Active clinical trials for "Pulmonary Embolism"

Identify risk factors for developing chronic thromboembolic pulmonary hypertension after acute pulmonary embolism. Determine echocardiographic predictors of chronic thromboembolic pulmonary hypertension. Determine the radiological predictors of chronic thromboembolic pulmonary hypertension in CT pulmonary angiography.

to detect the incidence of CTEPH patients. Primary outcome To predict CETHP in symptomatic patients after pulmonary embolism episode. Secondary outcome: On Echocardiography revealed RV dysfunction which are peak TR Velocity , the RV/LV basal diameter ratio, flattening of the IVS, RV acceleration time and/or midsystolic notching, IVC diameter with decreased inspiratory collapse and RA area.

Assess performance of PERFORM score in predicting outcome in CTPA confirmed patients. Compare PERFORM score with the currently validated PESI in risk stratification of patients

The clinical manifestations of pulmonary embolism vary greatly from the absence of specific clinical symptoms to cardiogenic shock or cardiac arrest. Clinical form of EP represented by "lung superinfection", also called "pulmonary embolism superinfected" is common and represents up to 30% of initial clinical presentations; she been few evaluations in clinical research. The reality of the bacterial infection remains controversial and the clinical presentation often leads to the prescription of empirical antibiotic therapy, often unnecessary in many cases. Number of antibiotic prescriptions are probably inappropriate. Fever has long been recognized as a sign associated with pulmonary embolism. Stein et al reported a temperature above 37.5 ° C on 50% of patients with acute pulmonary embolism without actually clarified whether this was related to temperature with a pulmonary embolism or other associated cause. Murray et al estimated that greater than 38 ° C was explained by pulmonary embolism in 57.1% of patients while in the PIOPED study, only 14% of patients had fever with no other cause identified as pulmonary embolism. Fever due to pulmonary embolism is often low intensity (often less than 38.3) and of short duration, with a peak on the day of pulmonary embolism and a gradual decrease of about 1 week. The pathophysiology of fever in pulmonary embolism has not yet was completely clarified. It is suggested that a combination of several factors involved pyrogenic myocardial tissue necrosis and releasing pro-inflammatory cytokines, hemorrhage, vascular irritation or inflammation, atelectasis or local superinfection. Since 2004, the PCT has become a marker helping the initiation of antibiotic therapy in patients with community-acquired pneumonia. This is especially verified in patients admitted for acute exacerbation of chronic obstructive bronchitis. In the latter case, the use of PCT reduces inappropriate antibiotic prescribing. Thus helping the clinician by measuring biomarkers such as PCT is based on writing an algorithm leading or not to use antibiotics. The use of an algorithm involving the PCT could just as for infectious pneumonia or COPD, of interest in the febrile pulmonary embolism to distinguish febrile forms related to bacterial infections febrile forms of EP to other causes.

Plastic and reconstructive surgeons consistently create large, raw surfaces as part of their operative procedures. Thus, plastic & reconstructive surgery patients are among those at highest risk for anticoagulant-associated bleeding adverse drug events (ADEs). This study seeks to optimize both the safety and effectiveness of post-operative enoxaparin by comparing aFXa levels, bleeding events, and VTE events among plastic & reconstructive surgery patients randomized to receive two different enoxaparin dose regimens.

Following acute pulmonary embolism (PE), up to a third of patients develop post-PE syndrome described as having persistent breathlessness (dyspnea), impaired exercise capacity, and a reduced quality of life. The post-PE syndrome includes patients with chronic thromboembolic pulmonary hypertension (CTEPH), patients with chronic thromboembolic disease (CTED) those with an obstruction of the pulmonary arteries without pulmonary hypertension, and patients with post-PE related dyspnea without obstruction or pulmonary hypertension. Although therapies exist for the most severe form of the post-PE syndrome (CTEPH) - for most patients there are no available disease specific therapies that reduce symptoms. Despite studies showing increased breathlessness and abnormal exercise responses in patients with CTED, a detailed examination of what causes breathlessness in post-PE syndrome has never been undertaken. It is suspected that reduced blood flow to the lungs contributes to the feelings of breathlessness, particularly during exercise. This study will use inhaled nitric oxide, a medication that increases blood flow to the lungs. Inhaled nitric oxide is used primarily in hospitalized patients in the intensive care unit with respiratory failure, its use in people with post-PE syndrome is experimental. The investigators believe use of this medication may help to relieve symptoms of breathlessness. In order to test this medication, in volunteers with post-PE syndrome, the following will be measured: 1) breathlessness, 2) the signal to breathe sent from the brain to the lungs, 3) the activity of the muscles involved with breathing and 4) the amount of different gasses in the blood during exercise. The investigators will compare breathlessness and exercise tolerance during exercise while receiving: 1) a placebo (normal medical grade air) and 2) inhaled nitric oxide (a medication that improves blood flow to the lungs). By comparing symptoms during these two conditions, it is hoped to obtain a better understanding of what causes breathlessness in people with post-PE syndrome. This clinical research study will recruit approximately 20 clinically stable participants with CTED or post-PE related breathlessness.

To date, the investigators have successfully employed a radiotracer (18F-sodium fluoride) as a marker of necrotic inflammation in human atherosclerosis. The investigators aim to further the mechanistic understanding of atherothrombosis by studying the activation of glycoprotein IIb/IIIa receptors in cardiovascular thrombus using the novel platelet radiotracer (18F-GP1). Binding of 18F-GP1 to activated platelets in venous and arterial thrombi has already been demonstrated in pre-clinical studies and a phase 1 trial in man. If successful, this study would define the role of the glycoprotein IIb/IIIa receptor within in vivo thrombosis across a range of cardiovascular diseases.

The central hypothesis of this proposal is that the addition of a theory-informed "nudge" to a clinical decision support (CDS) tool will address identified behavioral barriers to use and significantly improve adoption by providers. Nudges are applications of behavioral science, defined as positive reinforcement and indirect suggestions that have a non-forced effect on decision making. This study will use a behavioral theory-informed process to develop a new CDS tool that includes a nudge that addresses barriers to adoption.

This randomized phase III trial studies the side effects of and compares apixaban and dalteparin in reducing blood clots in patients with cancer-related venous thromboembolism. Venous thromboembolism is a condition in which a blood clot forms in a vein and then breaks off and moves through the bloodstream. Patients with cancer are at increased risk for venous thromboembolism. Apixaban and dalteparin are drugs used to prevent blood clots from forming or to treat blood clots that have formed. It is not yet known whether apixaban or dalteparin is more effective in reducing blood clots in patients with cancer related venous thromboembolism. ADAM-VTE

Epidemiological studies have shown a 2-3 fold increased long-term risk of arterial cardiovascular disease after venous thrombosis, most predominant in the first year following initial venous thrombosis. The results of recent observational studies that showed 40-50% risk reductions for first venous thrombosis occurrence when using a statin are in this aspect promising. The results are also somewhat surprising, because the mechanism behind this effect is unclear. Dyslipidemia may be the most plausible explanation to be considered. However, as dyslipidemia is not related to an increased risk of venous thrombosis, it is unlikely that statins decrease venous thrombosis risk by lipid lowering activities. Recent observations indicate that coagulation can activate the initial formation of atherosclerosis. Our hypothesis is therefore that the coagulation profile in persons with venous thrombosis is improved when using a statin, ultimately leading to less atherosclerosis: another well known property of statin use.