Active clinical trials for "Thrombosis"

The goal of this initial proof of principle single arm cohort trial is to determine if contemporary endovascular venous intervention, compared with a 1:1 propensity-matched medical therapy arm of the ATTRACT trial, significantly reduces the 2-year occurrence of Post Thrombotic Syndrome (PTS) in subjects with symptomatic proximal Deep Vein Thrombosis (DVT).

ST-elevation myocardial infarction (STEMI) is mostly caused by the rupture or the erosion of a vulnerable atherosclerotic plaque, initiating with intraluminal thrombosis and resulting in total occlusion of the coronary artery. Thrombus formation is a complex and dynamic process involving flow, blood cells and several plasma proteins, and it has not been clearly elucidated. To define - through proteomic approach - the composition of occluding thrombus and its time changes in patients with STEMI, trying to identify novel biomarkers of coronary thrombosis.

DESTINY D-Dimer is an observational feasibility study, and a collaboration between the University of South Wales and Cwm Taf Morgannwg University Health Board (CTMUHB). The study is based at St. John's Medical Practice in Aberdare, where participant recruitment will take place. Blood D-dimer data will be collected from CTMUHB Pathology Laboratory services, at Prince Charles Hospital. Study blood samples will be obtained by the research student, LAH, under the direction of Dr Owen Thomas at St John's Medical Centre. The participant data will be collected by the research student who will conduct a Wells' Risk Score and perform D-dimer POC tests to generate quantitative data. Data will later be compared by the research student with the diagnoses obtained from Secondary Care at Prince Charles Hospital via analysis of medical records to include a laboratory generated D-Dimer results and additional diagnostics (eg. Doppler). A laboratory based analytical verification of D-dimer POC tests will be undertaken to compare with the current laboratory method. The study will compare the data from the D-dimer POC tests and those gained using laboratory methods at Prince Charles Hospital.

The outbreak at covid-19 is caused by the SARS-CoV-2 virus. This virus can be responsible for severe respiratory failure but also for extra-respiratory organ dysfunctions associated with severe inflammatory stress. The endothelium is an important structure of the blood vessels and is implicated in the organ failure of many patients admitted in intensive care units. It could be affected by the virus and its alteration may explain the organ dysfunction of covid-19 ICU patients as well as the thrombotic processes frequently obstructed in this infection.

Patients with COVID-19 in the Intensive Care Unit (ICU) or hospitalized with severe form have a poor prognosis (almost 30% rate of death). They present often a high cardiovascular risk profile (almost 30% of hypertension and 19% of diabetes). Troponin has been described to be elevated in a high proportion of patients (one fifth of all patients and 50% of non-survivors) suggesting the possibility of cardiomyopathies. High levels of DDimers (81% of non survivors) and fibrin degradation products are also associated with increased risk of mortality suggesting also the possibility of venous thromboembolism. Therefore, screening for cardiomyopathies and venous thromboembolism could represent an important challenge for patients with COVID-19 management.

An estimated 22% of the global population is at an increased risk of a severe form of COVID-19, while one in four coronavirus patients admitted to intensive care unit will develop a pulmonary embolism. A major public health question remains to be investigated: why COVID-19 is mild for some, critically severe for others and why only a percentage of COVID-19 patients develop thrombosis, despite the disease's proven hypercoagulable state? Patients' intrinsic characteristics might be responsible for the deep variety of disease forms. Our study aims to assess the validity of the hypothesis according to which underlining genetic variations might be responsible for different degrees of severity and thrombotic events risks in the novel coronavirus disease. Moreover, we suspect that prothrombotic genotypes occuring in the genes that encode angiotensin-converting enzyme (ACE-DEL/INS) and angiotensinogen (AGT M235T) are involved in the unpredictable evolution of COVID-19, both in terms of severity and thrombotic events, due to the strong interactions of SARS-CoV-2 with the renin-angiotensin-aldosterone system (RAAS). Therefore, we also aim to assess the validity of the theory according to which there is a pre-existing atypical modulation of RAAS in COVID-19 patients that develop severe forms and/or thrombosis. Our hypothesis is based on various observations. Firstly, there is a substantial similarity with a reasonably related condition such as sepsis, for which there is a validated theory stating that thrombophilic mutations affect patients' clinical response. Secondly, racial and ethnic genetic differences are responsible for significant dissimilar thrombotic risks among various nations. Thirdly, an increase in stroke incidence has been reported in young patients with COVID-19, without essential thrombosis risk factors, favoring the idea that a genetic predisposition could contribute to increase the thrombotic and thromboembolic risk. Fourthly, the plasminogen activator inhibitor (PAI)-1 4G/5G inherited mutation was found to be responsible for a thrombotic state causing post-SARS osteonecrosis.

Portal vein thrombosis (PVT) is defined as an obstruction of the portal vein. The prevalence of PVT is 10-25% and incidence is about 16% in cirrhotic patients. PVT leads to increased intrahepatic resistance, decreased portal velocities, splanchnic vasodilatation, and stagnant flow. Portal vein recanalization (PVR) with transjugular intrahepatic portosystemic shunt (TIPS) is aimed at restoring main portal vein (PV) flow in chronic PVT. In this study, we will review the safety and outcomes of this approach.

This prospective controlled study examines the use of Doppler ultrasound as a means to screen elective plastic surgery patients for the presence of deep venous blood clots both before and after surgery. This is a noninvasive technique that is known to be both sensitive and specific for the detection of deep venous thromboses in the lower extremities. This method may make it unnecessary to select patients for prophylactic anticoagulation, which poses additional risks to the patient.

The retinal vein occlusion (RVO) is the second most common retinal disease after diabetic retinopathy, and is a common cause of unilateral visual loss. The risk factors that predispose to RVO are many and are generally the same as those found in vascular alterations involving other parts of the body, as in the case of stroke or coronary heart disease. Several authors have attempted to determine whether the pathogenesis of RVO can be of arterial type, considering the disease as consequent to atherosclerosis, rather than resulting from venous disease. Although less frequent than the other diseases RVO affects considerably on health care costs. Direct medical costs showed that in one year a patient with this disease has a higher than average cost for a patient with hypertension or glaucoma. Knowing the prevalence of the disease in Italy and identify modifiable risk factors, recognizing additional risk factors related to gender, genetic predisposition and especially the social-economic and cultural background in the pathogenesis of RVO, are the objectives that led to the planning of this study. In order to assess the prevalence of the disease and the current "clinical practice" we aim to create an online register between Italian specialist centers (ophthalmic emergency care and thrombosis centers) with immediate portability and usability of the data.

The aim of this study is to estimate the incidence of spontaneous and provoked recurrent VTE and the bleeding events during a 10-year follow-up in subjects experiencing a first VTE stratified according to % AT levels and to treatment schedule (long-term vs 6-12 months oral anticoagulation+transient prophylaxis during high risk periods)