Objective: Non-alcoholic fatty liver disease is a risk factor for atrial fibrillation. We assessed whether liver fibrosis markers are associated with atrial remodeling indicators in patients with atrial fibrillation in whom fatty liver disease has not been identified.
Methods: In this prospective, observational study, 174 patients with atrial fibrillation without chronic liver disease who underwent catheter ablation were enrolled.
A 54-year-old woman with multiple sclerosis treated with interferon-β (IFN-β)-1b for 15 years presented with sustained hypertension (240/124 mmHg) and retinal bleeding. She had proteinuria, anemia, thrombocytopenia, elevated serum creatinine levels, and haptoglobin depletion. Intravenous nicardipine stabilized her blood pressure, but her renal function and platelet count deteriorated.
View Article and Find Full Text PDFFactor Xa (FXa) inhibitors are recommended for use in fixed doses without laboratory monitoring. However, prior studies reported the importance of establishing biomarkers representing anticoagulation intensity related to bleeding or thrombotic events. To test the hypothesis that prothrombin activation fragment 1 and 2 (F1 + 2), a non-specific marker of thrombin generation, could be altered during FXa inhibitor treatment in patients with atrial fibrillation.
View Article and Find Full Text PDFAtrial fibrillation (AF) is the most common cardiac arrhythmia, but its proarrhythmic mechanism remains to be elucidated. Glutamate (Glu) and taurine (Tau) are present in the myocardium at substantially higher concentrations than in the plasma, suggesting their active role in myocardium. Here, we tested the hypothesis that the metabolism of Glu and Tau is altered in association with the generation of reactive oxygen species (ROS) in patients with AF.
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