Immunotherapy is one of the most effective methods of cancer therapy. There are five main groups of immunotherapy, including treatment with chimeric antigen receptor T cells, checkpoint inhibitors, anticancer vaccines, antibody-based targeted therapies, and oncolytic viruses. On the adult cohort of patients, immunotherapy has been proven to increase the survival rate of patients with cancer. At the same time, in some patients, it can cause an immune-mediated damage and contribute to unfavorable heart immune modulation and heart failure. Immunotherapy can target many components of the cardiovascular system, including the myocardium, blood vessels, electrical wiring, and the pericardium. Activated T lymphocytes (CD4 + and CD8 + T cells) penetrate the heart tissue and skeletal targets, which leads to local inflammation and damage. Additional theoretical mechanisms for side effects include autoantibody recognition of self-antigens and T cell-mediated damage to cardiomyocytes and stressed endothelial cells. After treatment with T cells, the level of proinflammatory cytokines may increase, which is often the cause of cytokine release syndrome, the occurrence of which is considered a “targeted, non-neoplastic” effect. Proinflammatory cytokines can have negative cytotoxic effects on cardiomyocytes, resulting in reduced myocardial contractility, cardiomyopathy, and hypotension. This review presents a clinical case of cardiotoxicity due to the use of antiGD2 monoclonal antibodies in a child with a refractory form of osteosarcoma.
Kulyova et al. (Mon,) studied this question.