Cardiology Letters 2024, 33(5):316-326

Cardiotoxic treatment in oncohaematology

Juraj Sokol¹, František Nehaj^{2, 3}, Juraj Chudej¹, Lenka Lisá¹, Ľudmila Lineková¹, Richard Jusko¹, Ivan Kecskés^{1, 4}, Ivana Plameňová¹

¹ Klinika hematológie a transfuziológie, Jesseniova lekárska fakulta v Martine, Univerzita Komenského v Bratislave, Bratislava

² Oddelenie arytmológie a kardiostimulácie, Národný ústav srdcových a cievnych chorôb, a. s., Bratislava

³ Klinika kardiológie a angiológie, Slovenská zdravotnícka univerzita, Bratislava

⁴ Onkologické centrum, Univerzitná nemocnica Martin, Martin, Slovenská republika

Chemotherapy and targeted therapy have significantly improved the prognosis of oncohaematological patients. Antineoplastic treatment can cause adverse cardiovascular effects known as cardiotoxicity, which requires modification, interruption or withdrawal of life-saving drugs. The onset of cardiotoxicity may depend on the class, dose, route, and duration of anticancer drug administration and individual risk factors. Standard chemotherapy exerts its toxic effect mainly by inducing oxidative stress and genomic instability. At the same time, new targeted molecules work by interfering with signalling pathways that are important for tumour cells and cardiomyocytes. For example, Bruton tyrosine kinase (BTK) inhibitors interfere with phosphatidylinositol-3-kinase isoforms involved in cardiac hypertrophy, contractility, and regulation of various proteins. Offtarget effects of BTK inhibitors are associated with an increased incidence of atrial fibrillation. This review summarises current knowledge about the cardiotoxic effects of targeted therapies used in haematology.

Keywords: oncohematology; cardiotoxicity; targeted therapy; pathomechanism; prevention; heart failure; atrial fibrillation

Published: May 1, 2024  Show citation