View clinical trials related to Atrial Fibrillation.
Filter by:Pulmonary vein isolation (PVI) is currently the cornerstone non pharmacological therapy for drug-refractory atrial fibrillation (AF). Where rhythm control has been shown to be inferior as compared to rate control in older trials. New data suggest that for patients with heart failure and AF PVI may improve prognosis (mortality) as compared to medical rate or rhythm control. Whether optimal rate control as can be achieved with atrioventricular node ablation is comparable with regard to all-cause mortality of heart failure hospitalization to PVI in patients with heart failure and AF is unknown.
BACKGROUND AND RATIONALE OF THE STUDY The analysis of the composition of the clot constitutes a promising tool for investigating the possible pathogenetic mechanisms underlying ischemic stroke. This analysis was made possible thanks to the numerous mechanical thrombectomy operations which have now become routine. Several studies have attempted to explore the possible relationship between the primary site of thrombus formation and clot composition, reporting that cardioembolic stroke may have a higher percentage of platelet-rich areas than noncardioembolic thrombosis. However, the data are conflicting and do not seem to support an association between clot histology and etiology. Furthermore, thrombus composition appears to influence thrombolysis and the efficacy of thrombectomy. For example, fibrin-rich thrombi appear to reduce the effectiveness of thrombolytic treatment and require more steps with mechanical thrombectomy treatment. Primary ENDPOINT: Evaluate how clot composition relates to stroke etiology according to the TOAST classification. Secondary ENDPOINT: - relationship between different clot components and the degree of thrombectomy recanalization as defined by treatment modified cerebral ischemia score (mTICI). - relationship between the different components of the clot and the number of steps required to achieve recanalization. - relationship between the different clot components and outcome indicators (NIHSS score and mRS score). TARGET POPULATION Patients with ischemic stroke with occlusion of large intracranial vessels will be included in the study if deemed suitable for mechanical thrombectomy therapy in accordance with national and international guidelines. INCLUSION CRITERIA - age > 18 years; - Patients diagnosed with large vessel occlusion stroke in the emergency room CT Angio-study, undergoing mechanical thrombectomy procedure. - Recovered thrombus available for analysis EXCLUSION CRITERIA ● Lack of written informed consent. MATERIALS AND METHODS The clot will be portioned. Part of the sample will be fixed in a 10% formalin solution (3.7% formaldehyde), part will be frozen in liquid nitrogen. Within 24-48 hours of fixation, formalin-fixed thrombi will be dehydrated by increasing the concentration of ethanol (70%, -80%, -95%, 100%) and paraffin-embedded allowing good preservation of tissue morphology and easy long-term storage. The included samples will be sectioned along the major axis of the thrombus, in slices with a thickness between 4 and 5 µm. Base staining will be used to visualize RBC, PLT and fibrin. - Hematoxylin and Eosin (H&E) will allow visualization of general thrombus structures and identification of aggregates of fibrin/platelets (colored pink), red blood cells (red), and nucleated cells (dark blue). - Martius Scarlet Blue (MSB), selectively stains fibrin (dark pink/red), red blood cells (yellow) and collagen (blue - Mallory-Azan for collagen and phosphotungstic acid hematoxylin for fibrin. - immunohistochemistry to detect the presence of - Platelets (CD42-Gp-Ib+, CD41a-Gp-IIb/IIIa+, CD61-GpIIIa), - white blood cells (CD45+, common leukocyte antigen), or monocytes/macrophages (CD14+, CD1a+, CD68+), - T lymphocytes (CD3+, CD8/CD4+), or natural killers (CD16+, CD56+), or mobile premature endothelial cells and blood progenitors (CD34+), or neutrophils (CD45+, CD16+), or fibrinogen or von Willebrand factor.
This pilot, prospective, interventional, monocentric, independent, and no-profit clinical trial aims to investigate and evaluate the proportion, acute and chronic characteristics, and outcomes of esophageal thermal injury (ETI) in AF ablation using a high-power, short-duration (HP-SD) setting with contact force (CF) sensing tip ablation catheter in standard clinical practice. The main questions it aims to answer are: - Evaluate the acute proportion of the ETI assessed by the mini-invasive esophagoscopy pre and post-procedure. In addition, clinical evaluations at 3, 6, and 12 months from the procedure are foreseen. - Evaluate the contribution of the factors influencing RF procedure (contact force, impedance, RF power, RF time) on ETI development. - Describe the relationship between the esophageal temperature (continuous monitoring) and ETI development.
The purpose of this study is to evaluate if milvexian is at least as effective as apixaban for reducing the risk of the composite stroke and non-central nervous system (CNS) systemic embolism.
The aim of this study is to test if stellate ganglion block can decrease the incidence of atrial fibrillation after video-assisted thoracoscopic surgery and the way it works.
The purpose of this study is to demonstrate safety and effectiveness of the ablation system (THERMOCOOL SMARTTOUCH SF [STSF] catheter and TRUPULSE generator) when used for isolation of the atrial pulmonary veins (PVs) in treatment of participants with paroxysmal atrial fibrillation (PAF).
Aim of the study is to investigate whether the influence of drugs inducing of CYP 3A4 isoenzyme of CYP450 and P-gp transporter significantly affect plasma levels of DOACs in patients with NVAF and venous thromboembolism
1050 patients with persistent/permanent atrial fibrillation (AF) will be studied using conventional and advanced (three-dimensional and deformation imaging) echocardiography. Patients with moderate/severe isolated secondary tricuspid regurgitation (STR) will undergo blood tests to assess their proteomic profile and cardiac CT to measure the tricuspid annulus geometry. The project will aim to 1. assess the prevalence of moderate/severe isolated STR in patients with AF; 2. identify the mechanisms associated with the development of moderate-severe STR in patients with AF; 3. identify the proteomic profile associated with significant growth of tricuspid valve leaflets as a mechanism to protect patients with AF from the development of moderate/severe STR; 4. evaluate the effects of the restoration of sinus rhythm on the severity of STR and the remodeling of the right heart cardiac structures (i.e. right ventricle, right atrium, and tricuspid valve apparatus).
The goal of this study is to test the feasibility of guiding as-needed pharmacological rate control of atrial fibrillation (AF) by implantable cardiac monitors and to assess the impact of continuous beta-blocker therapy versus as-needed rate control on the following outcomes: (1) exercise capacity, (2) AF burden, (3) symptomatic heart failure, (4) biomarker assessment of cardiac filling pressures and cardio-metabolic health, and (5) quality of life in patients with atrial fibrillation and stage II or III heart failure with preserved ejection fraction.
Atrial Fibrillation (AF) is an abnormal rhythm of the heart which is increasingly common and can be associated with serious consequences. We know that AF is associated with an increase in the scarring of the heart, the left atrium and it is thought that this scarring may be one of the drivers for this abnormal heart rhythm. The nature of this scarring in humans has been subject to limited study and generally only by indirect means such as cardiac MRI scans or measuring the voltage of the tissues. During cardiothoracic surgery, tissue from the left atrium is removed as a part of the procedure. This tissue is normally disposed of, but we would propose to consent patients to collect it to allow it to be analysed. Such analysis would examine the composition of the tissue, including the pattern of scarring, to allow us to gain a greater insight into the mechanisms of AF.