Circulation. 2026 Oct 6;154(14):1382-1403. doi: 10.1161/CIRCULATIONAHA.125.079141. Epub 2026 Oct 5.
ABSTRACT
The rapid development of novel cancer therapies has considerably improved the care of cancer patients and cancer-related survival; however, these therapies are associated with a broad range of adverse events that have become a major burden in this population. Alongside other cancer-related factors, vascular toxicity from anticancer therapies contributes to an increased risk of venous thromboembolism. Among anticancer drugs, chemotherapeutic agents (eg, anthracyclines, platinum-based drugs, antimetabolites), hormonal therapies (eg, selective estrogen receptor modulators), agents used for multiple myeloma (including immunomodulatory drugs and proteasome inhibitors), asparaginase, as well as targeted inhibitors to immune checkpoints, vascular endothelial growth factor, epidermal growth factor receptor, tyrosine kinases, cyclin-dependent kinases, and poly(ADP-ribose) polymerase are primarily associated with increased risk of venous thromboembolism. Vascular adverse events associated with anticancer drugs are frequently underestimated, and significant gaps remain in the risk stratification, prevention, and management of thromboembolic events in patients receiving systemic anticancer therapies. This review examines the evidence linking anticancer drug exposure to the incidence of venous thromboembolism, summarizes the key underlying pathobiological mechanisms, and highlights current guideline recommendations for the prevention and treatment of cancer-associated thrombosis. Arterial thrombotic events are also discussed where clinically or mechanistically relevant. This review also offers advanced cardio-oncology perspectives on the identification, risk stratification, and therapeutic targeting of drug-induced vascular toxicity.
PMID:42832625 | DOI:10.1161/CIRCULATIONAHA.125.079141