Mechanisms, Clinical Phenotype and Potential Risk Prediction for Cardiovascular Toxicity Induced by Tyrosine Kinase...

Area of Science:

• Cardiology
• Hematology
• Pharmacology

Background:

• Tyrosine kinase inhibitors (TKIs) are essential for chronic myeloid leukemia (CML) treatment.
• Long-term TKI use, especially newer generations, is linked to cardiovascular adverse events (CV-AEs).
• CV-AEs impact patient quality of life and treatment adherence.

Purpose of the Study:

• To systematically review mechanisms of TKI-induced cardiovascular toxicity.
• To propose the "Metabolism-Endothelium-Thrombosis Axis" as a unifying framework for TKI-related CV-AEs.
• To highlight the importance of risk prediction and cardioprotective strategies.

Main Methods:

• Narrative review of existing literature.
• Systematic elucidation of pathophysiological pathways.
• Integration of molecular, cellular, and clinical data.

Main Results:

• TKI-induced CV-AEs involve a complex cascade including endothelial dysfunction, metabolic changes, oxidative stress, inflammation, and platelet activation.
• The "Metabolism-Endothelium-Thrombosis Axis" integrates these mechanisms.
• Risk prediction models show value in identifying patients prone to CV-AEs, especially arterial occlusive events (AOEs).

Conclusions:

• Understanding the "Metabolism-Endothelium-Thrombosis Axis" is key to managing TKI-related cardiovascular risks.
• Identifying high-risk patients and implementing cardioprotective strategies are crucial.
• Further research is needed to refine TKI-specific toxicity understanding and risk prediction models.