EARLY DETECTION OF THE ANTHRACYCLINE-INDUCED CARDIOTOXICITY - A NONINVASIVE HEMODYNAMIC-STUDY

Citation
B. Massidda et al., EARLY DETECTION OF THE ANTHRACYCLINE-INDUCED CARDIOTOXICITY - A NONINVASIVE HEMODYNAMIC-STUDY, Anticancer research, 17(1B), 1997, pp. 663-668
Citations number
17
Categorie Soggetti
Oncology
Journal title
ISSN journal
02507005
Volume
17
Issue
1B
Year of publication
1997
Pages
663 - 668
Database
ISI
SICI code
0250-7005(1997)17:1B<663:EDOTAC>2.0.ZU;2-3
Abstract
Anthracyclines are the most frequent cause of iatrogenic congestive he art failure ranging from acute reversible minor, irreversible reductio n in the left ventricular ejection fraction and death despite preventi ve measures. Sensitive methods are needed to detect earliest preclinic al cardiotoxicity abong with the development of new protective agents. Thirty breast cancer patients were randomly treated with q 21 120 mg/ m(2) Epirubicin (EPI) x 3, alone (10 patients), or + ICRF-187 (1000 mg /m(2)) (10 patients) or + C(0)Q(10) (60 mg/day) (10 patients) and moni tored by Thoracic Electrical Bioimpedance (TEB) cardiography before (T -0) and at the end of chemotherapy (T-1), then at 1, 3, 6 months of fo llow up (F-1, F-2, F-3). a) The group treated with EPI alone showed, b etween F-1-F-2, a significant (p < 0.05) decrease in Stroke Index (SI) , Acceleration Index (ACI) and a significant (p < 0.05) increase in Sy stemic Vascular Resistance Index (SVRI), while between F-2 and F-3 it showed a significant (p < 0.05) recovery in SI and ACI. b) The group t reated with EPI + ICRF-187 showed, between F-1 and F-2 a significant d ecrease in SI and ACI (p < 0.05, p < 0.01 respectively) and a signific ant (p < 0.05) increase in SVRI; between F-2-F-3 ACI had a significant (p < 0.05) recovery; c) The group treated with EPI + C(1)Q(10) showed no modification in SI, ACI, and SVRI during the study. The ejection F raction (EF) remained unchanged during the study in all the groups. C( 1)Q(10) seems to prevent early decreased in cardiac performance and co ntractiling, thus avoiding an SVRI increase, while ICRF-187 did not. S ince ICRF-187 acts by binding iron, we deem that the earliest cardiac involvement, may occur before iron overload; therefore the role of ICR F-187 and C(1)Q(10) in acute or chronic heart toxicity was correlated with high-dose anthracycline and needs to be further investigated.