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Войти в исследования Cardio-oncology (London, England) · 2026
Cardiac magnetic resonance with myocardial strain as a predictor of anthracycline-induced cardiotoxicity in patients with lymphoma: a prospective multimodality study.
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da Silva Costa Isabela Bispo Santos, Assunção Bruna Morhy Borges Leal, Cruz Cecilia Beatriz Bittencourt Viana, Pavani Andrea Vinche Badra, Pereira Juliana, Buccheri Valéria, Bittar Cristina Salvadori, Fonseca Rafael Almeida, Osório Altamiro Ferraz, Negrão Carlos Eduardo, Kalil Filho Roberto, Nomura Cesar Higa, Rochitte Carlos Eduardo, Hajjar Ludhmila Abrahão
Аннотация
BACKGROUND: Cancer therapy-related cardiac dysfunction (CTRCD) is a frequent and clinically relevant complication in patients with lymphoma treated with anthracyclines. Early identification of subclinical myocardial injury is critical to prevent progression to overt heart failure and to avoid chemotherapy dose reductions that may compromise oncologic outcomes. We aimed to evaluate the role of cardiac magnetic resonance (CMR) with T1 mapping and feature-tracking myocardial strain, in comparison with transthoracic echocardiography (TTE) and circulating biomarkers, for the early detection of CTRCD in lymphoma patients receiving anthracycline-based chemotherapy.
METHODS: In this prospective, single-center observational study, forty-nine adult patients with lymphoma scheduled for anthracycline-based chemotherapy underwent serial assessment of high-sensitivity cardiac troponin T (hs-cTnT), NT-proBNP, TTE, and CMR at baseline (visit 0), after the third chemotherapy cycle (visit 1), and at chemotherapy completion (visit 2). TTE was repeated at 12-month follow-up (visit 3). CMR included cine imaging, T1 mapping with extracellular volume (ECV) quantification, late gadolinium enhancement, and feature-tracking strain analysis (global longitudinal [GLS], circumferential [GCS], and radial [GRS] strain). CTRCD was defined and graded according to the 2022 ESC Cardio-Oncology Guidelines.
RESULTS: The median age of patients was 46 (29.5-62) years; 53.1% were female. The mean cumulative doxorubicin dose was 295 ± 57 mg/m². hs-cTnT levels increased progressively from baseline (0.006 ± 0.005 ng/mL) to visit 2 (0.022 ± 0.016 ng/mL; p < 0.001), while NT-proBNP did not change significantly (p = 0.086). TTE showed a significant decline in LVEF by the Simpson method (62.92 ± 5.61% to 60.23 ± 5.41%; p = 0.037) and progressive worsening of GLS (- 19.84 ± 2.35% to - 18.31 ± 2.73%; p = 0.001). CMR-derived LVEF also declined (61.98 ± 6.08% to 57.34 ± 7.29%; p < 0.001), accompanied by significant deterioration of GLS, GCS, and GRS (p < 0.001 for all). CTRCD was identified in 7 patients (14.9%) by CMR and 5 (10.6%) by TTE (p = 0.625), with substantial agreement between modalities (κ = 0.619; p < 0.001). A relative GLS decline > 15% was observed by CMR in 34.1% of patients at visit 1 and 43.9% at visit 2, exceeding the corresponding TTE-detected rates (15.2% and 18.6%).
CONCLUSIONS: CMR-derived strain identified myocardial functional abnormalities during anthracycline therapy. Whether these abnormalities represent earlier manifestations of clinically relevant cardiotoxicity requires confirmation in larger prospective studies with longer follow-up.
METHODS: In this prospective, single-center observational study, forty-nine adult patients with lymphoma scheduled for anthracycline-based chemotherapy underwent serial assessment of high-sensitivity cardiac troponin T (hs-cTnT), NT-proBNP, TTE, and CMR at baseline (visit 0), after the third chemotherapy cycle (visit 1), and at chemotherapy completion (visit 2). TTE was repeated at 12-month follow-up (visit 3). CMR included cine imaging, T1 mapping with extracellular volume (ECV) quantification, late gadolinium enhancement, and feature-tracking strain analysis (global longitudinal [GLS], circumferential [GCS], and radial [GRS] strain). CTRCD was defined and graded according to the 2022 ESC Cardio-Oncology Guidelines.
RESULTS: The median age of patients was 46 (29.5-62) years; 53.1% were female. The mean cumulative doxorubicin dose was 295 ± 57 mg/m². hs-cTnT levels increased progressively from baseline (0.006 ± 0.005 ng/mL) to visit 2 (0.022 ± 0.016 ng/mL; p < 0.001), while NT-proBNP did not change significantly (p = 0.086). TTE showed a significant decline in LVEF by the Simpson method (62.92 ± 5.61% to 60.23 ± 5.41%; p = 0.037) and progressive worsening of GLS (- 19.84 ± 2.35% to - 18.31 ± 2.73%; p = 0.001). CMR-derived LVEF also declined (61.98 ± 6.08% to 57.34 ± 7.29%; p < 0.001), accompanied by significant deterioration of GLS, GCS, and GRS (p < 0.001 for all). CTRCD was identified in 7 patients (14.9%) by CMR and 5 (10.6%) by TTE (p = 0.625), with substantial agreement between modalities (κ = 0.619; p < 0.001). A relative GLS decline > 15% was observed by CMR in 34.1% of patients at visit 1 and 43.9% at visit 2, exceeding the corresponding TTE-detected rates (15.2% and 18.6%).
CONCLUSIONS: CMR-derived strain identified myocardial functional abnormalities during anthracycline therapy. Whether these abnormalities represent earlier manifestations of clinically relevant cardiotoxicity requires confirmation in larger prospective studies with longer follow-up.