Drug-induced myocardial dysfunction – recommendations for assessment in clinical and pre-clinical studies

Ebrahimi, Ahmad; Raichlen, Joel S.; Pointon, Amy; Gottfridsson, Christer; Munley, Jiefen; Hockings, Paul D.; Cartwright, James; Buss, Nicholas; Wikström, Johannes; Gan, Li‐Ming; Whittaker, Andrew K.; Khalil, Ali; George, Richard Т. De; Garkaviy, Pavlo; Brott, David

doi:10.1080/14740338.2020.1731471

Cited by 1 publication

(2 citation statements)

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“…B-type natriuretic peptides and N-terminal fragment of the prohormone brain natriuretic peptide are also considered routine biomarkers for cardiac dysfunction and HF diagnosis during chemotherapy. [44][45][46] The main disadvantage of these biomarkers is that they cannot be used as an early indicator of cardiotoxicity because their expressions occur after the irreversible cardiac damage. So there is an urgent need to identify new potential early detection biomarkers to provide early warning for chemotherapy-induced cardiotoxicity.…”

Section: Epigenetics and Aicmentioning

confidence: 99%

“…Several clinical studies reported that some cardiac biomarkers, such as troponin I and troponin T, could be used to confirm cardiotoxicity, and high levels of troponin indicate there is irreversible myocardial cell injury in patients with cancer who received chemotherapy. B‐type natriuretic peptides and N‐terminal fragment of the prohormone brain natriuretic peptide are also considered routine biomarkers for cardiac dysfunction and HF diagnosis during chemotherapy 44–46 . The main disadvantage of these biomarkers is that they cannot be used as an early indicator of cardiotoxicity because their expressions occur after the irreversible cardiac damage.…”

Section: Epigenetics and Aicmentioning

confidence: 99%

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Epigenetic Changes Associated With Anthracycline‐Induced Cardiotoxicity

Tantawy

Pamittan

Singh

et al. 2020

Clinical Translational Sci

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Advances in cancer treatment have significantly improved the survival of patients with cancer, but, unfortunately, many of these treatments also have long‐term complications. Cancer treatment‐related cardiotoxicities are becoming a significant clinical problem that a new discipline, Cardio‐Oncology, was established to advance the cardiovascular care of patients with growing cancer populations. Anthracyclines are a class of chemotherapeutic agents used to treat many cancers in adults and children. Their clinical use is limited by anthracycline‐induced cardiotoxicity (AIC), which can lead to heart failure. Early‐onset cardiotoxicity appears within a year of treatment, whereas late‐onset cardiotoxicity occurs > 1 year and even up to decades after treatment completion. The pathophysiology of AIC was hypothesized to be caused by generation of reactive oxygen species that lead to lipid peroxidation, defective mitochondrial biogenesis, and DNA damage of the cardiomyocytes. The accumulation of anthracycline metabolites was also proposed to cause mitochondrial damage and the induction of cardiac cell apoptosis, which induces arrhythmias, contractile dysfunction, and cardiomyocyte death. This paper will provide a general overview of cardiotoxicity focusing on the effect of anthracyclines and their epigenetic molecular mechanisms on cardiotoxicity.

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Section: Epigenetics and Aicmentioning

confidence: 99%

Section: Epigenetics and Aicmentioning

confidence: 99%