Belén Díaz-Antón1,2,3,4, Rodrigo Madurga5,5, Blanca Zorita2, Samantha Wasniewski6, Andrea Moreno‐Arciniegas2,3, Beatriz López‐Melgar2,3, Natalia Ramírez Merino7,4, Roberto Martín‐Asenjo8, Patricia Barrio2,3, Maximiliano Germán Amado Escañuela9,6, Jorge Solı́s1,10,11,11, Francisco Javier Jiménez2, Eva Ciruelos7,12, José M. Castellano1,11,2,13,4, Leticia Fernández‐Friera1,10,11,6,4
1Atria Clinic, Madrid, Spain
2Departamento de Cardiología HM Hospitales‐Centro Integral de Enfermedades Cardiovasculares HM CIEC Melchor Fernández Almagro 3 Madrid 28029 Spain
3Unidad de Imagen Cardiaca HM Hospitales‐Centro Integral de Enfermedades Cardiovasculares HM CIEC Madrid Spain
4Universidad CEU San Pablo, Madrid, Spain
5Facultad de Ciencias Experimentales, Universidad Francisco de Vitoria, Madrid, Spain
6Unidad de Imagen Cardiaca, HM Hospitales-Centro Integral de Enfermedades Cardiovasculares HM CIEC, Madrid, Spain
7Departamento de Oncología Médica HM Hospitales Madrid Spain
8Servicio de Cardiología, Hospital Universitario 12 de Octubre, Madrid, Spain
9Hospital General de Segovia, Segovia, Spain
10CIBER de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain
11Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain
12Servicio Oncología Hospital Universitario 12 de Octubre Madrid Spain
13Fundación de Investigación HM Hospitales, HM Hospitales, Madrid, Spain
Tóm tắt
AbstractAimsTo 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.
