Abstract
The mechanism of in-stent restenosis (ISR) remains elusive, and in-stent neoatherosclerosis (ISNA) may hold significant pathophysiologic implications. Nevertheless, the correlation between ISNA and the progression of untreated coronary segments affected by native atherosclerosis remains incompletely investigated. This study enrolled 225 patients diagnosed with coronary heart disease and multivessel disease. These patients underwent successful percutaneous coronary intervention and intraoperative placement of the drug-eluting stent, followed by optical coherence tomography assessment of the culprit stent. The mechanism of ISR was examined through qualitative and quantitative analysis of optical coherence tomography imaging. A significantly higher proportion of patients in the ISR with nontarget lesion progression (N-TLP) group exhibited lipid plaque formation compared with the ISR without N-TLP group (69.0% vs. 39.8%, P < 0.001). The incidence of thin-cap fibroatheroma (33.3% vs. 11.4%, P = 0.001) and ISNA (60.7% vs. 38.6%, P < 0.001) was markedly elevated in the ISR with N-TLP group compared with the ISR without N-TLP group. Regarding manifestations, heterogeneous hyperplasia was predominantly observed in the ISR with N-TLP group (76.2% vs. 38.6%, P < 0.001), whereas homogeneous hyperplasia was primarily presented in the ISR without N-TLP group (61.4% vs. 23.8%, P < 0.001). Patients displaying notable progression of naturally occurring atherosclerosis manifest histomorphologic features of ISR, primarily characterized by heterogeneous intimal hyperplasia and a higher prevalence of ISNA. In contrast, patients without substantial progression of naturally occurring atherosclerosis exhibit histomorphologic features of ISR primarily characterized by homogeneous intimal hyperplasia.