Cardiovascular toxicity associated with cellular therapies. (A) Current literature has identified several cardiotoxic side effects of CAR-Ts, including arrhythmia, coagulopathy, heart failure, pericardial disease, and hypotension/shock. Less is known about the cardiotoxicity of BTEs, with only coagulopathy myocarditis, and hypotension/shock having been associated with therapy. Finally, there has been no definitive association between cardiotoxicity and TILs, given their recent introduction. (B) The mechanism of cardiotoxicity associated with cellular therapies can be divided into 3 categories: CRS-mediated cardiovascular dysfunction, direct cardiotoxicity, and indirect cardiotoxicity. Activated CAR-Ts or BTEs release cytokines, including granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor (TNF), and interferon gamma (IFN-γ), which lead to macrophage activation, resulting in a proinflammatory cascade that causes oxidative stress, altered calcium cycling, and endothelial dysfunction, ultimately resulting in cardiovascular dysfunction. Indirect cardiotoxicity has been documented with CAR-Ts, in which engineered cells attack the sarcomeric protein titin as a crossantigen. Direct cardiotoxicity has been proposed as an alternative pathway in which CAR-Ts directly attack the myocardium. NO, nitric oxide.