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      Recent advances in cardio‐oncology: a report from the ‘Heart Failure Association 2019 and World Congress on Acute Heart Failure 2019’

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          Abstract

          While anti‐cancer therapies, including chemotherapy, immunotherapy, radiotherapy, and targeted therapy, are constantly advancing, cardiovascular toxicity has become a major challenge for cardiologists and oncologists. This has led to an increasing demand of cardio‐oncology units in Europe and a growing interest of clinicians and researchers. The Heart Failure 2019 meeting of the Heart Failure Association of the European Society of Cardiology in Athens has therefore created a scientific programme that included four dedicated sessions on the topic along with several additional lectures. The major points that were discussed at the congress included the implementation and delivery of a cardio‐oncology service, the collaboration among cardio‐oncology experts, and the risk stratification, prevention, and early recognition of cardiotoxicity. Furthermore, sessions addressed the numerous different anti‐cancer therapies associated with cardiotoxic effects and provided guidance on how to treat cancer patients who develop cardiovascular disease before, during, and after treatment.

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          Most cited references76

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          Immune checkpoint inhibitors and cardiovascular toxicity

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            Cardiotoxicity of Anticancer Drugs: The Need for Cardio-Oncology and Cardio-Oncological Prevention

            Due to the aging of the populations of developed countries and a common occurrence of risk factors, it is increasingly probable that a patient may have both cancer and cardiovascular disease. In addition, cytotoxic agents and targeted therapies used to treat cancer, including classic chemotherapeutic agents, monoclonal antibodies that target tyrosine kinase receptors, small molecule tyrosine kinase inhibitors, and even antiangiogenic drugs and chemoprevention agents such as cyclooxygenase-2 inhibitors, all affect the cardiovascular system. One of the reasons is that many agents reach targets in the microenvironment and do not affect only the tumor. Combination therapy often amplifies cardiotoxicity, and radiotherapy can also cause heart problems, particularly when combined with chemotherapy. In the past, cardiotoxic risk was less evident, but it is increasingly an issue, particularly with combination therapy and adjuvant therapy. Today's oncologists must be fully aware of cardiovascular risks to avoid or prevent adverse cardiovascular effects, and cardiologists must now be ready to assist oncologists by performing evaluations relevant to the choice of therapy. There is a need for cooperation between these two areas and for the development of a novel discipline, which could be termed cardio-oncology or onco-cardiology. Here, we summarize the potential cardiovascular toxicities for a range of cancer chemotherapeutic and chemopreventive agents and emphasize the importance of evaluating cardiovascular risk when patients enter into trials and the need to develop guidelines that include collateral effects on the cardiovascular system. We also discuss mechanistic pathways and describe several potential protective agents that could be administered to patients with occult or overt risk for cardiovascular complications.
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              Assessment of echocardiography and biomarkers for the extended prediction of cardiotoxicity in patients treated with anthracyclines, taxanes, and trastuzumab.

              Because cancer patients survive longer, the impact of cardiotoxicity associated with the use of cancer treatments escalates. The present study investigates whether early alterations of myocardial strain and blood biomarkers predict incident cardiotoxicity in patients with breast cancer during treatment with anthracyclines, taxanes, and trastuzumab. Eighty-one women with newly diagnosed human epidermal growth factor receptor 2-positive breast cancer, treated with anthracyclines followed by taxanes and trastuzumab were enrolled to be evaluated every 3 months during their cancer therapy (total of 15 months) using echocardiograms and blood samples. Left ventricular ejection fraction, peak systolic longitudinal, radial, and circumferential myocardial strain were calculated. Ultrasensitive troponin I, N-terminal pro-B-type natriuretic peptide, and the interleukin family member (ST2) were also measured. Left ventricular ejection fraction decreased (64 ± 5% to 59 ± 6%; P<0.0001) over 15 months. Twenty-six patients (32%, [22%-43%]) developed cardiotoxicity as defined by the Cardiac Review and Evaluation Committee Reviewing Trastuzumab; of these patients, 5 (6%, [2%-14%]) had symptoms of heart failure. Peak systolic longitudinal myocardial strain and ultrasensitive troponin I measured at the completion of anthracyclines treatment predicted the subsequent development of cardiotoxicity; no significant associations were observed for left ventricular ejection fraction, N-terminal pro-B-type natriuretic peptide, and ST2. Longitudinal strain was <19% in all patients who later developed heart failure. In patients with breast cancer treated with anthracyclines, taxanes, and trastuzumab, systolic longitudinal myocardial strain and ultrasensitive troponin I measured at the completion of anthracyclines therapy are useful in the prediction of subsequent cardiotoxicity and may help guide treatment to avoid cardiac side-effects.
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                Author and article information

                Contributors
                markus.anker@charite.de
                Journal
                ESC Heart Fail
                ESC Heart Fail
                10.1002/(ISSN)2055-5822
                EHF2
                ESC Heart Failure
                John Wiley and Sons Inc. (Hoboken )
                2055-5822
                28 December 2019
                December 2019
                : 6
                : 6 ( doiID: 10.1002/ehf2.v6.6 )
                : 1140-1148
                Affiliations
                [ 1 ] Division of Cardiology and Metabolism, Department of Cardiology Charité and Berlin Institute of Health Center for Regenerative Therapies (BCRT) and DZHK (German Centre for Cardiovascular Research) partner site Berlin and Department of Cardiology, Charité Campus Benjamin Franklin Berlin Germany
                [ 2 ] Sechenov Medical University Moscow Russia
                [ 3 ] Department of Cardiology Medical University of Vienna Vienna Austria
                [ 4 ] Department of Cardiology University of Groningen University Medical Center Groningen, Groningen The Netherlands
                [ 5 ] University of Cyprus Medical School Nicosia Cyprus
                [ 6 ] Department of Cardiology, Cardio‐Oncology Clinic, Heart Failure Unit Athens University Hospital ‘Attikon’, National and Kapodistrian University of Athens Athens Greece
                [ 7 ] Department of Cardiology and Pneumology, Heart Center Göttingen, German Center for Cardiovascular Medicine (DZHK) University of Göttingen Medical Center, Georg‐August‐University Göttingen Germany
                [ 8 ] Department of Community Cardiology, Clalit Health Fund, and Sackler Faculty of Medicine Tel Aviv University Tel Aviv Israel
                [ 9 ] Comprehensive Heart Failure Center (CHFC) University Clinic Würzburg Würzburg Germany
                [ 10 ] 1st Department of Medicine–Cardioangiology, Faculty of Medicine University Hospital Hradec Králové Czech Republic
                [ 11 ] Department of Internal Medicine American University of Beirut Medical Center Beirut Lebanon
                [ 12 ] Department of Cardiology, Lariboisière Hospital and U942 INSERM, BIOCANVAS (Biomarqueurs Cardiovasculaires) Paris University Paris France
                [ 13 ] Department of Translational Medical Sciences and Interdepartmental Center for Clinical and Translational Sciences (CIRCET) Federico II University Naples Italy
                [ 14 ] IRCCS San Raffaele Rome Italy
                [ 15 ] Faculty of Medicine and Heart Failure Center Belgrade University Medical Center, University of Belgrade Belgrade Serbia
                [ 16 ] Royal Brompton Hospital and Imperial College London London UK
                Author notes
                [*] [* ] Correspondence to: Markus S. Anker, Department of Cardiology, Charité Campus Benjamin Franklin (CBF), Charité University Medicine, Berlin, Germany. Email: markus.anker@ 123456charite.de

                Article
                EHF212551 ESCHF-19-00374
                10.1002/ehf2.12551
                6989292
                31884717
                eb1e710b-c2bd-473e-a175-2cedf88361ec
                © 2019 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 18 October 2019
                Page count
                Figures: 2, Tables: 0, Pages: 9, Words: 2834
                Categories
                ESC and HFA Paper
                ESC and HFA Papers
                Custom metadata
                2.0
                December 2019
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.7.5 mode:remove_FC converted:29.01.2020

                cardiotoxicity,heart failure,cancer
                cardiotoxicity, heart failure, cancer

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