Towards pre-treatment imaging prediction of chemotherapy-related cardiotoxicity
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Nuclear Medicine and Molecular Imaging Center, Clinical Hospital, University of the Republic, Montevideo, Uruguay Uruguayan Center of Molecular Imaging (CUDIM), Montevideo, Uruguay Cardiology Department, Clinical Hospital, University Cardiovascular Center, University of the Republic, Montevideo, Uruguay Nuclear Medicine Department, Assistance Center of the Medical Union of Uruguay (CASMU), Montevideo, Uruguay
Received Aug 31, 2020; accepted Aug 31, 2020 doi:10.1007/s12350-020-02368-x
See related article, https://doi.org/10.10 07/s12350-020-02277-z
Although the significant advances in cancer therapy obtained during the last decades have prolonged the survival of many patients, this improvement has been achieved at the expense of an increase in cardiovascular complications secondary to chemotherapy and/or radiotherapy.1 Consequently, cardiovascular (CV) disease is the first cause of death in patients who survive cancer.2 The pathogenic basis of this repercussion would be a direct toxicity of chemotherapy agents on cardiac structure and function or an accelerated development of CV disease, especially in subjects with previous risk factors. This cardiotoxicity can manifest itself in a wide clinical spectrum, which includes uni or biventricular systolic dysfunction, myocardial ischemia, valvular heart disease, arrhythmias, arterial hypertension, thromboembolic disease, and peripheral, pulmonary vascular or pericardial involvement.2 The most common manifestation is heart failure, a research endpoint that is usually a late phenomenon. However, the frequency and severity of this damage is a function of the drugs used,
Reprint requests: Rodolfo Ferrando Castagnetto, MD, MSc, Nuclear Medicine and Molecular Imaging Center, Clinical Hospital, University of the Republic, Montevideo, Uruguay; [email protected] J Nucl Cardiol 1071-3581/$34.00 Copyright Ó 2020 American Society of Nuclear Cardiology.
alone or in combination, and the dose administered in each patient.1 Thus, some cytostatic agents mainly determine systolic dysfunction of variable degree, such as anthracyclines and trastuzumab, while others, such as 5-fluorouracil and its prodrug, capecitabine, are more frequently associated with the development of acute myocardial ischemia.3 Observational clinical studies that explored the relationship between CV risk and cardiotoxicity found that age, hypertension, diabetes, smoking, previous radiotherapy and pre-existing CV disease are associated with an increased risk of post-chemotherapy myocardial damage. However, the causal relationship between treatment with different cytostatic agents and cardiotoxicity still remains uncertain.3 Although the detailed mechanisms underlying chemotherapy-related cardiotoxicity (CTRC) are unknown, a correct risk stratification prior to therapy represents a major clinical challenge, which can benefit from the contributions of various imaging techniques. It is then understood that, to optimize the therapy of cancer patients, a greater collaborative effort is required between
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