Cancer-related inflammation, anti-cancer treatment and other cancer-related comorbidities are proposed to affect atrial remodeling, increasing the susceptibility of lung cancer patients for developing atrial fibrillation. Moreover, cancer is assumed to modify the risk of thromboembolisms and bleeding. An association between AF and malignancy has been reported but incompletely defined. The earliest publications of cancer predisposing to AF came in the 1940s-50s with reports of neoplastic cardiac infiltration or mechanical pressure on the heart, and with oncologic thoracic surgery. Subsequently, multiple studies have reported an increased risk of AF after cancer therapy with surgery (particularly thoracic) and chemotherapy. However, the prevalence of AF appears to be higher in patients with cancer at the time of diagnosis even before undergoing therapy. The emerging field of cardio-oncology has revealed that these seemingly disparate disease processes are intertwined, owing to the cardiovascular sequelae of anticancer therapies, shared risk factors that predispose individuals to both cardiovascular disease and cancer, as well the possible potentiation of cancer growth by cardiac dysfunction. Although direct oral anticoagulants (DOAC) seem to represent a safe and effective option, compared to Vitamin K antagonists (VKA), in this population, this statement is based mainly on observational studies and sub analyses of pivotal trials of the DOAC.
Keywords: Atrial fibrillation; Cardiovascular events; Clinical outcomes; Lung cancer.
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