Cardiac and vascular toxicities of angiogenesis inhibitors: The other side of the coin

• Inhibition of vascular endothelial growth factor (VEGF) alters endothelial homeostasis, and causes hypertension, thrombosis and bleeding, but can also delay neointima formation.
• The presence of off-targets associated with multi-targeted tyrosine kinase inhibitors accounts for their increased cardiac toxicity.
• Several meta-analyses have reported an increased risk of congestive heart failure, left ventricular dysfunction and coronary arterial events with angiogenesis inhibitors.
• A novel strategy should include a comprehensive battery of clinical, laboratory and echocardiographic parameters to better delineate the magnitude of these adverse effects.

SummaryAngiogenesis is one of the best-described tumor hallmarks. Targeting angiogenesis is becoming a successful strategy to suppress cancer growth. Vascular endothelial growth factor (VEGF), the fulcrum of angiogenesis, contributes to vascular and cardiac homeostasis. Angiogenesis inhibitors classically associated with vascular side effects are increasingly recognized for cardiac adverse effects as reflected by several meta-analyses. A global approach to these findings is a pressing need, and future strategies involving collaboration among different medical specialties are highly encouraged.