to cardiovascular disease (CVD) risk factors. It also may affect cancer. But abdominal CTs use a contrast agent (CECT). Therefore, the Agatston score cannot be used. Researchers want to find a way to measure plaque in CECTs. This will help them use abdominal CTs to measure plaque without extra radiation. Objective: To measure atherosclerotic plaques on CECT in a group of males. Eligibility: Men ages 30-90 with prostate cancer (proven with biopsies) who have abdomen CT studies in the PACS (picture archiving system) in the Clinical Center. Also, men or women of all ages who have multiphase abdomen and pelvic CT studies that are in the PACS. Design: This study will use data gathered since 1/1/2013. Data will also be taken from protocol 03-CC-0128 and clinical trials 15-C-0124, 16-C-0048, 14-C-0112, and 04-C-0274. Participants from these studies have allowed their samples to be used in the future. Participants will be found via keyword searches on NIH databases. Their CT and MRI scans will be used. Data such as age, race, disease, and treatment will be used. Results of other tests may be used. The plaque in participants abdomen and iliac arteries will be measured. It will be compared with biomarkers related to CVD and prostate cancer, such as weight, age, and race. This study will take place at one site. Data will be stored on secure computers. Printouts will be kept in locked rooms.
Extensive arterial occlusion significantly reduces arterial perfusion, and may eventually lead to Critical Limb Ischemia (CLI). The pathology gives rise to symptoms such as ischemic pain, slow healing wounds at lower extremity and gangrene. It places patients with multi-segment occlusion at high risks of amputations and mortality. The treatment methods for such long occlusive lesions are limited. Traditionally, the standard of care would be surgical revascularization. This is because lesion length have been identified in several studies as an independent risk factor for the development of restenosis after angioplasty and/or stenting. However, thanks to recent advances in endovascular techniques, such as the utilization of subintimal technique for crossing long segment occlusions, it is now possible to employ endovascular techniques for suitable patients.The re-establishment of an in-line flow, even if only temporary, can allow tissue healing, which is vital in achieving limb salvage. In addition, the use of Drug Coated Balloons (DCB) can potentially reduce restenosis rate, as Sirolimus have an anti-proliferative effect. To date, there are few studies that have evaluated the performance of DCB in lesions that are longer than 10cm. The investigators hope to evaluate the performance of the Selution DCB when used in treatment of such lesions
Non-obstructive coronary artery disease (CAD), particularly common in women, has been associated with impaired quality of life and risk of recurrent hospitalizations. Several studies have also demonstrated increased risk of incident acute coronary events and mortality. The main objective of the project is to assess the association between coronary artery plaque features by coronary CT angiography and long term prognosis in a large unselected population undergoing CT coronary angiography due to stable angina and suspected myocardial ischemia from the Norwegian Registry for Invasive Cardiology (NORIC) diagnosed with non-obstructive CAD by coronary CT angiography.
The aim of this prospective, open-label, randomized, single center study is to compare the effect of usual dose rosuvastatin plus ezetimibe and high-dose rosuvastatin on modifying atherosclerotic plaque.
Aim 1: To determine whether therapy with Alirocumab, compared to pre-treatment, will effectively improve carotid atherosclerotic plaque characteristics by reducing Ktrans and LRNC size. To achieve this goal, we will (a) enroll 30 subjects who are intolerant to high intensity statin therapy and only able to tolerate low potency statin or low weekly dose of high potency statin and have LDL-C ≥70 mg/dl; (b) initiate alirocumab at 150mg subcutaneously injection every 2 weeks; (c) perform carotid DCE-MRI scans at baseline, 3, 6 and 12 months; (d) perform quantitative analysis for vascular inflammation and plaque LRNC volume and other plaque characteristics; (e) compare vascular inflammation and LRNC volume between pre- and post-alirocumab at 3, 6 and 12 months. Aim 2: To examine associations between reductions in atherogenic lipids (LDL-C, Lp(a), non-HDL-C) and changes in atherosclerotic plaque characteristics. To achieve this goal, we will (a) perform laboratory assessments of lipids, lipoproteins and apo-lipoproteins at baseline and during the study; (b) compare lipids, lipoproteins and apo-lipoproteins levels between pre- and post-alirocumab; (c) correlate reductions in atherogenic lipids with changes atherosclerotic plaque characteristics.
To describe the natural history of the coronary atherosclerotic plaque development and progression over time by CCTA with demographic and laboratory data for refinement of risk stratification of patients referred for CCTA.
The EMERALD trial is a multinational, multicenter study. The patients presented with AMI/definite evidence of plaque rupture and had underwent coronary CT angiography from 1 month to 2 year prior to the event will be retrospectively searched. Plaques in the non-culprit vessels will be regarded as internal control to the ruptured plaque in the culprit vessel.