Cancer-Associated Arterial Thrombosis: Mechanisms and Risk Factors

Cancer-associated thrombosis (CAT) is a leading cause of morbidity and mortality among cancer patients. While venous thromboembolic events have been extensively studied due to their higher incidence, arterial thrombosis in cancer patients—referred to as cancer-associated arterial thromboembolism (CA-ATE)—is less well understood but may pose a greater danger. The pathophysiology of CA-ATE involves complex interactions between the tumor microenvironment, cancer cells, patient-related factors, and cancer therapies. Some chemotherapeutic agents, particularly platinum-based compounds (cisplatin, oxaliplatin), gemcitabine, taxanes, and targeted therapies such as tyrosine kinase inhibitors (TKIs), have been associated with an increased risk of arterial thrombosis. In certain patient populations, hormonal therapy and selective estrogen receptor modulators may also contribute to this risk. Additionally, factors such as patient age, cancer type, and stage contribute to an increased risk of arterial thrombosis in this population. Key mechanisms driving CA-ATE include endothelial injury, hypercoagulability, and platelet activation. Certain malignancies, notably lung and pancreatic cancers, are associated with a higher incidence of arterial thrombotic events. The aim of this review is to enhance understanding of the underlying mechanisms of cancer-related arterial thromboembolism and to highlight the various therapeutic, cancer-related, and patient-related factors that contribute to the occurrence of cancer-associated arterial thrombotic events.