RT Journal Article SR Electronic T1 Doxorubicin Effect on Myocardial Metabolism as a Prerequisite for Subsequent Development of Cardiac Toxicity: A Translational 18F-FDG PET/CT Observation JF Journal of Nuclear Medicine JO J Nucl Med FD Society of Nuclear Medicine SP 1638 OP 1645 DO 10.2967/jnumed.117.191122 VO 58 IS 10 A1 Matteo Bauckneht A1 Giulia Ferrarazzo A1 Francesco Fiz A1 Silvia Morbelli A1 Matteo Sarocchi A1 Fabio Pastorino A1 Alberto Ghidella A1 Elena Pomposelli A1 Maurizio Miglino A1 Pietro Ameri A1 Laura Emionite A1 Flavia Ticconi A1 Eleonora Arboscello A1 Ambra Buschiazzo A1 Elena Augusta Massimelli A1 Salvatore Fiordoro A1 Anna Borra A1 Vanessa Cossu A1 Annalisa Bozzano A1 Adalberto Ibatici A1 Mirco Ponzoni A1 Paolo Spallarossa A1 Andrea Gallamini A1 Paolo Bruzzi A1 Gianmario Sambuceti A1 Cecilia Marini YR 2017 UL http://jnm.snmjournals.org/content/58/10/1638.abstract AB The present translational study aimed to verify whether serial 18F-FDG PET/CT predicts doxorubicin cardiotoxicity. Methods: Fifteen athymic mice were treated intravenously with saline (n = 5) or with 5 or 7.5 mg of doxorubicin per kilogram (n = 5 each) and underwent dynamic small-animal PET beforehand and afterward to estimate left ventricular (LV) metabolic rate of glucose (MRGlu). Thereafter, we retrospectively identified 69 patients who had been successfully treated with a regimen of doxorubicin, bleomycin, vinblastine, and dacarbazine for Hodgkin disease (HD) and had undergone 4 consecutive 18F-FDG PET/CT scans. Volumes of interest were drawn on LV myocardium to quantify mean SUV. All patients were subsequently interviewed by telephone (median follow-up, 30 mo); 36 of them agreed to undergo electrocardiography and transthoracic echocardiography. Results: In mice, LV MRGlu was 17.9 ± 4.4 nmol × min−1 × g−1 at baseline. Doxorubicin selectively and dose-dependently increased this value in the standard-dose (27.9 ± 9 nmol × min−1 × g−1, P < 0.05 vs. controls) and high-dose subgroups (37.2 ± 7.8 nmol × min−1 × g−1, P < 0.01 vs. controls, P < 0.05 vs. standard-dose). In HD patients, LV SUV showed a progressive increase during doxorubicin treatment that persisted at follow-up. New-onset cardiac abnormalities appeared in 11 of 36 patients (31%). In these subjects, pretherapy LV SUV was markedly lower with respect to the remaining patients (1.53 ± 0.9 vs. 3.34 ± 2.54, respectively, P < 0.01). Multivariate analysis confirmed the predictive value of baseline LV SUV for subsequent cardiac abnormalities. Conclusion: Doxorubicin dose-dependently increases LV MRGlu, particularly in the presence of low baseline 18F-FDG uptake. These results imply that low myocardial 18F-FDG uptake before the initiation of doxorubicin chemotherapy in HD patients may predict the development of chemotherapy-induced cardiotoxicity, suggesting that prospective clinical trials are warranted to test this hypothesis.