Abstract
Case Presentation A 72 year old man presented with progressive dyspnea on exertion, only able to climb 4 stairs prior to symptom onset. He had a history of diffuse large B-cell lymphoma for which he had completed chemotherapy with cyclophosphamide, doxorubicin, rituximab, vincristine, and prednisone a year prior to presentation with recent PET scan showing complete remission. EKG showed rate-controlled atrial fibrillation. TTE confirmed a severely reduced systolic function with LVEF 25% and global hypokinesis. Coronary angiogram revealed no obstructive disease. Cardiac MRI (CMR) was then performed with no evidence of myocardial infarction, infiltration, or scarring on delayed gadolinium enhancement (DGE). T2 mapping, DIR, and TIR sequencing did not show any myocardial edema. However, baseline pre-contrast T1 relaxation time was increased at 1140-1153ms [Figure 1A] with a calculated ECV [Figure 1B] elevated at 37-40%, concerning for anthracycline-induced cardiomyopathy (AIC). Discussion Anthracyclines, such as doxorubicin, are important chemotherapeutic agents; however, their utility is often limited by development of progressive cardiotoxicity. Cumulative dose-dependent exposure can lead to apoptotic myocyte loss, myocardial fibrosis, and dysmotility. DGE usually identifies focal myocardial fibrosis; however, anthracycline-induced fibrosis is frequently diffuse and can be missed by qualitative analysis and DGE burden assessment. Diffuse fibrosis is better demonstrated with use of hematocrit adjusted ECV and pre-/post-T1 mapping. CMR provides additional information about decrease in the LV mass, aortic stiffness, myocardial strain, early fibrosis detection, and myocardial edema that can aid in early detection of cardiotoxicity during anthracycline therapy. Use of CMR parametric imaging is complementary and essential in accurately diagnosing AIC in patients with prior exposure and merits widespread consideration in cardio-oncology.
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