Among patients with AF undergoing catheter ablation, atrial tissue fibrosis estimated by delayed enhancement MRI was independently associated with likelihood of recurrent arrhythmia. The clinical implications of this association warrant further investigation.
NOACs; (8) NOAC plasma level measurement: rare indications, precautions, and potential pitfalls; (9) How to deal with dosing errors; (10) What to do if there is a (suspected) overdose without bleeding, or a clotting test is indicating a potential risk of bleeding; (11) Management of bleeding under NOAC therapy; (12) Patients undergoing a planned invasive procedure, surgery or ablation; (13) Patients requiring an urgent surgical intervention; (14) Patients with AF and coronary artery disease; (15) Avoiding confusion with NOAC dosing across indications; (16) Cardioversion in a NOAC-treated patient; (17) AF patients presenting with acute stroke while on NOACs; (18) NOACs in special situations; (19) Anticoagulation in AF patients with a malignancy; and (20) Optimizing dose adjustments of VKA. Additional information and downloads of the text and anticoagulation cards in different languages can be found on an EHRA website (www.NOACforAF.eu).
Stent integration is a multifactorally triggered process with proliferating SMCs generating regenerative tissue. In the early phase predominantly thrombotic material can be observed at the site of stenting, followed by the invasion of SMCs, T lymphocytes and macrophages. The incidence of delayed reendothelializations and the occurrence of deep dissections may be associated with excessive SMC hyperplasia.
Esophageal perforation is a dreaded complication of atrial fibrillation ablation that occurs in 0.1% to 0.25% of atrial fibrillation ablation procedures. Delayed diagnosis is associated with the development of atrial-esophageal fistula (AEF) and increased mortality. The relationship between the esophagus and the left atrial posterior wall is variable, and the esophagus is most susceptible to injury where it is closest to areas of endocardial ablation. Esophageal ulcer seems to precede AEF development, and postablation endoscopy documenting esophageal ulcer may identify patients at higher risk for AEF. AEF has been reported with all modalities of atrial fibrillation ablation despite esophageal temperature monitoring. Despite the name AEF, fistulas functionally act 1 way, esophageal to atrial, which accounts for the observed symptoms and imaging findings. Because of the rarity of AEF, evaluation and validation of strategies to reduce AEF remain challenging. A high index of suspicion is recommended in patients who develop constitutional symptoms or sudden onset chest pain that start days or weeks after atrial fibrillation ablation. Early detection by computed tomography scan with oral and intravenous contrast is safe and feasible, whereas performance of esophageal endoscopy in the presence of AEF may result in significant neurological injury resulting from air embolism. Outcomes for esophageal stenting are poor in AEF. Aggressive intervention with skilled cardiac and thoracic surgeons may improve chances of stroke-free survival for all types of esophageal perforation.
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