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Optimizing Cardiovascular Care in Children With Acute Myeloid Leukemia to Improve Cancer-Related Outcomes
Saro H Armenian1, Matthew J Ehrhardt2
11 City of Hope Comprehensive Cancer Center, Duarte, CA.
Insights
This case study highlights a young patient with acute myeloid leukemia (AML) who experienced significant cardiac dysfunction during chemotherapy. It emphasizes the importance of cardiac monitoring during intensive AML treatment, especially with anthracycline-based regimens.
Area of Science:
- Hematology
- Cardiology
- Oncology
Background:
- Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy requiring intensive chemotherapy.
- Anthracyclines, commonly used in AML treatment, are known cardiotoxic agents.
- Cardiac monitoring is crucial during AML therapy to detect and manage potential cardiotoxicity.
Purpose of the Study:
- To present a case of a 14-year-old female diagnosed with acute myeloid leukemia (AML).
- To illustrate the development of chemotherapy-induced cardiotoxicity during AML treatment.
- To underscore the importance of serial echocardiographic monitoring in AML patients receiving cardiotoxic agents.
Main Methods:
- A case report of a 14-year-old African American female with AML (FAB M2, t[8;21]).
- Treatment involved multi-agent chemotherapy including daunorubicin and mitoxantrone.
- Serial echocardiograms were performed to assess left ventricular (LV) systolic function (ejection fraction [EF], shortening fraction [SF]).
Main Results:
- The patient developed severe left ventricular systolic dysfunction (EF 28%, SF 14%) during intensification 2 of chemotherapy.
- Cardiac dysfunction occurred after receiving daunorubicin and mitoxantrone, with a possible contributing factor of sepsis.
- Initial echocardiogram showed normal LV function (EF 60%, SF 32%), which decreased to low-normal (EF 53%, SF 27%) after sepsis and prior to the severe decline.
Conclusions:
- Intensive chemotherapy regimens for AML, particularly those including anthracyclines like daunorubicin and mitoxantrone, can lead to significant cardiotoxicity.
- Serial echocardiographic monitoring is essential for early detection of cardiac dysfunction in AML patients undergoing treatment.
- Prompt recognition and management, including dose modification or omission of cardiotoxic agents, may be necessary to prevent irreversible cardiac damage.
Abstract:
The Oncology Grand Rounds series is designed to place original reports published in the Journal into clinical context. A case presentation is followed by a description of diagnostic and management challenges, a review of the relevant literature, and a summary of the authors' suggested management approaches. The goal of this series is to help readers better understand how to apply the results of key studies, including those published in Journal of Clinical Oncology, to patients seen in their own clinical practice. A 14-year-old African American female presented with fatigue, easy bruising, and fever. On examination, she had scattered bruising, lymphadenopathy, and hepatosplenomegaly. Laboratory evaluation revealed pancytopenia with peripheral blasts, and acute myeloid leukemia (AML; French-American-British M2, t[8;21][q22;q22.1]) was diagnosed on bone marrow biopsy. A baseline echocardiogram revealed normal left ventricular (LV) systolic function (ejection fraction [EF], 60%; shortening fraction [SF], 32%), and conventional chemotherapy was initiated that consisted of two cycles of remission induction (cytarabine, etoposide, and daunorubicin [50 mg/m2 × 3 days per cycle]) followed by intensification 1 (high-dose cytarabine and etoposide), intensification 2 (high-dose cytarabine and mitoxantrone [12 mg/m2/dose daily; four total doses]), and intensification 3 (high-dose cytarabine and l-asparaginase). Of note, an echocardiogram was not repeated before the start of intensification 1. During intensification 1, the patient developed Streptococcus viridans sepsis, which required 4 days in the intensive care unit with antimicrobial and inotropic support. Repeat echocardiogram after recovery from the sepsis episode demonstrated low-normal LV systolic function (EF, 53%; SF, 27%), and she subsequently began intensification 2. On day 3 of intensification 2, the patient developed afebrile tachypnea, tachycardia, and an increasing oxygen requirement. Chest x-ray revealed cardiomegaly and pulmonary vascular congestion. Cardiac troponins were normal, whereas N-terminal pro B-type natriuretic peptide was 10 times the upper limit of normal. Repeat echocardiogram showed an enlarged LV with moderate to severely depressed LV function (EF, 28%; SF, 14%). Day 4 mitoxantrone was omitted and a cardiology consult obtained.
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