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Cardiac monitoring
Source: Childhood Acute Myeloid Leukemia Treatment (PDQ®)–Health Professional Version, National Cancer Institute.
Source updated: April 15, 2025 · Captured 2026-09-09.
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Context: Treatment of Childhood AML / Induction Therapy / Supportive care
Bacteremia or sepsis and anthracycline use have been identified as significant risk factors in the development of cardiotoxicity, manifested as reduced left ventricular function.[52,53] Monitoring of cardiac function through the use of serial exams during therapy is an effective method for detecting cardiotoxicity and adjusting therapy as indicated. The use of dexrazoxane in conjunction with bolus dosing of anthracyclines can effectively reduce the risk of cardiac dysfunction during therapy.[54]
Evidence (cardiac monitoring/dexrazoxane impact):
In the COG AAML0531 (NCT00372593) trial, 8.6% of enrolled patients experienced left ventricular systolic dysfunction (LVSD) during protocol therapy, with a cumulative incidence of LVSD of 12% within 5 years of completing therapy.[52]
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In the COG AAML0531 (NCT00372593) trial, 8.6% of enrolled patients experienced left ventricular systolic dysfunction (LVSD) during protocol therapy, with a cumulative incidence of LVSD of 12% within 5 years of completing therapy.[52]
Risk factors for LVSD during therapy included Black race, older age, underweight body mass, and bacteremia.
In the COG AAML0531 (NCT00372593) trial, 8.6% of enrolled patients experienced left ventricular systolic dysfunction (LVSD) during protocol therapy, with a cumulative incidence of LVSD of 12% within 5 years of completing therapy.[52]
The occurrence of LVSD adversely impacted 5-year EFS (HR, 1.57; 95% CI, 1.16–2.14; P = .004) and OS (HR, 1.59; 95% CI, 1.15–2.19; P = .005), which was primarily a result of nonrelapse mortality.
In the COG AAML0531 (NCT00372593) trial, 8.6% of enrolled patients experienced left ventricular systolic dysfunction (LVSD) during protocol therapy, with a cumulative incidence of LVSD of 12% within 5 years of completing therapy.[52]
In patients who experienced LVSD during therapy, there was a 12-fold greater risk of LVSD in the 5 years after the completion of therapy.
The use of dexrazoxane was assessed in patients enrolled on the COG AAML1031 (NCT01371981) trial.[54]
Source links and citations
The use of dexrazoxane was assessed in patients enrolled on the COG AAML1031 (NCT01371981) trial.[54]
This trial mandated prospective cardiac monitoring with each cycle and in follow-up and found a higher LVSD incidence (39%) occurring at a median of 3.8 months from enrollment (interquartile range, 2–6.2 months) than was seen in the preceding trial.
The use of dexrazoxane was assessed in patients enrolled on the COG AAML1031 (NCT01371981) trial.[54]
Approximately 10% of children (96 of 1,014) electively received dexrazoxane with each dose of anthracycline. The incidence of LVSD (defined as ejection fraction <55% or shortening fraction <28%) was significantly less in these patients (26.5% vs. 42.2%; HR, 0.55; 95% CI, 0.36–0.86; P = .009) than in the patients who did not elect to receive dexrazoxane. This was also evident for risk of LVSD grade 2 or higher (60% lower). Patients who received dexrazoxane also had persistently better cardiac function after therapy (median follow-up, 3.5 years).
The use of dexrazoxane was assessed in patients enrolled on the COG AAML1031 (NCT01371981) trial.[54]
Patients who received dexrazoxane had a lower treatment-related mortality (5.7% vs. 12.7%; P = .068), although the improved OS, EFS, and relapse risk outcomes did not reach statistical significance.
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