Active clinical trials for "Atrial Fibrillation"

Atrial fibrillation (AF) occurs in 20% to 40% of patients after Coronary artery bypass grafting (CABG) and is associated with numerous detrimental sequelae. In postoperative period, the patient may be exposed to several proarrhythmogenic factors as increased endogenous catecholamines, inflammatory and oxidative mediators secondary to surgical stress and the systemic response to cardiopulmonary bypass, use of inotropic support. Steroids suppress the release of the above-mentioned inflammatory mediators. Dexmedetomidine is sympatholytic, along with anti-inflammatory properties. so combined use of both drugs may have synergistic effect to prevent post operative AF (POAF)

Post-operative atrial fibrillation (POAF) is commonly observed in patients post cardiac surgery without a previous history of atrial fibrillation (AF) or other arrythmias. It's associated with significant postoperative complications including infection, bleeding reoperation, increased hospital length of stay (LOHS) and mortality. Magnesium has been identified as a potentially interesting compound with easy access and low toxicity. Hypomagnesemia has been observed frequently immediately after cardiac surgery. Both reduction of abnormal atomicity of atrial myocardium and prolongation of the atrial refractory period caused by administration of magnesium may prevent AF. The POMPAE trial will analyse the effectiveness of MgSO4 versus placebo (double blind randomized trial) in the prevention of POAF after cardiac surgery.

Atrial fibrillation (AF) is a cardiac rhythm disorder particularly common in intensive care patients. Some meta-analyzes report a prevalence of new onset AF ranging from 4.5% to 29.5% in polyvalent intensive care. In our department, a recent month-long survey showed that more than 30% of the patients who were unhealthy on admission suffer from an episode of new onset AF during their stay. The occurrence of AF in intensive care has a pejorative effect on the patient's outcome, and this through two factors. On the one hand, the decreasing of cardiac output by degradation of the ventricular filling in diastole time, on the other hand the FA is responsible for an over-risk of ischemic stroke. In fact, it has been shown that the occurrence of new onset AF in intensive care is associated with a higher level of severity and a higher mortality. It is also important to underline the medico-economic impact of this rhythmic disorder as complication of shock due to the frequent prescription of various anti-arrhythmic or anticoagulant medication. Various factors have been mentioned to explain the frequent occurrence of AF in shocked patients. The shock state, whatever its origin, is characterized by the occurrence of a systemic inflammatory response syndrome in which is observed a particularly important releasing of stress hormones and endogenous catecholamines involved in the occurrence of a rapid multi-organ failure without treatment. Systemic humoral elements are possibly involved in the occurrence of new onset AF, such as high level of inflammation that characterizes shock states. In addition, physiological factors such as hypoxia, hypovolemia, hyperthermia or ionic disorders are also implicated, but their non-systemic association with intensive care new onset FA suggests that humoral factors may play an important and independent role. Among these humoral factors, the proteins of chromogranin family particularly Vasostatin-I (VS-I) seem possibly involved in the genesis of AF in the aggressed intensive care patients. Several studies have highlighted the beneficial regulatory role of VS-I on the cardiovascular system, particularly in a study on a canine model Stavrakis and al. have shown the VS-I protective role on the FA occurrence. However, as has been demonstrated in a prospective study in intensive care, the rates of circulating VS-I were significantly higher in the most severe patients and those whose prognosis was the most pejorative, thus not supporting the thesis of the protective effect of VS-I. An explanation exists for this discrepancy: VS-I is present in two distinct forms in the circulating blood. In vitro work carried out within the U1121 INSERM team with has made it possible to highlight the coexistence of two forms of VS-1: an aggregated "inactive" form and an "active" disaggregated form. In our hypothesis, the inactive aggregated form would be predominant during the states of acute pathological aggressions such as the shock and thus would not exert the anti arrhythmic and cardio protector expected functions. The first aim of our study is therefore to confirm that the onset of new onset FA during the shock state is associated with a significant decrease in the VS-I plasma level in its monomeric form called "active", even when high levels of total VS-1 are detected by ELISA in the plasma of patients. Our project is a pilot and unpublished translational work. The link between VS-I and new onset AF in intensive care severe patients has never been studied in vivo, and the recent work of the associated INSERM team provides advances in understanding the function of VS-I over time shock conditions. Nevertheless, our experimental hypothesis require confirmation in humans. A better understanding of the factors influencing the occurrence of cardiac arrhythmias in intensive care patients is a major ambition as it would be a step forward in the development of a preventive strategy or new treatment for the benefit of patients.

Multinational, investigator-initiated study of oral anticoagulation versus no anticoagulation for the prevention of stroke and other adverse cardiovascular events in patients with transient perioperative atrial fibrillation after noncardiac surgery and additional stroke risk factors.

Atrial fibrillation (AF) is the most common form of irregular heart rhythm. In people with AF, blood clots often form in the heart, which can travel to the brain. Blockage of brain arteries by these clots is a major cause of stroke. This type of stroke is called an ischaemic stroke and approximately 15% of all ischaemic strokes are caused by AF. People with AF are often prescribed a medication called an anticoagulant, which makes it less likely for blood clots to form and thus can prevent ischaemic strokes. However, anticoagulants also increase the risk of bleeding, so they are not suitable for everyone. Some people who have AF have had a different type of stroke which is caused by bleeding in the brain, an intracerebral haemorrhage (ICH). These people are at increased risk of suffering both an ischaemic stroke (due to AF) and another ICH. It is not known whether it is best for these people to take an anticoagulant medication or not, as previous research studies did not include this group of people. PREvention of STroke in Intracerebral haemorrhaGE survivors with Atrial Fibrillation (PRESTIGE-AF) is a research study on the best stroke prevention in people with atrial fibrillation (AF) who have recently had a bleeding in their brain, (ICH). This is a trial where half of the participants will take an anticoagulant medication, preventing blood clot formation, and half will not receive an anticoagulant. The direct oral anticoagulants (DOACs) that will be used in this trial are all licenced for use in the United Kingdom and within the European Union (EU) to prevent strokes in people with AF. However, the current licence does not extend to use with people who have had an ICH because it has not been tested in this group with a randomised controlled trial. DOACs will be tested in ICH survivors with AF because previous research trials have shown that people are up to 50% less likely to have bleeding complications in the brain with DOACs than with Warfarin (another commonly used anticoagulant). The aim of PRESTIGE-AF is to answer the question of whether people with ICH and AF should take an anticoagulant medication or if it is better for them to avoid it.

Current clinical society guidelines and statements are non-specific and relatively open-ended regarding the optimal timing to restart non-warfarin oral anticoagulant (NOAC) after gastrointestinal bleeding (GIB) in patients with atrial fibrillation (AF) who require the prophylactic medication for stroke prevention. These patients are at increased risk for devastating future thromboembolic events including stroke if NOAC is not resumed promptly, whilst premature resumption of anticoagulants can result in recurrent GIB, haemorrhage, anaemia, myocardial ischaemia and infarction in those with ischaemic heart disease, and even death. However, the question as to how early a NOAC can be safely restarted after acute GIB has not been previously answered, and there remains an important knowledge gap.

The purpose of the study is to evaluate a new radiotracer called 64Cu-FBP8 for PET-MR imaging of thrombosis. The tracer has the potential of detecting thrombosis anywhere in the body, for instance in the left atrial appendage of patients with atrial fibrillation, and thereby may provide a non-invasive alternative to the current standard-of-care methods.

The study evaluates the effects of antithrombotic drugs (anticoagulant drugs or antiplatelet drugs) for prevention of ischaemic events in patients With recent intracerebral haemorrhage.

Randomised controlled trials (RCTs) demonstrate a substantial benefit from oral anticoagulant drugs for the prevention of stroke and systemic embolism in non-valvular atrial fibrillation (AF). However, these RCTs excluded patients with prior intracerebral haemorrhage (ICH). Therefore, guidelines are unable to recommend whether oral anticoagulant drugs, in particular non-vitamin K antagonist (called direct OAC) - can be used for patients with AF after an intracerebral haemorrhage. Roughly 30% of adults with ICH have AF but in 2017 it remains unclear whether they should start oral anticoagulant drugs, be treated with left atrial appendage closure (LAAC) or avoid anticoagulation and LAAC.

To test the impacts of different exercise training programs to the cardiopulmonary function, muscle metabolism, and body mass composition