Researchers discover the mechanism for heart complications from immune checkpoint inhibitor

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Myocarditis is a complication that can occur in cancer patients treated with immune checkpoint inhibitors.  

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Although the adverse event is rare -; affecting less than 1% of patients given the immunotherapy -; the mortality rate is nearly 50%. Now, researchers from Vanderbilt-Ingram Cancer Center have identified the mechanism for the deadly heart inflammation. 

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The researchers discovered that T-cells recognizing the cardiac antigen α-myosin are the mechanism for this complication, setting the framework to identify biomarkers so at-risk patients can be recognized and medical strategies developed for them to tolerate the immunotherapy. 

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This discovery represents the next important step to making these often-effective therapies safer in patients." 

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The research team obtained cardiac samples and peripheral blood from three patients who had suffered severe myocarditis after being treated with immune checkpoint inhibitors. 

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Clinicians currently do not have a clear understanding for why immunotherapy-related myocarditis occurs in some patients. Although early treatment with steroids can improve survival chances, a more effective treatment is needed 

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The study is the first to identify the role of α-myosin in the mechanism of heart complications from immune checkpoint inhibitors. 

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"While autoreactive T cells are the presumed mechanism for many toxicities to immunotherapies, tracing the condition back to a specific T cell receptor (often unique to each patient) and antigen source (drawing from tens- to hundreds- of thousands of potential antigens in the human body) is a daunting task," 

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