Anticancer therapy-induced vascular toxicity: VEGF inhibition and beyond

Int J Cardiol. 2017 Jan 15:227:11-17. doi: 10.1016/j.ijcard.2016.11.174. Epub 2016 Nov 9.

Abstract

Cardiotoxicity induced by chemotherapeutic agents and radiotherapy is a growing problem. In recent years, an increasing number of new drugs with targeted action have been designed. These molecules, such as monoclonal antibodies and tyrosine kinase inhibitors, can cause different type of toxicities compared to traditional chemotherapy. However, they can also cause cardiac complications such as heart failure, arterial hypertension, QT interval prolongation and arrhythmias. Currently, a field of intense research is the vascular toxicity induced by new biologic drugs, particularly those which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGF-R) and other tyrosine kinases. In this review, we aim at focusing on the problem of vascular toxicity induced by new targeted therapies, chemotherapy and radiotherapy, and describe the main mechanisms and emphasizing the importance of early diagnosis of vascular damage, in order to prevent clinical complications.

Keywords: Cardio-oncology; Cardiotoxicity; Chemotherapy; New target therapy; Radiotherapy; VEGF; Vascular toxicity.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / adverse effects*
  • Cardiotoxicity
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / metabolism
  • Endothelium, Vascular / radiation effects
  • Heart Diseases / blood
  • Heart Diseases / chemically induced*
  • Heart Diseases / diagnosis*
  • Humans
  • Reactive Oxygen Species / blood
  • Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors
  • Receptors, Vascular Endothelial Growth Factor / blood
  • Vascular Endothelial Growth Factor A / antagonists & inhibitors*
  • Vascular Endothelial Growth Factor A / blood

Substances

  • Antineoplastic Agents
  • Reactive Oxygen Species
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • Receptors, Vascular Endothelial Growth Factor