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atrial fibrillation/protease
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Pharmacological Inhibition of Serine Proteases to Reduce Cardiac Inflammation and Fibrosis in Atrial Fibrillation.
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Systemic inflammation correlates with an increased risk of atrial fibrillation (AF) and thrombogenesis. Systemic inflammation alters vessel permeability, allowing inflammatory and immune cell migration toward target organs, including the heart. Among inflammatory cells infiltrating the atria,
Association of circulating factor seven activating protease (FSAP) and of oral Omega-3 fatty acids supplements with clinical outcome in patients with atrial fibrillation: the OMEGA-AF study.
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Factor VII Activating Protease (FSAP) activates factor VII (FVII) as well as pro-urokinase (uPA). Our goal was to evaluate the relation between plasma levels of FSAP and clinical instability in atrial fibrillation (AF) and possible effects of oral omega-3 fatty acids (FA) supplements. 101 patients
Prognostic value of plasma von Willebrand factor and its cleaving protease ADAMTS13 in patients with atrial fibrillation.
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BACKGROUND
The von Willebrand factor (vWF) is essential for platelet adhesion and arterial thrombosis. It is degraded into less active multimers by ADAMTS13. Patients with atrial fibrillation (AF) exhibit higher plasma vWF and lower ADAMTS13 antigen levels. The vWF/ADAMTS13-ratio might help to
Successful co-administration of dabigatran etexilate and protease inhibitors ritonavir/lopinavir in a patient with atrial fibrillation.
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[Morphological remodeling in atrial fibrillation].
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In the recent years, a tremendous amount has been learned about the pathophysiology of atrial fibrillation (AF). AF induces electrophysiological changes in the atria causing a perpetuation of the arrhythmia ("electrical remodeling"). Besides such AF-induced electrophysiological changes, which
Changes in plasma von Willebrand factor and ADAMTS13 levels associated with left atrial remodeling in atrial fibrillation.
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BACKGROUND
Previous studies have shown raised plasma von Willebrand factor (VWF) levels in patients with atrial fibrillation (AF). However, little is known about changes of VWF associated with VWF-cleaving protease (ADAMTS13) in AF. The aim of this study was to examine the relationship between
Edoxaban suppresses the progression of atrial fibrosis and atrial fibrillation in a canine congestive heart failure model.
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Coagulation factor Xa activates the protease-activated receptor 2 (PAR2) and causes tissue fibrosis; however, the effects of Xa inhibitor edoxaban on atrial fibrosis and atrial fibrillation (AF) have not been investigated. We examined the effect of edoxaban on the progression of atrial fibrosis in a
Data regarding the effects of thrombin and dabigatran-inhibited thrombin on protease-activated receptor 1 and activation of human atrial fibroblasts.
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The data presented here are related to the research paper entitled "Thrombin induces protease-activated receptor 1 signaling and activation of human atrial fibroblasts and dabigatran prevents these effects" (Altieri et al., 2018) [1]. Data show that silencing of protease-activated receptor 1 (PAR1)
Degradation of a connexin40 mutant linked to atrial fibrillation is accelerated.
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Several Cx40 mutants have been identified in patients with atrial fibrillation (AF). We have been working to identify physiological or cell biological abnormalities of several of these human mutants that might explain how they contribute to disease pathogenesis. Wild type (wt) Cx40 or four different
Atrial Fibrillation Ablation Increases Inflammation - Chemokine Modulation Suppresses Activation of Leukocytes Isolated after Ablation.
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Atrial fibrillation (AF) ablation is associated with increased circulating markers of inflammation. Innate immune or inflammation pathways up-regulate mononuclear cell responses and may increase the risk for recurrent arrhythmia. Chemokines and serine protease coagulation pathways both activate
[Upstream therapy for atrial fibrillation].
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In recent years a tremendous amount has been learned about the pathophysiology of atrial fibrillation (AF) which induces electrophysiological changes in the right and left atrium. Besides calcium-dependent tissue changes which are induced by activation of proteases and phosphatases, such as calpain
Mechanisms with clinical implications for atrial fibrillation-associated remodeling: cathepsin K expression, regulation, and therapeutic target and biomarker.
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BACKGROUND
The cysteine protease cathepsin K (CatK) has been implicated in the pathogenesis of cardiovascular disease. We sought to determine the link between atrial fibrillation (AF) and plasma CatK levels and to investigate the expression of and therapeutic target for CatK in vivo and in
Levels of von Willebrand factor and ADAMTS13 determine clinical outcome after cardioversion for atrial fibrillation.
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Von Willebrand factor (vWF) plays an essential role in platelet adhesion and thrombus formation. Patients with atrial fibrillation (AF) exhibit higher plasma vWF and lower ADAMTS13 antigen levels compared to controls. Little is known about vWF and ADAMTS13 in AF patients treated with cardioversion
Increased plasma corin levels in patients with atrial fibrillation.
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BACKGROUND
NPPA mutations/polymorphisms were associated with atrial fibrillation (AF), and plasma proatrial natriuretic peptide (proANP) concentrations were increased in AF patients. Corin, as a transmembrane protease that processes proANP in the heart, may play a potential role in AF.
METHODS
To
Thrombin induces protease-activated receptor 1 signaling and activation of human atrial fibroblasts and dabigatran prevents these effects.
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BACKGROUND
Data with animal cells and models suggest that thrombin activates cardiac fibroblasts (Fib) to myofibroblasts (myoFib) via protease-activated receptor 1 (PAR1) cleavage, and in this way promotes adverse atrial remodeling and, thereby, atrial fibrillation (AF).
OBJECTIVE
Here, we explored
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