Cardiotoxicity of Selected Vascular Endothelial Growth Factor Receptor Tyrosine Kinase Inhibitors in Patients with...

Area of Science:

• Oncology
• Cardiology
• Pharmacology

Background:

• Renal cell carcinoma (RCC) is a common kidney cancer.
• Advanced RCC treatments include vascular endothelial growth factor receptor (VEGFR)-targeted tyrosine kinase inhibitors (TKIs).
• VEGFR-TKIs offer therapeutic benefits but may increase cardiotoxicity risk, especially in combination therapy.

Purpose of the Study:

• To explore the mechanisms of cardiotoxicity associated with VEGFR-TKIs in metastatic RCC.
• To highlight the challenges in identifying the specific pathways responsible for cardiotoxicity.
• To discuss the implications of VEGF signaling inhibition on cardiac function and potential patient monitoring strategies.

Main Methods:

• Review of existing literature on VEGFR-TKIs and their cardiovascular side effects.
• Analysis of the role of VEGF signaling in cardiomyocyte homeostasis and cardiac function.
• Discussion of potential mechanisms linking VEGF inhibition to adverse cardiac events.

Main Results:

• VEGF signaling is crucial for maintaining normal heart function; its inhibition can lead to cardiotoxicity.
• Cardiotoxicity may manifest as endothelial dysfunction, impaired revascularization, dilated cardiomyopathy, cardiac hypertrophy, and altered vascular load.
• The complex interplay of signaling pathways makes pinpointing the exact cause of cardiotoxicity challenging.

Conclusions:

• VEGFR-TKIs, while effective against RCC, pose a risk of cardiotoxicity due to interference with vital VEGF signaling pathways.
• Understanding these mechanisms is critical for managing treatment-related cardiovascular adverse events.
• Clinical surveillance, particularly for high-risk patients within the initial weeks of therapy, is suggested, though consensus on optimal strategies is lacking.