“…In studies of the late effects of anthracyclines, patients treated with anthracyclines 82 months previously were found to have higher ECV values than matched controls (54) and this was independent of underlying cancer or cardiovascular conditions (55). These findings have not however been replicated in scans in lower risk patients receiving contemporary doses of anthracyclines with and without trastuzumab (56,57). While LGE offers prognostic information in a variety of cardiovascular diseases, it is not commonly found in cardiomyopathy related to anthracyclines or HER2 therapy where histology has shown diffuse interstitial rather than focal fibrosis (53,54,(58)(59)(60).…”
Advances in cancer therapy have led to significantly longer cancer-free survival times over the last 40 years. Improved survivorship coupled with increasing recognition of an expanding range of adverse cardiovascular effects of many established and novel cancer therapies has highlighted the impact of cardiovascular disease in this population. This has led to the emergence of dedicated cardio-oncology services that can provide pre-treatment risk stratification, surveillance, diagnosis, and monitoring of cardiotoxicity during cancer therapies, and late effects screening following completion of treatment. Cardiovascular imaging and the development of imaging biomarkers that can accurately and reliably detect pre-clinical disease and enhance our understanding of the underlying pathophysiology of cancer treatment-related cardiotoxicity are becoming increasingly important. Multi-parametric cardiovascular magnetic resonance (CMR) is able to assess cardiac structure, function, and provide myocardial tissue characterization, and hence can be used to address a variety of important clinical questions in the emerging field of cardio-oncology. In this review, we discuss the current and potential future applications of CMR in the investigation and management of cancer patients.
“…In studies of the late effects of anthracyclines, patients treated with anthracyclines 82 months previously were found to have higher ECV values than matched controls (54) and this was independent of underlying cancer or cardiovascular conditions (55). These findings have not however been replicated in scans in lower risk patients receiving contemporary doses of anthracyclines with and without trastuzumab (56,57). While LGE offers prognostic information in a variety of cardiovascular diseases, it is not commonly found in cardiomyopathy related to anthracyclines or HER2 therapy where histology has shown diffuse interstitial rather than focal fibrosis (53,54,(58)(59)(60).…”
Advances in cancer therapy have led to significantly longer cancer-free survival times over the last 40 years. Improved survivorship coupled with increasing recognition of an expanding range of adverse cardiovascular effects of many established and novel cancer therapies has highlighted the impact of cardiovascular disease in this population. This has led to the emergence of dedicated cardio-oncology services that can provide pre-treatment risk stratification, surveillance, diagnosis, and monitoring of cardiotoxicity during cancer therapies, and late effects screening following completion of treatment. Cardiovascular imaging and the development of imaging biomarkers that can accurately and reliably detect pre-clinical disease and enhance our understanding of the underlying pathophysiology of cancer treatment-related cardiotoxicity are becoming increasingly important. Multi-parametric cardiovascular magnetic resonance (CMR) is able to assess cardiac structure, function, and provide myocardial tissue characterization, and hence can be used to address a variety of important clinical questions in the emerging field of cardio-oncology. In this review, we discuss the current and potential future applications of CMR in the investigation and management of cancer patients.
“…Heart failure is a serious side effect following DOX treatment (Cardinale et al, 2015;Maestrini et al, 2017), so this study explored the effects of AL on heart function in zebrafish. Heart rate (beats/minute) of zebrafish larvae was used as a parameter for cardiotoxicity.…”
Section: Al and Cardiotoxicitymentioning
confidence: 99%
“…Chemotherapy drugs, such as doxorubicin (DOX), induce cell death (apoptosis) or permanent growth arrest (cellular senescence) in cancer cells (Gonzalez et al, 2016). Although DOX is effective in preventing cancer progression, it damages normal tissues, including heart tissue, causing structural alterations, left ventricular dysfunction, and congestive heart failure (Cardinale et al, 2015;Maestrini et al, 2017). Hence, cardiotoxicity is a major concern during chemotherapy, as it may lead to morbidity and mortality of cancer patients (Khan et al, 2016).…”
DOX also induces cellular senescence and activates the inflammatory marker nuclear factor-kappa B (NFκB), creating a pro-inflammatory environment which
“…Gadolinium-based contrast agents can be administered to detect focal myocardial scarring and fibrosis, and the distribution and extent of myocardial scar can be used both to differentiate aetiologies of myocardial disease (for example ischaemic cardiomyopathy versus myocarditis) and to estimate prognosis [74, 75]. Although experimental models of anthracycline cardiotoxicity [76] demonstrated focal scarring on late gadolinium enhancement (LGE) imaging, clinical studies suggest LGE is rarely detected, and is not associated with outcomes [77, 78]. Rather than focal scarring, anthracyclines are thought to cause diffuse interstitial fibrosis, via excess collagen deposition.…”
Section: Imaging Biomarkers To Understand the Pathophysiology Of Ctrcdmentioning
confidence: 99%
“…T1 mapping has been explored as a biomarker of early anthracycline cardiotoxicity, with several small studies showing elevated myocardial T1 and extracellular volume fraction (ECV) in patients treated with anthracyclines compared with age- and sex-matched controls [81, 82]. Other studies have however failed to reproduce these results [78, 83], particularly in lower risk patients. This conflicting data therefore means that, at least currently, T1 mapping is not a tool for anthracycline- or HER2-related mainstream cardiotoxicity screening.Fig.…”
Section: Imaging Biomarkers To Understand the Pathophysiology Of Ctrcdmentioning
Opinion statement
Early detection and treatment of cardiotoxicity from cancer therapies is key to preventing a rise in adverse cardiovascular outcomes in cancer patients. Over-diagnosis of cardiotoxicity in this context is however equally hazardous, leading to patients receiving suboptimal cancer treatment, thereby impacting cancer outcomes. Accurate screening therefore depends on the widespread availability of sensitive and reproducible biomarkers of cardiotoxicity, which can clearly discriminate early disease. Blood biomarkers are limited in cardiovascular disease and clinicians generally still use generic screening with ejection fraction, based on historical local expertise and resources. Recently, however, there has been growing recognition that simple measurement of left ventricular ejection fraction using 2D echocardiography may not be optimal for screening: diagnostic accuracy, reproducibility and feasibility are limited. Modern cancer therapies affect many myocardial pathways: inflammatory, fibrotic, metabolic, vascular and myocyte function, meaning that multiple biomarkers may be needed to track myocardial cardiotoxicity. Advanced imaging modalities including cardiovascular magnetic resonance (CMR), computed tomography (CT) and positron emission tomography (PET) add improved sensitivity and insights into the underlying pathophysiology, as well as the ability to screen for other cardiotoxicities including coronary artery, valve and pericardial diseases resulting from cancer treatment. Delivering screening for cardiotoxicity using advanced imaging modalities will however require a significant change in current clinical pathways, with incorporation of machine learning algorithms into imaging analysis fundamental to improving efficiency and precision. In the future, we should aspire to personalized rather than generic screening, based on a patient’s individual risk factors and the pathophysiological mechanisms of the cancer treatment they are receiving. We should aspire that progress in cardiooncology is able to track progress in oncology, and to ensure that the current ‘one size fits all’ approach to screening be obsolete in the very near future.
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