title: Anthracycline chemotherapy impairs the structure and diastolic function of the left ventricle and induces negative arterial remodelling.
abstract: BACKGROUND
  Anthracycline affects various cell lines, which may contribute to left ventricular (LV) dysfunction and vascular remodelling.
  
  
  OBJECTIVE
  To assess the complex influence of anthracycline chemotherapy on the echocardiographic parameters of LV systolic and diastolic function and indices of vascular function and structure.
  
  
  METHODS
  35 women (age 50 ± 9 years old) with breast cancer scheduled for standard anthracycline chemotherapy were enrolled into the study. Examinations were performed at the baseline and six months after the last dose of anthracycline with a clinical follow-up of 9-12 months. LV systolic and diastolic function were assessed by: ejection fraction, transmitral flow, isovolumetric relaxation time, Tei index, mitral ring movement velocity and E/E' ratio. Vascular parameters, including flow-mediated dilatation, intima-media thickness (IMT), aortic compliance, common carotid artery (CCA) compliance, and stiffness indices b were measured.
  
  
  RESULTS
  None of the patients revealed any cardiovascular symptoms during follow-up. LV systolic function parameters remained normal. However, LV end-diastolic diameter (46 ± 3.5 vs. 48 ± 4 mm, p = 0.004) and LV end-diastolic volume (101 ± 25 vs. 112 ± 26 mL, p = 0.01) increased. The diastolic function changed - the Tei index increased (0.49 ± 0.09 vs. 0.54 ± 0.1, p = 0.04) and E' (p = 0.049), A' (p = 0.02) and S (p = 0.01) decreased. The E/E' index increased (p < 0.0001) within the LV lateral wall. We observed an increase in carotid IMT (p < 0.0001), a decrease in aortic compliance (p = 0.042) and CCA compliance (p = 0.004), and an increase in aorta as well as the CCA stiffness indices (p = 0.046, p = 0.003, respectively).
  
  
  CONCLUSIONS
  Standard-dose anthracycline chemotherapy is associated with LV dilatation and diastolic dysfunction, regardless of the preserved global systolic function. It coexists with negative structural arterial remodelling.
authors.affiliation: First Department of Cardiology, Medical University of Silesia, Upper Silesian Medical Centre, Katowice, Poland. kmizia@op.pl
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Mizia-Stec
authors.forename: Adrianna
authors.initials: A
authors.lastname: Gościńska
authors.forename: Magdalena
authors.initials: M
authors.lastname: Mizia
authors.forename: Maciej
authors.initials: M
authors.lastname: Haberka
authors.forename: Artur
authors.initials: A
authors.lastname: Chmiel
authors.forename: Wojciech
authors.initials: W
authors.lastname: Poborski
authors.forename: Zbigniew
authors.initials: Z
authors.lastname: Gąsior
mesh_terms: D000328:Adult; D018943:Anthracyclines / Q000009:adverse effects*; D000970:Antineoplastic Agents / Q000009:adverse effects*; D001158:Arteries / Q000187:drug effects; D001943:Breast Neoplasms / Q000188:drug therapy*; D005260:Female; D006801:Humans; D008875:Middle Aged; D018487:Ventricular Dysfunction, Left / Q000139:chemically induced* / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D018943:Anthracyclines; D000970:Antineoplastic Agents