Figure 1.

ISR physiopathology (adapted from an open–access source [32]). (Left): Coronary restenosis after conventional balloon angioplasty primarily arises from the phenomenon of elastic recoil of the arterial vessel wall. Moreover, the trauma inflicted on the coronary artery triggers the initiation of smooth muscle cell proliferation, their migration, and the deposition of an extracellular matrix. This cascade of events culminates in the formation of neointimal hyperplasia, which ultimately contributes to the pathogenesis of restenosis. (Center): The deployment of a BMS is associated with a heightened level of vascular injury, thereby augmenting the magnitude of neointimal hyperplasia and elevating the risk of in-stent restenosis. (Right): DESs dispense antiproliferative agents, effectively mitigating the extent of neointimal hyperplasia and correspondingly diminishing the susceptibility to in-stent restenosis.