Anticancer therapy-induced vascular toxicity: VEGF inhibition and beyond

Area of Science:

• Oncology
• Cardiology
• Pharmacology

Background:

• Chemotherapy and radiotherapy are established causes of cardiotoxicity.
• Emerging targeted therapies, including monoclonal antibodies and tyrosine kinase inhibitors, present novel toxicity profiles.
• Vascular toxicity, particularly from agents targeting vascular endothelial growth factor (VEGF) and its receptor (VEGF-R), is a significant concern.

Purpose of the Study:

• To review the vascular toxicity associated with novel targeted therapies, chemotherapy, and radiotherapy.
• To elucidate the mechanisms underlying treatment-induced vascular damage.
• To emphasize the critical role of early diagnosis in preventing clinical sequelae.

Main Methods:

• Literature review of cardiotoxicity and vascular toxicity from cancer treatments.
• Analysis of mechanisms of action for targeted therapies and their impact on vasculature.
• Synthesis of current understanding of cardiac complications.

Main Results:

• Targeted therapies can induce cardiac complications like heart failure, hypertension, QT prolongation, and arrhythmias.
• Inhibition of VEGF and VEGF-R by targeted agents is a key mechanism for vascular toxicity.
• Chemotherapy and radiotherapy also contribute to vascular damage.

Conclusions:

• New targeted therapies introduce distinct cardiovascular risks compared to traditional chemotherapy.
• Understanding the mechanisms of vascular toxicity is crucial for managing patients undergoing cancer treatment.
• Early detection and intervention for vascular damage are essential to mitigate severe clinical outcomes.