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VEGFR-TKI Cardiac Toxicity — SCE Medical Oncology MCQ

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HardImmunotherapy & Targeted TherapyVEGFR-TKI Cardiac ToxicitySCE Medical Oncology

A 55-year-old man on sunitinib for RCC develops hypertension and heart failure (LVEF dropped from 60% to 35%). He has no prior cardiac history. What is the mechanism of VEGFR-TKI cardiac toxicity?

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Correct answer: B — VEGFR-TKI cardiac toxicity is primarily caused by afterload-mediated cardiomyopathy (severe hypertension → increased cardiac workload) plus direct inhibition of myocardial pro-survival kinase pathways — it is often reversible with drug cessation and cardiac treatment

VEGFR-TKI cardiac toxicity differs from anthracycline cardiotoxicity: it is primarily mediated by (1) afterload increase from severe hypertension (anti-VEGF effect) imposing increased cardiac workload, and (2) direct inhibition of myocardial pro-survival kinase pathways (PDGFR, RAF, VEGFR on cardiomyocytes). Unlike anthracycline cardiomyopathy (irreversible myocyte destruction), VEGFR-TKI cardiomyopathy is often partially reversible with drug cessation, blood pressure control and standard heart failure therapy (ACEi, beta-blocker, diuretic).

Reference: ESMO 2024 Cardio-Oncology; Schmidinger et al Lancet Oncol 2008