title: Anthracycline-induced cardiomyopathies evaluated by tissue Doppler tracking system and strain rate imaging.
abstract: OBJECTIVE
  Anthracycline cardiotoxicity is known to occur from the subendocardial side of the left ventricular wall. Recent advances of tissue Doppler echocardiography may allow the evaluation of anthracycline cardiotoxicity by dividing the left ventricular wall into the subendocardial half and subepicardial half. The present study assessed the feasibility using the tissue Doppler echo tracking system (M-mode) and myocardial strain rate imaging (B-mode) to noninvasively detect anthracycline cardiotoxicity.
  
  
  METHODS
  The tissue Doppler echo tracking system (M-mode) was used to measure systolic thickening of the subendocardial layer (delta Endo), subepicardial layer (delta Epi), and whole wall (delta Total) of the left ventricular posterior wall in 41 normal subjects and three groups of patients receiving anthracycline: 34 patients in the low dose group, 19 in the middle dose group, and 12 in the high dose group. Strain rate is the spatial gradient of local velocities, reflecting local compression and expansion rates not affected by overall heart motion. Myocardial strain rate imaging (B-mode) was used in 25 normal subjects, 9 patients in the low dose group, and 10 patients in the high dose group. The ratio of peak systolic strain rate of subendocardium to that of subepicardium (peak strain rate endo/epi), and the ratio of integrated strain rate during ejection time of subendocardium to that of subepicardium (integrated strain rate endo/epi) were measured.
  
  
  RESULTS
  Tissue Doppler echo tracking system (M-mode) measurement of delta Endo/delta Epi showed the most distinct difference and the least overlap of the data between normal subjects and patients, whereas delta Total failed to show significant differences. Myocardial strain rate imaging (B-mode) measurement of integrated strain rate endo/epi showed the most distinct difference and the least overlap of the data between normal subjects and patients, but ejection fraction failed to show statistically significant differences.
  
  
  CONCLUSIONS
  These methods are highly sensitive tools for monitoring anthracycline cardiotoxicity.
authors: Department of Laboratory Medicine, Faculty of Medicine, University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-8655, Japan.
authors: K
authors: K
authors: Takenaka
authors: Y
authors: Y
authors: Kuwada
authors: M
authors: M
authors: Sonoda
authors: K
authors: K
authors: Uno
authors: M
authors: M
authors: Asakawa
authors: S
authors: S
authors: Sakurai
authors: T
authors: T
authors: Takahashi
authors: K
authors: K
authors: Sasaki
authors: M
authors: M
authors: Matsuzaki
authors: A
authors: A
authors: Kikuchi
authors: R
authors: R
authors: Amagai
authors: N
authors: N
authors: Furudate
authors: R
authors: R
authors: Nagai
mesh_terms: D018943:Anthracyclines / Q000009:adverse effects*; D009202:Cardiomyopathies / Q000139:chemically induced* / Q000000981:diagnostic imaging*; D015150:Echocardiography, Doppler; D006801:Humans; D013318:Stroke Volume; D013599:Systole
chemical_list: D018943:Anthracyclines