Background: Atrial 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. Methods: This 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. Results: Cancer 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. Conclusion: AF 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.

Background: Tirzepatide, a dual GIP/GLP‐1 receptor agonist, offers a novel cardiometabolic strategy beyond glycemic control with important implications for heart failure care. By producing potent, sustained weight reduction and favourable changes in lipids, blood pressure, systemic inflammation and endothelial biology, tirzepatide targets central pathophysiologic drivers of obesity‐related HFpEF. Methods: We conducted this review to synthesise current evidence on the mechanisms, clinical efficacy and therapeutic implications of tirzepatide for heart failure management, with emphasis on obesity‐related HFpEF, cardiorenal effects and safety considerations. Randomised clinical programmes and the SUMMIT outcomes trial have demonstrated symptomatic and functional improvements, reverse cardiac remodelling on imaging, reduced circulating markers of myocardial stress and fewer worsening heart‐failure events versus placebo, alongside signals of renal stabilisation. Results: The tolerability profile aligns with the GLP‐1 class, with gastrointestinal events predominating and a low risk of clinically important hypoglycemia; biliary events may be more likely at higher doses, while pancreatitis risk has not been clearly elevated. Data in HFrEF remain limited and caution is advised given prior mixed results with incretin therapies and theoretical concerns about rapid weight loss in advanced systolic failure. Conclusion: This review integrates mechanistic insights and contemporary trial evidence to clarify how dual incretin agonism may modify the trajectory of obesity‐driven heart failure, to inform multidisciplinary clinical decision making, and to highlight key unanswered questions and research priorities needed to define tirzepatide's full role in heart failure management.