title: Myocyte cell damage after administration of doxorubicin or mitoxantrone in breast cancer patients assessed by indium 111 antimyosin monoclonal antibody studies.
abstract: OBJECTIVE
  To compare myocyte cell damage induced by doxorubicin or mitoxantrone, we performed left ventricular ejection fraction (LVEF) measurements and indium 111 antimyosin antibody studies in a group of patients with advanced breast cancer who had been treated with these anthracycline derivatives.
  
  
  METHODS
  We studied 35 patients eligible to receive chemotherapy including the anthracyclines: doxorubicin or mitoxantrone (cumulative dose of doxorubicin, 500 mg/m2; or mitoxantrone, 120 mg/m2). LVEF was measured before and after 10 cycles of chemotherapy. Antimyosin uptake in the myocardium was quantified by means of a heart-to-lung ratio (HLR).
  
  
  RESULTS
  Patients treated with doxorubicin presented with a significant decrease in LVEF after chemotherapy (before, 60.4% +/- 8.92%; after, 49.8% +/- 9.71%; P = .001). Antimyosin uptake was observed in all patients with a HLR of 2.03 +/- 0.25. Seven of eight patients with a HLR greater than 2.03 had a greater than 10% decrease in LVEF. Patients treated with mitoxantrone did not present with a decrease in LVEF after chemotherapy (before, 55.4% +/- 6.25%; after, 55.8% +/- 7.25%; not significant). Antimyosin uptake was observed in 14 of 17 patients with a HLR of 1.77 +/- 0.18 (P < .05).
  
  
  CONCLUSIONS
  111In antimyosin monoclonal antibodies defect myocardial cell damage produced by doxorubicin and mitoxantrone. In patients with advanced breast cancer, cumulative doses of 120 mg/m2 of mitoxantrone produce less myocardial cell damage than cumulative doses of 500 mg/m2 of doxorubicin. 111In antimyosin uptake without decrease in LVEF after treatment with mitoxantrone indicates the presence of myocyte cell damage, but not to the extent necessary to deteriorate function. These results indicate that 111In antimyosin antibody studies are useful in the noninvasive comparative assessment of cardiotoxicity produced by different anthracycline derivatives.
authors.affiliation: Department of Nuclear Medicine, Hospital de Sant Pau, Barcelona, Spain.
authors.forename: M
authors.initials: M
authors.lastname: Estorch
authors.forename: I
authors.initials: I
authors.lastname: Carrió
authors.forename: D
authors.initials: D
authors.lastname: Martínez-Duncker
authors.forename: L
authors.initials: L
authors.lastname: Berná
authors.forename: G
authors.initials: G
authors.lastname: Torres
authors.forename: C
authors.initials: C
authors.lastname: Alonso
authors.forename: B
authors.initials: B
authors.lastname: Ojeda
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000009:adverse effects; D001943:Breast Neoplasms / Q000188:drug therapy*; D004317:Doxorubicin / Q000009:adverse effects*; D005260:Female; D006331:Heart Diseases / Q000139:chemically induced* / Q000000981:diagnostic imaging / Q000473:pathology; D006801:Humans; D007205:Indium Radioisotopes; D008875:Middle Aged; D008942:Mitoxantrone / Q000009:adverse effects*; D009206:Myocardium / Q000473:pathology; D009218:Myosins / Q000276:immunology; D016719:Radioimmunodetection; D013318:Stroke Volume / Q000187:drug effects; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D000911:Antibodies, Monoclonal; D007205:Indium Radioisotopes; D004317:Doxorubicin; D008942:Mitoxantrone; D009218:Myosins