Nikita P Patel1, Peter G Doukas1, Leo I Gordon2, Nausheen Akhter3. 1. Department of Medicine, Northwestern Feinberg School of Medicine, 676 N. St. Clair St., Arkes Suite 2330, Chicago, IL, 60611, USA. 2. Division of Hematology and Oncology, Northwestern Feinberg School of Medicine, 675 N. St. Clair St. Ste 21-100, Chicago, IL, 60611, USA. 3. Division of Cardiology, Northwestern Feinberg School of Medicine, 675 N. St. Clair St. Ste 19-100, Chicago, IL, 60611, USA. n-akhter@northwestern.edu.
Abstract
PURPOSE OF REVIEW: This review provides a contemporary overview of current studies outlining the incidence and characteristics of CAR T-cell cardiotoxicity in an effort to identify future directions for research and potential opportunities for prevention and intervention. RECENT FINDINGS: Cardiovascular events occurred in anywhere between 10 and 36% of patients in CAR T-cell clinical trials, ranging from tachycardia, hypotension, arrhythmia, decreased left ventricular systolic function to cardiogenic shock and death. Cardiac events are more often associated higher grades (> 2) of cytokine release syndrome and frequently proceeded by an elevated troponin. There is a growing recognition of cardiotoxicities of CAR T-cell therapy but has a limited study in this area. The mechanism of left ventricular dysfunction due to CAR T-cell therapy is also unknown. As CAR T-cell use expands, it becomes imperative to truly understand the mechanism behind cardiac injury and to assess long-term follow-up data as this will allow for surveillance, early intervention, and potentially prevention of cardiotoxicity.
PURPOSE OF REVIEW: This review provides a contemporary overview of current studies outlining the incidence and characteristics of CAR T-cell cardiotoxicity in an effort to identify future directions for research and potential opportunities for prevention and intervention. RECENT FINDINGS: Cardiovascular events occurred in anywhere between 10 and 36% of patients in CAR T-cell clinical trials, ranging from tachycardia, hypotension, arrhythmia, decreased left ventricular systolic function to cardiogenic shock and death. Cardiac events are more often associated higher grades (> 2) of cytokine release syndrome and frequently proceeded by an elevated troponin. There is a growing recognition of cardiotoxicities of CAR T-cell therapy but has a limited study in this area. The mechanism of left ventricular dysfunction due to CAR T-cell therapy is also unknown. As CAR T-cell use expands, it becomes imperative to truly understand the mechanism behind cardiac injury and to assess long-term follow-up data as this will allow for surveillance, early intervention, and potentially prevention of cardiotoxicity.
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