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Echocardiography. 2016 Aug;33(8):1166-77. doi: 10.1111/echo.13245. Epub 2016 Apr 24.

Mitoxantrone-Induced Cardiotoxicity in Acute Myeloid Leukemia-A Velocity Vector Imaging Analysis.

Author information

1
Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts.
2
Department of Medicine, Providence Holy Cross Medical Center, Mission Hills, California.
3
Division of Hematology-Oncology, Baystate Medical Center, Springfield, Massachusetts.
4
Division of Cardiology, University of Massachusetts Medical School, Worcester, Massachusetts.
5
Division of Hematology-Oncology, University of Massachusetts Medical School, Worcester, Massachusetts.

Abstract

BACKGROUND:

The purpose of this investigation was to: (1) determine incidence and predictors of mitoxantrone-induced early cardiotoxicity and (2) study left ventricular mechanics before and after receiving mitoxantrone.

METHOD AND RESULTS:

We retrospectively analyzed 80 subjects diagnosed with acute myeloid leukemia (AML) who underwent chemotherapy with bolus high-dose mitoxantrone. Echocardiographic measurements were taken at baseline and at a median interval of 55 days after receiving mitoxantrone. Thirty-five (44%) of the patients developed clinically defined early cardiotoxicity, 29 (36%) of which developed heart failure. There was a significant decrease in the ejection fraction (EF) not only in the cardiotoxicity group (17.6 ± 14.8%, P < 0.001) but also in the noncardiotoxicity group (5.3 ± 8.4%, P < 0.001). Decrease in global longitudinal strain (GLS) (-3.7 ± 4.5, P < 0.001 vs. -2.4 ± 4.3, P = 0.01) and global circumferential strain (GCS) (-5.6 ± 9, P = 0.003 vs. -5.3 ± 8.7, P < 0.001) was significant in both the cardiotoxicity and noncardiotoxicity group, respectively. A multivariate model including baseline left ventricular end-systolic diameter, baseline pre-E/A ratio, and baseline pre-E/e' ratio was found to be the best-fitted model for prediction of mitoxantrone-induced early clinical cardiotoxicity.

CONCLUSION:

High-dose mitoxantrone therapy is associated with an excellent remission rate but with a significantly increased risk of clinical and subclinical early cardiotoxicity and heart failure. Mitoxantrone-induced systolic dysfunction is evident from reduction in EF, increase in Tei index, and significant reduction in GLS and GCS. Baseline impaired ventricular relaxation evident from higher E/e' ratio and lower E/A ratio independently predicts increased risk of mitoxantrone-induced early cardiotoxicity.

KEYWORDS:

Tei index; anthracyclines; chemotherapy; diastolic dysfunction; dyssynchrony; heart failure; leukemia; myocardial performance index; strain

PMID:
27109429
DOI:
10.1111/echo.13245
[Indexed for MEDLINE]

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