Adoptive cell therapy using chimeric antigen receptor (CAR) T cells augments the ability of the patient’s immune system to recognize and destroy cancer cells. Genetically modified autologous T-cell agents that target CD-19, tisagenlecleucel and axicabtagene ciloleucel, are currently approved for the treatment of children with B-cell acute lymphocytic leukemia and adults with aggressive B-cell lymphoma. Cytokine release syndrome (CRS) is a frequent adverse effect of CAR T-cell therapy and has been associated with cardiotoxicity.1 The pathophysiology of CAR T cell–associated cardiac dysfunction is unclear, but potential mechanisms include interleukin-6–mediated myocardial depression during CRS2 and direct cardiotoxicity attributed to off-target cross-reactivity of T cells against titin.3 In this study, we examined the incidence and impact of CAR T-cell therapy–associated cardiomyopathy.

This retrospective cohort study included all patients who received CAR T-cell therapy for refractory or relapsed, aggressive non-Hodgkin lymphoma at the Dana Farber Cancer Institute, in Boston, Massachusetts, and at the University of Michigan, Ann Arbor, Michigan, between February 2016 and April 2019. The respective institutional review boards approved this study and waived the requirement for informed consent. All patients underwent baseline echocardiography to assess left ventricular ejection fraction (LVEF).

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