А patient with acute decompensation of chronic heart failure and chronic myeloid leukemia during imatinib therapy. Cardiotoxicity or acute myocardial infarction?

This article presents a clinical case of acute decompensation of chronic heart failure in a patient with chronic myeloid leukemia (CML) during targeted therapy with a tyrosine kinase inhibitor — imatinib. The patient was admitted to a multidisciplinary clinic with pronounced clinical signs of heart failure (HF). Upon admission to the hospital, blood tests revealed severe pancytopenia and elevated cardio-specific enzymes. According to echocardiography — a low left ventricular ejection fraction (LVEF), decreased global contractility of the left ventricle, and decreased regional contractility of the left ventricle were noted. The condition was interpreted as a type 2 acute myocardial infarction (AMI) due to severe anemia. Intensive therapy was conducted in the intensive care unit, during which a significant positive dynamic was achieved. Follow-up echocardiography showed disappearance of regional wall motion abnormalities and an increase in LVEF according to Simpson (from 30% to 42%). During subsequent follow-up — further increase in LVEF (from 42% to 69%) and resolution of heart failure symptoms were observed. Given the complete regression of clinical symptoms following imatinib withdrawal, heart failure could have been associated with the cardiotoxicity of this drug.