Current Data and Future Perspectives on Patients with Atrial Fibrillation and Cancer.

Simple Summary: Atrial fibrillation is a very common comorbidity in cancer patients. Both cancer and cancer treatment increase the risk of developing new AF, resulting in increased morbidity and mortality. Heart rate and rhythm control, together with anticoagulant therapy, are the mainstays of atrial fibrillation treatment, even in patients with cancer. However, treatment adjustments may be necessary due to drug interactions with concomitant chemotherapy. In addition, cancer and advanced age increase the risk of both thromboembolism and hemorrhage. The risk of these complications is further increased by concomitant cancer therapy, frailty, poor nutrition status, and coexisting geriatric syndromes. In this review, we address the complex mechanisms linking arrhythmia to cancer and the difficult therapeutic challenges faced by oncologists and cardiologists in best managing these two conditions. Atrial fibrillation (AF) is an increasingly recognized comorbidity in patients with cancer. Indeed, cancer patients have a significantly higher incidence of AF than that observed in the general population. A reciprocal relationship between these two diseases has been observed, as much as some assume AF to be a marker for occult cancer screening, especially in older adults. The pathophysiological mechanisms are many and varied, including the underlying pro-inflammatory state, specific treatments (chemo- and radiotherapy), and surgery. The therapeutic management of patients with cancer and AF involves the same rhythm and frequency control strategies as the general population; however, the numerous interactions with chemotherapeutics, which lead to a significant increase in side effects, as well as the extreme fragility of the patient, should be considered. Anticoagulant therapy is also a complex challenge to address, as bleeding and stroke risk scores have not been fully assessed in this subpopulation. Furthermore, in large studies establishing the efficacy of direct oral anticoagulants (DOACs), cancer patients have been underrepresented. In this review, we elaborate on the mechanisms linking AF to cancer patients with a particular focus on the therapeutic challenges in this population. [ABSTRACT FROM AUTHOR]