Abstract 16605: Left Ventricular Global Longitudinal Strain in Mitoxantrone-Induced Cardiotoxicity - A Velocity Vector Imaging Analysis
Background: Definite risk factors have not been identified for mitoxantrone-induced cardiotoxicity. The purpose of this investigation was to (a) study left ventricular mechanics [global longitudinal strain (εl), time-to-peak strain (TPKε), and dyssynchrony] before and after receiving mitoxantrone; and (b) to determine predictors of mitoxantrone-induced early cardiotoxicity.
Method: We analyzed 45 subjects diagnosed with acute myeloid leukemia who underwent chemotherapy with bolus high dose mitoxantrone. Echocardiographic measurements were done at baseline and at an approximate 3 month interval. An offline analysis using velocity vector imaging (TomTec Imaging Systems) was done to measure εl, and TPKε. The median follow up was close to one year.
Results: Mean εl decreased from -16.3 ± 0.6 to -13.6 ± 0.6 (p<0.0004). A total of 15 (33.3%) subjects developed HF. Mean interval for development of HF was 12 weeks (Range: 4-18). There was a significant decrease in εl in both the HF and non-HF group. Left ventricular end-systolic diameter index showed a trend whereas baseline ejection fraction (EF) and delta-EF were found to be independent predictors of heart failure in an adjusted regression analysis (Figure).
Conclusion: Strain significantly decreased in patients who developed HF with reduced EF. Interestingly, significant decrease in εl in patients who did not develop HF may be indicative of sub-clinical cardiotoxicity, and may predict decrease in EF in subjects at risk for delayed cardiotoxic effects of mitoxantrone. We also found that increase in estimated left ventricular filling pressure might have resulted in symptomatic HF. Baseline EF and decrease in EF were found to be independent risk factors for heart failure. Surprisingly, neither strain nor delta-strain were found to be independent predictors for heart failure; we speculate that compensatory increase in circumferential/radial strain might have played a role in EF preservation in the non-HF group.
- © 2013 by American Heart Association, Inc.