Predictors and Mechanisms of Nonculprit Plaque Progression in Patients With Acute Coronary Syndromes: An In-Vivo...

Plaque progression is vital in the relationship between baseline phenotypes and future adverse events. Serial optical coherence tomography (OCT) has enabled the comprehensive assessment of plaque progression in vivo. This study aimed to explore the predictors of nonculprit plaque progression in patients with acute coronary syndrome (ACS) and assess the underlying mechanisms of progression using serial OCT. Patients diagnosed with ACS who underwent baseline and 12 ± 3 months of follow-up OCT scans between September 2013 and August 2022 were retrospectively enrolled. OCT defined plaque progression as a reduction in minimal lumen area of ≥0.84 mm² at follow-up. A total of 406 patients with ACS and 1,054 nonculprit plaques met the inclusion criteria, with a median follow-up duration of 369 days. Lesion location, luminal severity and the prevalence of vulnerable features significantly differed between the progression and nonprogression groups. In the multivariate analysis, thin-cap fibroatheroma (TCFA) (OR: 2.028, 95% CI: 1.287 to 3.196), macrophages (OR: 1.919, 95% CI: 1.212 to 3.040), microchannels (OR: 1.941, 95% CI: 1.353-2.782), and layered plaques (OR: 1.660, 95% CI: 1.178 to 2.339) were independent predictors of plaque progression. Two mechanisms of lesion progression were observed: Type I (54.6%): lesion progression without silent event(s). Type II (45.4%): lesion progression accompanied by silent event(s), including new layer formation and/or new intra-plaque hemorrhage. In conclusion, TCFA, macrophages, microchannels, and layered plaques independently predict nonculprit plaque progression in patients with ACS. Serial OCT examinations can identify distinct mechanisms of plaque progression that vary dramatically among different plaque phenotypes.