Acute cardiotoxicity after initiation of the novel tyrosine kinase inhibitor gilteritinib for acute myeloid leukemia

Figures

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  Fig. 1. Admission electrocardiogram demonstrating sinus tachycardia (left upper) with negative T waves in leads V1-V3 and admission chest radiograph showing no acute cardiopulmonary disease (left lower). After four doses of gilteritinib and five days after admission, a repeat electrocardiogram is unremarkable (upper right). A repeat chest radiograph demonstrates interval cardiomegaly and diffuse pulmonary interstitial edema (lower right)

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  Fig. 2. Echocardiogram after four doses of gilteritinib demonstrating acutely reduced systolic function and global hypokinesis. After four doses of gilteritinib targeted therapy, an echocardiogram showed moderately reduced left ventricular systolic function, an estimated ejection fraction of 36% with global hypokinesis and regional abnormalities of the septum

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  Fig. 3. Cardiac magnetic resonance imaging (MRI) after six days of gilteritinib targeted therapy. After gilteritinib initiation, the patient developed significant clinical heart failure. Cardiac MRI revealed new left ventricular dilation and depressed systolic function with evidence of myocardial edema/ inflammation on T2 mapping (red arrows; max T2 of 70 milliseconds, normal < 53 ms), as well as patchy correlating non-ischemic patterned fibrosis with late gadolinium enhancement (LGE). Myocardial extracellular volume fraction was also elevated (not shown here). However, five months after therapeutic cessation, systolic function normalized with injury resolution (green arrows)