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Chemotherapy-induced Cardiotoxicity and Mitigation / Angiogenesis and VEGF in Cancer · Journal article
Journal of Vascular Diseases · September 9, 2026
A consensus or society position rather than new primary data.
This narrative review synthesizes evidence on venous thromboembolism in cancer patients receiving VEGF-targeted therapies, reporting VTE incidence of 2.5–15.7% depending on agent, cancer type, and study design. It identifies key pathogenic mechanisms (PAI-1 upregulation, endothelial dysfunction, tissue factor activation) and recommends risk stratification, thromboprophylaxis, and individualized anticoagulation, with direct oral anticoagulants (particularly apixaban) favored over traditional agents.
Narrative review. Cancer patients receiving VEGF-targeted therapies; evidence drawn from clinical trials, observational studies, pharmacovigilance analyses, and preclinical investigations.. Intervention: VEGF-targeted therapies (bevacizumab and other VEGF inhibitors), direct oral anticoagulants (particularly apixaban).. Compared with: Traditional anticoagulants; patients not receiving VEGF inhibitors (inferred from context)..
VTE incidence ranges from 2.5% to 15.7% across studies with substantial heterogeneity by agent, cancer type, and setting. Bevacizumab-treated patients receiving chemotherapy showed increased arterial and venous thromboembolism risk with relative risk 1.32–2.45. PAI-1 upregulation, endothelial dysfunction, and tissue factor activation identified as key pathogenic mechanisms.
Apixaban efficacy and safety in cancer-associated VTE stated qualitatively; comparative efficacy and safety data not quantified. Direct oral anticoagulants, particularly apixaban, demonstrate favorable efficacy and safety compared to traditional anticoagulants in cancer-associated VTE.
Clinicians managing cancer patients on VEGF inhibitors should use validated risk-stratification systems, implement thromboprophylaxis, and consider direct oral anticoagulants (particularly apixaban) for VTE management. The wide heterogeneity in VTE incidence underscores the need for individualized patient assessment based on specific agent, cancer type, and concomitant therapy.
A comprehensive narrative review synthesizing evidence from trials, observational studies, and pharmacovigilance to provide clinical guidance on VTE risk, mechanisms, and management in VEGF-inhibitor-treated patients.
As stated by the source record.
Quoted from the source exactly as published.
Clinicians managing cancer patients on VEGF inhibitors should use validated risk-stratification systems, implement thromboprophylaxis, and consider direct oral anticoagulants (particularly apixaban) for VTE management. The wide heterogeneity in VTE incidence underscores the need for individualized patient assessment based on specific agent, cancer type, and concomitant therapy.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Vascular endothelial growth factor (VEGF)-targeted therapies have been associated with thromboembolic events, although the magnitude and nature of this risk vary substantially according to the specific agent, mechanism of VEGF-pathway inhibition, malignancy, concomitant therapy, and patient-related factors. This comprehensive narrative review examines the epidemiology, mechanisms, clinical characteristics, and management of VTE in cancer patients receiving VEGF inhibitors. Evidence from clinical trials, observational studies, pharmacovigilance analyses, and preclinical investigations is synthesized to provide a clinically oriented overview of VEGF-targeted therapy-associated thrombosis. Reported VTE incidence ranges from 2.5% to 15.7% across studies, with substantial heterogeneity according to the VEGF-targeted agent, cancer type, treatment setting, and study design. Bevacizumab-treated patients receiving chemotherapy demonstrated increased arterial and venous thromboembolism risk (relative risk 1.32–2.45). Plasminogen activator inhibitor-1 (PAI-1) upregulation, endothelial dysfunction, and tissue factor activation represent key pathogenic mechanisms. Careful patient selection, risk stratification using validated scoring systems, thromboprophylaxis strategies, and individualized anticoagulation approaches are essential for managing this complication. Direct oral anticoagulants, particularly apixaban, demonstrate favorable efficacy and safety profiles compared to traditional anticoagulants in cancer-associated VTE. This review provides clinicians with comprehensive, evidence-based guidance for preventing and managing VTE in the growing population of cancer patients receiving VEGF-directed therapies.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.