This article has been reviewed so that we could detect how Cancer immunotherapy with immune checkpoint inhibitors (ICIs) has revolutionized the management of a wide variety of malignancies. ICIs, such as monoclonal antibodies targeting PD-1 (programmed cell death protein 1; nivolumab, pembrolizumab), PD-L1 (programmed death-ligand 1; atezolizumab), or CTLA-4 (cytotoxic T-lymphocyte-associated protein 4; ipilimumab), stimulate previously inactivated cytotoxic T-cells to recognize and target cancer cells. Interference with the CTLA-4 and PD-1 axes can cause immune-related adverse events, which in some cases lead to serious and potentially fatal cardiovascular toxicity.1 Numerous reports of fulminant myocarditis, fatal heart failure, and acute coronary syndromes have been described, as well as conduction disease, pericardial disease, and even Takotsubo-like cardiomyopathy.
The atherosclerosis progression was associated with markedly increased monocyte recruitment, and the loss of CTLA-4 leads to a promotion of lymphoproliferation, suppressed atherosclerotic T-cell activation by multiorgan CD4+ (cluster of differentiation 4) and CD8+ (cluster of differentiation 8) T-lymphocyte infiltration, and tissue destruction, with particularly severe myocarditis and pancreatitis. This suggests that PD-1/PD-L1 and CTLA-4 chemokine axes could play important roles in limiting T-cell–mediated autoimmune inflammation.1,2 Activated T cells produce large amounts of proatherogenic cytokines that may contribute to both the growth and destabilization of atherosclerotic plaques.
Reference link- https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.120.048708
