title: Left ventricular systolic and diastolic function after anthracycline chemotherapy in childhood.
abstract: BACKGROUND
  In childhood, late cardiotoxicity is characterized by inappropriately thin wall and consequent increased end-systolic wall stress, but the associations of impaired left ventricular geometry and function occurring under these circumstances need further investigation.
  
  
  OBJECTIVE
  The purpose of this study was to assess anthracycline late effects on the relationships occurring between increased end-systolic stress (ESS) and changes in both M-mode systolic measurements (i.e., endocardial and midwall fractional shortening) and Doppler diastolic indices in the pediatric age.
  
  
  METHODS
  The population consisted of 101 children treated with anthracyclines for at least 12 months and 91 healthy children. Using M-mode echocardiography, end-systolic wall stress was calculated as index of afterload, and endocardial and midwall fractional shortening as systolic indices. Doppler transmitral measurements were made as diastolic indices.
  
  
  RESULTS
  Patients treated with anthracyclines showed significantly lower relative wall thickness and left ventricular mass index, greater end-systolic wall stress, reduced endocardial and midwall fractional shortening and peak E/A ratio, prolonged deceleration, and isovolumic relaxation times. Direct relationships were found between end-systolic wall stress and both endocardial and midwall shortening. The use of midwall shortening in the relation showed a greater, but not significant increase (from 3 to 6%) in the proportion of patients with depressed systolic function than did endocardial shortening. In the anthracycline group, end-systolic wall stress was also inversely related to relative wall thickness and directly to isovolumic relaxation time.
  
  
  CONCLUSIONS
  In childhood, reduced myocardial thickness and increased afterload explain much of systolic and diastolic dysfunction of late anthracycline toxicity. Midwall fractional shortening does not seem to add useful information for identifying subsets of children more prone to the development of heart failure.
authors.affiliation: Cattedra di Cardiologia, Istituto Medico Chirurgico di Cardiologia, Dipartimento di Pediatria, Seconda Università di Napoli, Italy.
authors.forename: D
authors.initials: D
authors.lastname: Iarussi
authors.forename: M
authors.initials: M
authors.lastname: Galderisi
authors.forename: G
authors.initials: G
authors.lastname: Ratti
authors.forename: M A
authors.initials: MA
authors.lastname: Tedesco
authors.forename: P
authors.initials: P
authors.lastname: Indolfi
authors.forename: F
authors.initials: F
authors.lastname: Casale
authors.forename: M T
authors.initials: MT
authors.lastname: Di Tullio
authors.forename: O
authors.initials: O
authors.lastname: de Divitiis
authors.forename: A
authors.initials: A
authors.lastname: Iacono
mesh_terms: D000293:Adolescent; D000903:Antibiotics, Antineoplastic / Q000494:pharmacology*; D002648:Child; D003971:Diastole / Q000187:drug effects* / Q000502:physiology; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D008297:Male; D013599:Systole / Q000187:drug effects* / Q000502:physiology; D013997:Time Factors; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D000903:Antibiotics, Antineoplastic