“…Proposed mechanisms include direct endothelial injury and changes in vascular smooth muscle cell reactivity [ 45 ]. ACS can also be triggered by destabilization of atherosclerotic lesions, leading to plaque rupture and immediate term accelerated atherosclerosis [ 46 ]. The classical cytotoxic agent associated was cisplatin; however, multiple targeted therapies such as BCR-ABL TKI, ICI, and vascular endothelial growth factor inhibitors have such off-target effects.…”