Key result
Anthracycline chemotherapy raises LV SUVmax to ~4.8, indicating altered glucose uptake linked to cardiotoxicity.
Why the study?
To investigate anthracycline-induced cardiotoxicity myocardial metabolism changes by integrating 18F-FDG PET/CT and data-independent acquisition proteomics to provide novel prediction targets.
Does anthracycline-based chemotherapy alter myocardial energy metabolism as measured by 18F-FDG PET/CT and DIA proteomics in patients with diffuse large B-cell lymphomas?
Population
17 patients with DLBCL receiving anthracycline-based chemotherapy and 13 non-oncologic controls without organic heart disease
Comparison
Anthracycline-treated DLBCL patients (before vs after 6 cycles) vs non-oncologic controls
Design
Observational cohort study
Follow-up
6 cycles of chemotherapy
Authors
Loading...
May enable earlier PET/CT detection of anthracycline cardiotoxicity; hypothesis-generating for surveillance before echocardiographic changes.
Does anthracycline-based chemotherapy alter myocardial energy metabolism as measured by 18F-FDG PET/CT and DIA proteomics in patients with diffuse large B-cell lymphomas?
Anthracycline-based chemotherapy induces early myocardial metabolic remodeling characterized by decreased fatty acid oxidation and increased glucose uptake, detectable by 18F-FDG PET/CT before functional echocardiographic changes occur.
Xu et al. (2026) studied this question. After anthracycline chemotherapy, LV SUV max increased significantly to 4.82, indicating altered myocardial glucose uptake and decreased fatty acid oxidation associated with cardiotoxicity.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: