Cancer treatment-related ischemic arterial events: Focus on peripheral arterial disease and cerebrovascular events

Cancer therapies, including VEGF inhibitors, BCR-ABL tyrosine kinase inhibitors (TKIs), immune checkpoint inhibitors (ICIs), multiple myeloma and hormonal therapies, are associated with an increased risk of arterial thrombotic events (ATEs). While most studies have focused on myocardial and cerebral ischemia, this review highlights the underreported peripheral arterial complications, peripheral arterial disease (PAD) and cerebrovascular events. VEGF inhibitors, such as bevacizumab and VEGFR-TKIs (e.g., sorafenib, sunitinib), significantly elevate the risk of ATEs, with hypertension and proteinuria as common comorbidities. BCR-ABL-TKIs, especially nilotinib and ponatinib, are linked to rapid-onset PAD, even in patients without prior cardiovascular risk factors. ICIs triple the progression of aortic plaque volume, increasing the risk of ischemic stroke and myocardial infarction. Hormonal therapies, including tamoxifen and androgen deprivation therapy, also contribute to ATEs through metabolic and vascular mechanisms. Radiotherapy further exacerbates arterial disease, particularly carotid stenosis and iliofemoral atherosclerosis, in head, neck, and pelvic cancer survivors. Monitoring and prevention strategies, such as regular cardiovascular risk assessments, lipid management, and arterial ultrasound surveillance, are critical for high risk patients. Multidisciplinary onco-vascular teams are essential to mitigate these risks and optimize patient outcomes.