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Atrial fibrillation (AF), the most prevalent sustained cardiac arrhythmia, is intricately linked with atrial functional tricuspid regurgitation (AFTR), a condition distinguished from ventricular functional tricuspid regurgitation by its unique pathophysiological mechanisms and clinical implications. This review article delves into the multifaceted aspects of AFTR, exploring its epidemiology, pathophysiology, diagnostic evaluation, and management strategies. Further, we elucidate the mechanisms underlying AFTR, including tricuspid annular dilatation, right atrial enlargement, and dysfunction, which collectively contribute to the development of tricuspid regurgitation in the absence of significant pulmonary hypertension or left-sided heart disease.

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Background/aim: Atrial fibrillation (AF) and heart failure (HF) commonly co-occur, significantly increasing morbidity and mortality. Poorly controlled AF can contribute to complications like HF and is associated with conditions, such as stroke and pulmonary embolism (PE). This report involves a man with AF who had persistent respiratory symptoms and left-sided chest pain, initially suspected to be PE, but eventually diagnosed as HF.

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Background: In patients with adult congenital heart disease (ACHD), significant atrioventricular valve regurgitation is an important risk factor for poor outcomes, such as heart failure. However, in many cases, transcatheter intervention may reduce the risk profile to avoid a high surgical risk.

Case Summary: A 44-year-old man with complex ACHD in the form of a double-inlet left ventricle, congenitally corrected transposition of the great arteries, pulmonary atresia, atrial septal defect, and patent ductus arteriosus was referred for the treatment of severe tricuspid regurgitation.

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Introduction Parenteral heparin is widely used as bridging therapy while optimising oral anticoagulation(OAC). Newer Direct-Acting OACs(DOACs) attain therapeutic effect very quickly. We report the use of dabigatran as bridging therapy during warfarin optimization for cardioembolic stroke in two patients who opted to receive warfarin for long-term anticoagulation for secondary stroke prevention.

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Emery-Dreifuss muscular dystrophy type 2 (EDMD2) is a rare autosomal dominant neuromuscular disorder caused by LMNA gene mutations and characterized by progressive skeletal muscle weakness and significant cardiac involvement. We report the case of a 45-year-old woman who presented with sudden-onset, left-sided hemiparesis and dysarthria. Initial imaging was unremarkable, and symptoms transiently improved, suggesting a transient ischemic attack.

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