Anthracycline Cardiotoxicity in Patients with Acute Myeloid Leukemia: Cardiovascular Risk Assessment, Monitoring and Management.

Introduction:
Cardiotoxicity of anthracyclines during treatment for acute myelocytic leukemia (AML) remains a significant cause of mortality. Close monitoring of cardiac function and risk factor management is crucial for early recognition and treatment, although not mandated by current guidelines.

Methods:
The study included 55 patients with AML who received induction anthracycline-based chemotherapy between February 1, 2007 and March 1, 2015. Cardiotoxicity was defined as a decrease in the left ventricular ejection fraction (LVEF) of >10%, to a value <53%. We also evaluated Sorror Index (SI) a risk assessment tool before allogeneic transplant. SI>2 determines high risk of mortality.

Results:
The mean age was 58 years and 49.1% were females. Overall 13 (23.6%) of the 55 patients who received chemotherapy treatment developed cardiotoxicity: 7(12.7%) - permanent decrease of LVEF, 6 (10.9%) – transient LVEF decrease with subsequent improvement to baseline. SI >2 was observed in five of seven patients with permanent LVEF decrease, while in group of patients with transient LVEF decrease only in one case SI was >2.

Only three of seven patients with permanent LVEF decrease after chemotherapy were treated with beta-blockers (BB), ACEi/ARB and MRA. Only two of six patients with a temporary decrease in EF were these disease-modifying medications. Five of thirteen patients with cardiotoxicity were not even referred for cardiology follow-up.

Conclusion:
Not all patients who met criteria for cardiotoxicity with left ventricular dysfunction (LVD) were initiated on optimal heart failure medications nor seen by a cardiologist. The implementation of a standard protocol for cancer patients receiving cardiotoxic medications may enable better detection and early management of LVD before the onset of clinical heart failure. Sorror index may be used to determine subgroup of patients who may be given prophylactic “cardioprotective” therapy.