Table 1.

Summary of Main Vascular Toxicities Associated With Traditional Cancer Therapies and Proposed Mechanisms for Toxicities

Cancer Therapy	Proposed Mechanisms of Vascular Toxicity	Vascular Toxicities*
Antimetabolites: fluoropyrimidines	Endothelial injury Vasospasm Increased endothelin-1 bioactivity	Coronary vasospasm Raynaud phenomenon
Antimicrotubule agents: taxanes	Interference with basic endothelial cell functions by affecting the cytoskeleton	Capillary leak Peripheral neuropathy
Antimicrotubule agents: vinca alkaloids (vincristine, vinblastine)	Caspase-mediated apoptosis Inhibition of endothelial cell proliferation	Chest pain presentations Hypertension Myocardial ischemia Raynaud phenomenon Thromboembolism
Alkyl-like agents: platinum compounds	Injury to endothelial cells Increased platelet aggregation Reduced NO availability	Cerebrovascular events Hypertension Myocardial ischemia/MI Raynaud phenomenon Venous thromboembolic disease
Alkylating agents: cyclophosphamide	Injury to endothelial cells Increased platelet aggregation Decreased angiotensin-converting enzyme activity	Cerebrovascular events Hepatic veno-occlusive disease Hypertension Myocardial ischemia/MI Pulmonary hypertension Raynaud phenomenon
Antitumor antibiotics: anthracycline	Production of reactive oxygen species DNA double-stranded breaks Mitochondrial dysfunction Injury to endothelial cells	Endothelial dysfunction
Antitumor antibiotics: bleomycin	Inhibition of endothelial cell proliferation/migration Endothelial cell apoptosis	Myocardial ischemia/MI Pulmonary hypertension Raynaud phenomenon
Other older therapies: IL-2	Cytotoxic effects by lymphokine-activated killer cells Direct effects of IL-2 on endothelial cells Induction of inflammatory cytokines	Vascular leak syndrome

IL indicates interleukin; MI, myocardial infarction; and NO, nitric oxide.

^*Vascular toxicities are presented in alphabetical order. Order does not reflect prevalence of respective toxicities.