Why the study?
Does CMR T2 mapping detect early anthracycline-induced cardiotoxicity before LVEF decline in a preclinical pig model?
Does CMR T2 mapping detect early anthracycline-induced cardiotoxicity before LVEF decline in a preclinical pig model?
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CMR T2 mapping shows promise as an early imaging marker of reversible anthracycline cardiotoxicity, potentially allowing for timely cardioprotective interventions.
A nthracycline-based chemotherapy has played an important role in cancer care since the 1960s, either as a single agent or in combination with other chemotherapeutics, to treat a broad range of hematological and solid tumor malignancies in children and adults. Anthracyclines, however, are associated with an increased risk of cardiotoxicity, manifest by left ventricular dysfunction and/or heart failure (1). Anthracycline cardiotoxicity is at least in part mediated through the formation of reactive oxygen species, leading to oxidative stress and mitochondrial dysfunction (2). Anthracyclines bind to cardiomyocyte-specific topoisomerase-IIb and cause DNA double strand breaks and transcriptome changes that are responsible for regulation of mitochondrial bioenergetics, generation of reactive oxygen species, and oxidative phosphorylation (3). Risk stratification and early detection of anthracycline cardiotoxicity are 2 important aspects of cardio-oncology care, as they provide an opportunity to initiate cardioprotective strategies and ultimately mitigate the risk of myocardial injury and heart failure. Major risk factors for anthracycline cardiotoxicity include high cumulative anthracycline dose, age, radiation exposure to the heart, and concomitant treatment with other cardiotoxic therapies, such
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Yu et al. (2019) conducted an editorial in Anthracycline-induced cardiotoxicity (n=20). CMR T2 mapping vs. Control group was evaluated on T2 relaxation time prolongation.
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