Early detection of anthracycline‐ and trastuzumab‐induced cardiotoxicity: value and optimal timing of serum biomarkers and echocardiographic parameters
Aims To evaluate echocardiographic and biomarker changes during chemotherapy, assess their ability to early detect and predict cardiotoxicity and to define the best time for their evaluation. Methods and results Seventy‐two women with breast cancer (52 ± 9.8 years) treated with anthracyclines (26 al...
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| Published in | ESC Heart Failure Vol. 9; no. 2; pp. 1127 - 1137 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley & Sons, Inc
01.04.2022
John Wiley and Sons Inc Wiley |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Aims
To evaluate echocardiographic and biomarker changes during chemotherapy, assess their ability to early detect and predict cardiotoxicity and to define the best time for their evaluation.
Methods and results
Seventy‐two women with breast cancer (52 ± 9.8 years) treated with anthracyclines (26 also with trastuzumab), were evaluated for 14 months (6 echocardiograms/12 laboratory tests). We analysed: high‐sensitivity cardiac troponin T, NT‐proBNP, global longitudinal strain (GLS), left ventricle end‐systolic volume (LVESV), left ventricle end‐diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF). Cardiotoxicity was defined as a reduction in LVEF>10% compared with baseline with LVEF<53%. High‐sensitivity troponin T levels rose gradually reaching a maximum peak at 96 ± 13 days after starting chemotherapy (P < 0.001) and 62.5% of patients presented increased values during treatment. NT‐proBNP augmented after each anthracycline cycle (mean pre‐cycle levels of 72 ± 68 pg/mL and post‐cycle levels of 260 ± 187 pg/mL; P < 0.0001). Cardiotoxicity was detected in 9.7% of patients (mean onset at 5.2 months). In the group with cardiotoxicity, the LVESV was higher compared with those without cardiotoxicity (40 mL vs. 29.5 mL; P = 0.045) at 1 month post‐anthracycline treatment and the decline in GLS was more pronounced (−17.6% vs. −21.4%; P = 0.03). Trastuzumab did not alter serum biomarkers, but it was associated with an increase in LVESV and LVEDV (P < 0.05). While baseline LVEF was an independent predictor of later cardiotoxicity (P = 0.039), LVESV and GLS resulted to be early detectors of cardiotoxicity [odds ratio = 1.12 (1.02–1.24), odds ratio = 0.66 (0.44–0.92), P < 0.05] at 1 month post‐anthracycline treatment. Neither high‐sensitivity troponin T nor NT‐proBNP was capable of predicting subsequent cardiotoxicity.
Conclusions
One month after completion of anthracycline treatment is the optimal time to detect cardiotoxicity by means of imaging parameters (LVESV and GSL) and to determine maximal troponin rise. Baseline LVEF was a predictor of later cardiotoxicity. Trastuzumab therapy does not affect troponin values hence imaging techniques are recommended to detect trastuzumab‐induced cardiotoxicity. |
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| AbstractList | AIMSTo evaluate echocardiographic and biomarker changes during chemotherapy, assess their ability to early detect and predict cardiotoxicity and to define the best time for their evaluation. METHODS AND RESULTSSeventy-two women with breast cancer (52 ± 9.8 years) treated with anthracyclines (26 also with trastuzumab), were evaluated for 14 months (6 echocardiograms/12 laboratory tests). We analysed: high-sensitivity cardiac troponin T, NT-proBNP, global longitudinal strain (GLS), left ventricle end-systolic volume (LVESV), left ventricle end-diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF). Cardiotoxicity was defined as a reduction in LVEF>10% compared with baseline with LVEF<53%. High-sensitivity troponin T levels rose gradually reaching a maximum peak at 96 ± 13 days after starting chemotherapy (P < 0.001) and 62.5% of patients presented increased values during treatment. NT-proBNP augmented after each anthracycline cycle (mean pre-cycle levels of 72 ± 68 pg/mL and post-cycle levels of 260 ± 187 pg/mL; P < 0.0001). Cardiotoxicity was detected in 9.7% of patients (mean onset at 5.2 months). In the group with cardiotoxicity, the LVESV was higher compared with those without cardiotoxicity (40 mL vs. 29.5 mL; P = 0.045) at 1 month post-anthracycline treatment and the decline in GLS was more pronounced (-17.6% vs. -21.4%; P = 0.03). Trastuzumab did not alter serum biomarkers, but it was associated with an increase in LVESV and LVEDV (P < 0.05). While baseline LVEF was an independent predictor of later cardiotoxicity (P = 0.039), LVESV and GLS resulted to be early detectors of cardiotoxicity [odds ratio = 1.12 (1.02-1.24), odds ratio = 0.66 (0.44-0.92), P < 0.05] at 1 month post-anthracycline treatment. Neither high-sensitivity troponin T nor NT-proBNP was capable of predicting subsequent cardiotoxicity. CONCLUSIONSOne month after completion of anthracycline treatment is the optimal time to detect cardiotoxicity by means of imaging parameters (LVESV and GSL) and to determine maximal troponin rise. Baseline LVEF was a predictor of later cardiotoxicity. Trastuzumab therapy does not affect troponin values hence imaging techniques are recommended to detect trastuzumab-induced cardiotoxicity. To evaluate echocardiographic and biomarker changes during chemotherapy, assess their ability to early detect and predict cardiotoxicity and to define the best time for their evaluation. Seventy-two women with breast cancer (52 ± 9.8 years) treated with anthracyclines (26 also with trastuzumab), were evaluated for 14 months (6 echocardiograms/12 laboratory tests). We analysed: high-sensitivity cardiac troponin T, NT-proBNP, global longitudinal strain (GLS), left ventricle end-systolic volume (LVESV), left ventricle end-diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF). Cardiotoxicity was defined as a reduction in LVEF>10% compared with baseline with LVEF<53%. High-sensitivity troponin T levels rose gradually reaching a maximum peak at 96 ± 13 days after starting chemotherapy (P < 0.001) and 62.5% of patients presented increased values during treatment. NT-proBNP augmented after each anthracycline cycle (mean pre-cycle levels of 72 ± 68 pg/mL and post-cycle levels of 260 ± 187 pg/mL; P < 0.0001). Cardiotoxicity was detected in 9.7% of patients (mean onset at 5.2 months). In the group with cardiotoxicity, the LVESV was higher compared with those without cardiotoxicity (40 mL vs. 29.5 mL; P = 0.045) at 1 month post-anthracycline treatment and the decline in GLS was more pronounced (-17.6% vs. -21.4%; P = 0.03). Trastuzumab did not alter serum biomarkers, but it was associated with an increase in LVESV and LVEDV (P < 0.05). While baseline LVEF was an independent predictor of later cardiotoxicity (P = 0.039), LVESV and GLS resulted to be early detectors of cardiotoxicity [odds ratio = 1.12 (1.02-1.24), odds ratio = 0.66 (0.44-0.92), P < 0.05] at 1 month post-anthracycline treatment. Neither high-sensitivity troponin T nor NT-proBNP was capable of predicting subsequent cardiotoxicity. One month after completion of anthracycline treatment is the optimal time to detect cardiotoxicity by means of imaging parameters (LVESV and GSL) and to determine maximal troponin rise. Baseline LVEF was a predictor of later cardiotoxicity. Trastuzumab therapy does not affect troponin values hence imaging techniques are recommended to detect trastuzumab-induced cardiotoxicity. Aims To evaluate echocardiographic and biomarker changes during chemotherapy, assess their ability to early detect and predict cardiotoxicity and to define the best time for their evaluation. Methods and results Seventy‐two women with breast cancer (52 ± 9.8 years) treated with anthracyclines (26 also with trastuzumab), were evaluated for 14 months (6 echocardiograms/12 laboratory tests). We analysed: high‐sensitivity cardiac troponin T, NT‐proBNP, global longitudinal strain (GLS), left ventricle end‐systolic volume (LVESV), left ventricle end‐diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF). Cardiotoxicity was defined as a reduction in LVEF>10% compared with baseline with LVEF<53%. High‐sensitivity troponin T levels rose gradually reaching a maximum peak at 96 ± 13 days after starting chemotherapy (P < 0.001) and 62.5% of patients presented increased values during treatment. NT‐proBNP augmented after each anthracycline cycle (mean pre‐cycle levels of 72 ± 68 pg/mL and post‐cycle levels of 260 ± 187 pg/mL; P < 0.0001). Cardiotoxicity was detected in 9.7% of patients (mean onset at 5.2 months). In the group with cardiotoxicity, the LVESV was higher compared with those without cardiotoxicity (40 mL vs. 29.5 mL; P = 0.045) at 1 month post‐anthracycline treatment and the decline in GLS was more pronounced (−17.6% vs. −21.4%; P = 0.03). Trastuzumab did not alter serum biomarkers, but it was associated with an increase in LVESV and LVEDV (P < 0.05). While baseline LVEF was an independent predictor of later cardiotoxicity (P = 0.039), LVESV and GLS resulted to be early detectors of cardiotoxicity [odds ratio = 1.12 (1.02–1.24), odds ratio = 0.66 (0.44–0.92), P < 0.05] at 1 month post‐anthracycline treatment. Neither high‐sensitivity troponin T nor NT‐proBNP was capable of predicting subsequent cardiotoxicity. Conclusions One month after completion of anthracycline treatment is the optimal time to detect cardiotoxicity by means of imaging parameters (LVESV and GSL) and to determine maximal troponin rise. Baseline LVEF was a predictor of later cardiotoxicity. Trastuzumab therapy does not affect troponin values hence imaging techniques are recommended to detect trastuzumab‐induced cardiotoxicity. Abstract Aims To evaluate echocardiographic and biomarker changes during chemotherapy, assess their ability to early detect and predict cardiotoxicity and to define the best time for their evaluation. Methods and results Seventy‐two women with breast cancer (52 ± 9.8 years) treated with anthracyclines (26 also with trastuzumab), were evaluated for 14 months (6 echocardiograms/12 laboratory tests). We analysed: high‐sensitivity cardiac troponin T, NT‐proBNP, global longitudinal strain (GLS), left ventricle end‐systolic volume (LVESV), left ventricle end‐diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF). Cardiotoxicity was defined as a reduction in LVEF>10% compared with baseline with LVEF<53%. High‐sensitivity troponin T levels rose gradually reaching a maximum peak at 96 ± 13 days after starting chemotherapy (P < 0.001) and 62.5% of patients presented increased values during treatment. NT‐proBNP augmented after each anthracycline cycle (mean pre‐cycle levels of 72 ± 68 pg/mL and post‐cycle levels of 260 ± 187 pg/mL; P < 0.0001). Cardiotoxicity was detected in 9.7% of patients (mean onset at 5.2 months). In the group with cardiotoxicity, the LVESV was higher compared with those without cardiotoxicity (40 mL vs. 29.5 mL; P = 0.045) at 1 month post‐anthracycline treatment and the decline in GLS was more pronounced (−17.6% vs. −21.4%; P = 0.03). Trastuzumab did not alter serum biomarkers, but it was associated with an increase in LVESV and LVEDV (P < 0.05). While baseline LVEF was an independent predictor of later cardiotoxicity (P = 0.039), LVESV and GLS resulted to be early detectors of cardiotoxicity [odds ratio = 1.12 (1.02–1.24), odds ratio = 0.66 (0.44–0.92), P < 0.05] at 1 month post‐anthracycline treatment. Neither high‐sensitivity troponin T nor NT‐proBNP was capable of predicting subsequent cardiotoxicity. Conclusions One month after completion of anthracycline treatment is the optimal time to detect cardiotoxicity by means of imaging parameters (LVESV and GSL) and to determine maximal troponin rise. Baseline LVEF was a predictor of later cardiotoxicity. Trastuzumab therapy does not affect troponin values hence imaging techniques are recommended to detect trastuzumab‐induced cardiotoxicity. Abstract Aims To evaluate echocardiographic and biomarker changes during chemotherapy, assess their ability to early detect and predict cardiotoxicity and to define the best time for their evaluation. Methods and results Seventy‐two women with breast cancer (52 ± 9.8 years) treated with anthracyclines (26 also with trastuzumab), were evaluated for 14 months (6 echocardiograms/12 laboratory tests). We analysed: high‐sensitivity cardiac troponin T, NT‐proBNP, global longitudinal strain (GLS), left ventricle end‐systolic volume (LVESV), left ventricle end‐diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF). Cardiotoxicity was defined as a reduction in LVEF>10% compared with baseline with LVEF<53%. High‐sensitivity troponin T levels rose gradually reaching a maximum peak at 96 ± 13 days after starting chemotherapy ( P < 0.001) and 62.5% of patients presented increased values during treatment. NT‐proBNP augmented after each anthracycline cycle (mean pre‐cycle levels of 72 ± 68 pg/mL and post‐cycle levels of 260 ± 187 pg/mL; P < 0.0001). Cardiotoxicity was detected in 9.7% of patients (mean onset at 5.2 months). In the group with cardiotoxicity, the LVESV was higher compared with those without cardiotoxicity (40 mL vs. 29.5 mL; P = 0.045) at 1 month post‐anthracycline treatment and the decline in GLS was more pronounced (−17.6% vs. −21.4%; P = 0.03). Trastuzumab did not alter serum biomarkers, but it was associated with an increase in LVESV and LVEDV ( P < 0.05). While baseline LVEF was an independent predictor of later cardiotoxicity ( P = 0.039), LVESV and GLS resulted to be early detectors of cardiotoxicity [odds ratio = 1.12 (1.02–1.24), odds ratio = 0.66 (0.44–0.92), P < 0.05] at 1 month post‐anthracycline treatment. Neither high‐sensitivity troponin T nor NT‐proBNP was capable of predicting subsequent cardiotoxicity. Conclusions One month after completion of anthracycline treatment is the optimal time to detect cardiotoxicity by means of imaging parameters (LVESV and GSL) and to determine maximal troponin rise. Baseline LVEF was a predictor of later cardiotoxicity. Trastuzumab therapy does not affect troponin values hence imaging techniques are recommended to detect trastuzumab‐induced cardiotoxicity. AimsTo evaluate echocardiographic and biomarker changes during chemotherapy, assess their ability to early detect and predict cardiotoxicity and to define the best time for their evaluation.Methods and resultsSeventy‐two women with breast cancer (52 ± 9.8 years) treated with anthracyclines (26 also with trastuzumab), were evaluated for 14 months (6 echocardiograms/12 laboratory tests). We analysed: high‐sensitivity cardiac troponin T, NT‐proBNP, global longitudinal strain (GLS), left ventricle end‐systolic volume (LVESV), left ventricle end‐diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF). Cardiotoxicity was defined as a reduction in LVEF>10% compared with baseline with LVEF<53%. High‐sensitivity troponin T levels rose gradually reaching a maximum peak at 96 ± 13 days after starting chemotherapy (P < 0.001) and 62.5% of patients presented increased values during treatment. NT‐proBNP augmented after each anthracycline cycle (mean pre‐cycle levels of 72 ± 68 pg/mL and post‐cycle levels of 260 ± 187 pg/mL; P < 0.0001). Cardiotoxicity was detected in 9.7% of patients (mean onset at 5.2 months). In the group with cardiotoxicity, the LVESV was higher compared with those without cardiotoxicity (40 mL vs. 29.5 mL; P = 0.045) at 1 month post‐anthracycline treatment and the decline in GLS was more pronounced (−17.6% vs. −21.4%; P = 0.03). Trastuzumab did not alter serum biomarkers, but it was associated with an increase in LVESV and LVEDV (P < 0.05). While baseline LVEF was an independent predictor of later cardiotoxicity (P = 0.039), LVESV and GLS resulted to be early detectors of cardiotoxicity [odds ratio = 1.12 (1.02–1.24), odds ratio = 0.66 (0.44–0.92), P < 0.05] at 1 month post‐anthracycline treatment. Neither high‐sensitivity troponin T nor NT‐proBNP was capable of predicting subsequent cardiotoxicity.ConclusionsOne month after completion of anthracycline treatment is the optimal time to detect cardiotoxicity by means of imaging parameters (LVESV and GSL) and to determine maximal troponin rise. Baseline LVEF was a predictor of later cardiotoxicity. Trastuzumab therapy does not affect troponin values hence imaging techniques are recommended to detect trastuzumab‐induced cardiotoxicity. |
| Author | Castellano, José María Wasniewski, Samantha Zorita, Blanca Amado Escañuela, Maximiliano German Martín‐Asenjo, Roberto Madurga, Rodrigo Barrio, Patricia Moreno‐Arciniegas, Andrea Ramírez Merino, Natalia Ciruelos, Eva Solís, Jorge López‐Melgar, Beatriz Fernández‐Friera, Leticia Parra Jiménez, Francisco Javier Díaz‐Antón, Belén |
| AuthorAffiliation | 2 Unidad de Imagen Cardiaca HM Hospitales‐Centro Integral de Enfermedades Cardiovasculares HM CIEC Madrid Spain 10 Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) Madrid Spain 8 Servicio de Cardiología Hospital Universitario 12 de Octubre Madrid Spain 12 CIBER de enfermedades CardioVasculares (CIBERCV) Madrid Spain 11 Servicio Oncología Hospital Universitario 12 de Octubre Madrid Spain 1 Departamento de Cardiología HM Hospitales‐Centro Integral de Enfermedades Cardiovasculares HM CIEC Melchor Fernández Almagro 3 Madrid 28029 Spain 6 Facultad de Ciencias Experimentales Universidad Francisco de Vitoria Madrid Spain 5 Fundación de Investigación HM Hospitales HM Hospitales Madrid Spain 7 Departamento de Oncología Médica HM Hospitales Madrid Spain 9 Hospital General de Segovia Segovia Spain 3 Universidad CEU San Pablo Madrid Spain 4 Atria Clinic Madrid Spain |
| AuthorAffiliation_xml | – name: 7 Departamento de Oncología Médica HM Hospitales Madrid Spain – name: 1 Departamento de Cardiología HM Hospitales‐Centro Integral de Enfermedades Cardiovasculares HM CIEC Melchor Fernández Almagro 3 Madrid 28029 Spain – name: 8 Servicio de Cardiología Hospital Universitario 12 de Octubre Madrid Spain – name: 6 Facultad de Ciencias Experimentales Universidad Francisco de Vitoria Madrid Spain – name: 4 Atria Clinic Madrid Spain – name: 2 Unidad de Imagen Cardiaca HM Hospitales‐Centro Integral de Enfermedades Cardiovasculares HM CIEC Madrid Spain – name: 12 CIBER de enfermedades CardioVasculares (CIBERCV) Madrid Spain – name: 5 Fundación de Investigación HM Hospitales HM Hospitales Madrid Spain – name: 9 Hospital General de Segovia Segovia Spain – name: 10 Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) Madrid Spain – name: 11 Servicio Oncología Hospital Universitario 12 de Octubre Madrid Spain – name: 3 Universidad CEU San Pablo Madrid Spain |
| Author_xml | – sequence: 1 givenname: Belén surname: Díaz‐Antón fullname: Díaz‐Antón, Belén organization: Atria Clinic – sequence: 2 givenname: Rodrigo surname: Madurga fullname: Madurga, Rodrigo organization: Universidad Francisco de Vitoria – sequence: 3 givenname: Blanca surname: Zorita fullname: Zorita, Blanca organization: HM Hospitales‐Centro Integral de Enfermedades Cardiovasculares HM CIEC – sequence: 4 givenname: Samantha surname: Wasniewski fullname: Wasniewski, Samantha organization: HM Hospitales‐Centro Integral de Enfermedades Cardiovasculares HM CIEC – sequence: 5 givenname: Andrea surname: Moreno‐Arciniegas fullname: Moreno‐Arciniegas, Andrea organization: HM Hospitales‐Centro Integral de Enfermedades Cardiovasculares HM CIEC – sequence: 6 givenname: Beatriz surname: López‐Melgar fullname: López‐Melgar, Beatriz organization: HM Hospitales‐Centro Integral de Enfermedades Cardiovasculares HM CIEC – sequence: 7 givenname: Natalia surname: Ramírez Merino fullname: Ramírez Merino, Natalia organization: HM Hospitales – sequence: 8 givenname: Roberto surname: Martín‐Asenjo fullname: Martín‐Asenjo, Roberto organization: Hospital Universitario 12 de Octubre – sequence: 9 givenname: Patricia surname: Barrio fullname: Barrio, Patricia organization: HM Hospitales‐Centro Integral de Enfermedades Cardiovasculares HM CIEC – sequence: 10 givenname: Maximiliano German surname: Amado Escañuela fullname: Amado Escañuela, Maximiliano German organization: Hospital General de Segovia – sequence: 11 givenname: Jorge surname: Solís fullname: Solís, Jorge organization: CIBER de enfermedades CardioVasculares (CIBERCV) – sequence: 12 givenname: Francisco Javier surname: Parra Jiménez fullname: Parra Jiménez, Francisco Javier organization: HM Hospitales‐Centro Integral de Enfermedades Cardiovasculares HM CIEC – sequence: 13 givenname: Eva surname: Ciruelos fullname: Ciruelos, Eva organization: Hospital Universitario 12 de Octubre – sequence: 14 givenname: José María surname: Castellano fullname: Castellano, José María organization: CIBER de enfermedades CardioVasculares (CIBERCV) – sequence: 15 givenname: Leticia surname: Fernández‐Friera fullname: Fernández‐Friera, Leticia email: lafernandez@cnic.es organization: CIBER de enfermedades CardioVasculares (CIBERCV) |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35106939$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2022 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology. 2022. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| DOI | 10.1002/ehf2.13782 |
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| DocumentTitleAlternate | Early detection of anthracycline‐induced and trastuzumab‐induced cardiotoxicity: value and optimal timing of serum biomarkers and echocardiographic parameters |
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| Issue | 2 |
| Keywords | Anthracyclines Global longitudinal strain Cardiotoxicity High-sensitivity cardiac troponin Trastuzumab |
| Language | English |
| License | Attribution-NonCommercial 2022 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
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| Notes | José María Castellano and Leticia Fernández‐Friera contributed equally to the manuscript. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
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| PublicationDate | April 2022 |
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| PublicationTitle | ESC Heart Failure |
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The EACVI/ASE inter‐vendor comparison study publication-title: J Am Soc Echocardiogr – volume: 28 start-page: 1 year: 2015 end-page: 39 article-title: Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the ASE and the EACVI publication-title: J Am Soc Echocardiogr – volume: 50 start-page: 46 year: 2014 end-page: 52 article-title: Assessment and comparison of acute cardiac toxicity during high‐dose cyclophosphamide and high‐dose etoposide stem cell mobilization regimens with N‐terminal pro‐B‐type natriuretic peptide publication-title: Transfus Apher Sci – volume: 39 start-page: 168 year: 2014 end-page: 174 article-title: Incidence and risk‐factors of CHOP/R‐CHOP‐related cardiotoxi‐ city in patients with aggressive non‐Hodgkin's lymphoma publication-title: J Clin Pharm Ther – volume: 135 start-page: 1397 year: 2017 end-page: 1412 article-title: Detailed echocardiographic phenotyping in breast cancer patients associations with ejection fraction decline, recovery, and heart failure symptoms over 3 years of follow‐up publication-title: Circulation – volume: 16 start-page: 300 year: 2014 end-page: 308 article-title: Two‐dimensional speckle tracking echocardiography combined with high‐sensitive cardiac troponin T in early detection and prediction of cardiotoxicity during epirubicine‐based chemotherapy publication-title: Eur J Heart Fail – volume: 63 start-page: 2751 year: 2014 end-page: 2760 article-title: Use of myocardial strain imaging by echocardiography for the early detection of cardiotoxicity in patients during and after cancer chemotherapy. A systematic review publication-title: J Am Coll Cardiol – volume: 37 start-page: 2768 year: 2016 end-page: 2801 article-title: 2016 ESC position paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC Committee for Practice Guidelines publication-title: Eur Heart J – volume: 18 start-page: 392 year: 2017 end-page: 401 article-title: Assessment of global longitudinal strain at low dose anthracycline‐based chemotherapy, for the prediction of subsequent cardiotoxicity publication-title: Eur Heart J Cardiovasc Imaging – volume: 26 start-page: 493 year: 2013 end-page: 498 article-title: Independent and incremental value of deformation indices for prediction of trastuzumab‐induced cardiotoxicity publication-title: J Am Soc Echocardiogr – volume: 107 start-page: 1375 year: 2011 end-page: 1380 article-title: Early detection and prediction of cardiotoxicity in chemotherapy‐treated patients publication-title: Am J Cardiol – ident: e_1_2_8_14_1 doi: 10.1016/j.echo.2014.10.003 – ident: e_1_2_8_21_1 doi: 10.1136/heartjnl-2014-305533 – ident: e_1_2_8_25_1 doi: 10.1161/CIRCIMAGING.121.012459 – ident: e_1_2_8_2_1 doi: 10.1016/S0140-6736(05)66544-0 – ident: e_1_2_8_20_1 doi: 10.1161/CIRCULATIONAHA.116.023463 – ident: e_1_2_8_5_1 doi: 10.1093/eurheartj/ehw211 – ident: e_1_2_8_18_1 doi: 10.1002/ejhf.8 – ident: e_1_2_8_3_1 doi: 10.1111/jcpt.12124 – ident: e_1_2_8_16_1 doi: 10.2174/1871529X19666190912150942 – ident: e_1_2_8_19_1 doi: 10.1159/000500204 – ident: e_1_2_8_6_1 doi: 10.1093/annonc/mdf170 – ident: e_1_2_8_23_1 doi: 10.1016/j.transci.2013.12.001 – ident: e_1_2_8_7_1 doi: 10.1161/01.CIR.0000130926.51766.CC – ident: e_1_2_8_8_1 doi: 10.1016/j.jacc.2014.01.073 – ident: e_1_2_8_17_1 doi: 10.1161/CIRCIMAGING.112.973321 – ident: e_1_2_8_4_1 doi: 10.1016/j.mayocp.2014.05.013 – ident: e_1_2_8_9_1 doi: 10.1016/j.echo.2014.07.012 – ident: e_1_2_8_10_1 doi: 10.1002/ejhf.1631 – ident: e_1_2_8_22_1 doi: 10.1186/2193-1801-3-620 – ident: e_1_2_8_24_1 doi: 10.1200/JCO.2015.65.7916 – ident: e_1_2_8_13_1 doi: 10.1016/j.echo.2013.02.008 – ident: e_1_2_8_11_1 doi: 10.1016/j.amjcard.2011.01.006 – ident: e_1_2_8_12_1 doi: 10.1016/j.echo.2015.06.011 – volume: 18 start-page: 392 year: 2017 ident: e_1_2_8_15_1 article-title: Assessment of global longitudinal strain at low dose anthracycline‐based chemotherapy, for the prediction of subsequent cardiotoxicity publication-title: Eur Heart J Cardiovasc Imaging contributor: fullname: Charbonnel C |
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| SubjectTerms | Anthracyclines Anthracyclines - adverse effects Beta blockers Biomarkers Breast cancer Cardiotoxicity Chemotherapy Early Detection of Cancer Echocardiography - methods Female Global longitudinal strain High‐sensitivity cardiac troponin Humans Monoclonal antibodies Original Patients Radiation therapy Risk factors Statistical analysis Stroke Volume Targeted cancer therapy Trastuzumab Trastuzumab - adverse effects Ultrasonic imaging Ventricular Function, Left |
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| Title | Early detection of anthracycline‐ and trastuzumab‐induced cardiotoxicity: value and optimal timing of serum biomarkers and echocardiographic parameters |
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