Abstract
BackgroundAtrial fibrillation (AF) is a frequent and serious cardiovascular complication in oncology patients, driven by shared pathophysiological mechanisms of inflammation, thrombosis, and cardiac remodeling. Cancer and its therapies significantly increase AF risk, impacting survival, quality of life, and management complexity.MethodsThis narrative review synthesizes current evidence on the epidemiology, pathogenesis, and management of AF in cancer, emphasizing inflammatory and prothrombotic pathways, treatment-related cardiotoxicity, and cardio-oncology strategies. Literature was retrieved from PubMed and recent cardio-oncology guidelines to provide an integrated overview of mechanistic insights and therapeutic implications.ResultsCancer patients exhibit up to a 10-fold higher risk of AF than the general population, particularly with esophageal, lung, and hematologic malignancies. Mechanistically, the NLRP3 inflammasome, neutrophil extracellular traps, and hypercoagulability promote atrial fibrosis and electrical instability. Cancer therapies-including anthracyclines, platinum agents, tyrosine kinase inhibitors, immunotherapies, and thoracic radiation-further potentiate AF. Management is challenging due to drug-drug interactions, bleeding risks, and altered pharmacokinetics. Evidence supports the use of direct oral anticoagulants when feasible and emphasizes multidisciplinary cardio-oncology collaboration. Personalized anticoagulation, vigilant rhythm monitoring, and shared decision-making are key to optimizing outcomes.ConclusionAF in cancer arises from a convergence of inflammation, thrombosis, and therapy-induced injury. A structured, multidisciplinary cardio-oncology approach integrating early risk stratification, tailored anticoagulation, and preventive strategies is essential. Future research should focus on oncology-specific risk prediction tools, biomarker-guided management, and randomized trials to refine evidence-based care for this high-risk population.