Active clinical trials for "Pulmonary Embolism"

The primary objective is to demonstrate the clinical benefits of diclofenac (added to standard anticoagulant therapy) over placebo in normotensive patients with acute symptomatic pulmonary embolism and right ventricular dysfunction. The secondary objective is to assess the safety after administration of diclofenac in normotensive patients with acute symptomatic pulmonary embolism and right ventricular dysfunction.

The purpose of this study is to determine if tenecteplase plus enoxaparin is safe and effective in the treatment of patients with severe submassive pulmonary embolism.

To investigate venous thromboembolism in two carefully conducted prospective epidemiologic studies of African American and white adults -- the Atherosclerosis Risk in Communities (ARIC) Study and the Cardiovascular Health Study (CHS).

The purpose of this study is to examine the degree to which pulmonary embolism (clot) can be dissolved when treated with a very low dose of a systemic thrombolytic drug (clot buster) along with standard anticoagulant therapy as compared to the standard of care anticoagulant therapy alone.

In an open-label parallel groups blinded-endpoint randomized clinical trial, the investigators aim to assess the safety and efficacy of conventional catheter-directed thrombolysis (CDT) vs anticoagulation monotherapy on outcomes of patients with acute intermediate-high risk pulmonary embolism. The investigators hypothesize that CDT will have a superior efficacy and safety compared with anticoagulation-only therapy regarding the proportion of patients with a right ventricle to left ventricle (RV/LV) ratio > 0.9 at a 3-month follow-up by an imaging core laboratory, major bleeding, severe thrombocytopenia, or vascular access complication.

This prospective, multicenter, multinational, phase IV, interventional single-armed (management) trial will focus on the safety, efficacy and cost-effectiveness of a new oral anticoagulant in the treatment of patients with acute intermediate-risk PE based on validated imaging (echocardiographic or CT angiographic) and laboratory biomarker (circulating levels of cardiac troponins and natriuretic peptides) parameters and their combinations.

Blood clots in the leg veins, known as deep vein thrombosis, are important because they may travel to the lung (known as pulmonary embolism) and cause death. Blood clots are treated with blood thinners, or anticoagulants. The preferred treatment is an anticoagulant known as low molecular weight heparin (LMWH). LMWH is given by an injection under the skin, which is convenient for patients because they can self-administer this medication at home, and no blood testing is required. However, LMWH is cleared from the body through the kidneys, so patients who have kidney failure are generally not treated with LMWH because they may be at a higher risk of bleeding. One type of LMWH, known as tinzaparin, may be less dependent on the kidneys for clearance and may not increase in patients with kidney failure. The investigators would like to use tinzaparin to treat patients who have deep vein thrombosis or pulmonary embolism, and who also have kidney failure. The purpose of this study is to determine whether the blood thinning effects of tinzaparin build up, or accumulate, in patients with varying degrees of kidney failure compared to patients without kidney failure. The blood thinning effects will be measured using a blood test known as an anti-Xa level. Patients will be followed over the time they receive tinzaparin and those patients who are found to have potentially high levels of tinzaparin (based on the anti-Xa level) will have their tinzaparin dose adjusted. The investigators believe that the levels of tinzaparin will not accumulate to potentially dangerous levels in a significant number of patients with kidney failure.

This study seeks to uncover potential genetic determinants of pulmonary embolism (PE). Our translational goal is to ultimately identify certain genetic markers that will allow us to stratify patients in terms of their PE risk post total knee or total hip arthroplasty. The clinical implications for this study would allow for better patient care by lowering the risk of post-operative bleeding while still preventing symptomatic PEs and deep vein thromboses (DVTs). We look to sample patients who have a history of PE after undergoing total knee or total hip arthroplasty. We will sample these patients' blood DNA for a set of DNA genetic markers. To do so, we will utilize the Taqman assay, which is a PCR-based 5'-nuclease allelic discrimination assay to determine single nucleotide polymorphism (SNP) genotypes at specified loci. The region flanking the SNP is amplified using two allele-specific fluorescent probes, allowing for the detection of each allele in a single tube. Using this assay, there is no post-PCR processing because the probes are included in the PCR reaction (Hui). Using this approach, we will measure the frequency of genetic mutations in patients who have developed a PE after a total joint arthroplasty. This data would then be used to perform a prospective study to determine a subset of genetic markers that can definitively be used to risk stratify patients.

The goal of this NIH-sponsored study is to characterize three biomarkers derived from 129Xe gas exchange MRI and to understand how they change in response to interventions.

There is no randomized controlled trial examining surveillance ultrasonography for lower limb DVT in high-risk medical-surgical ICU patients compared to a clinician-directed approach. The DETECT randomized controlled trial addresses the question of whether surveillance ultrasound in critically ill patients by facilitating DVT detection reduces the incidence of PE and lowers all cause 90-day mortality. The primary outcome is 90-day all-cause mortality.