Abstract 4363863: Does Lipoprotein(a) Associate with In-Stent Neoatherosclerosis and Plaque Vulnerability Detected by Optical Coherence Tomography in Patients with Acute Coronary Syndrome?

Background: Recently, lipoprotein(a) [Lp(a)], a genetically determined low-density lipoprotein-like particle, has been recognized as a potential therapeutic target for residual cardiovascular risk. In-stent restenosis remains one of major clinical challenges for patients undergoing stent implantation. This study aimed to investigate the association between Lp(a) level and optical coherence tomography (OCT)-defined ISNA as well as plaque vulnerability in patients with acute coronary syndrome (ACS). Methods: From January 2017 to December 2021, 146 ACS patients with ISR undergoing OCT-guided intervention were enrolled. Baseline serum Lp(a) levels were measured via latex particle-enhanced turbidimetric immunoassay (Roche Diagnostics) and categorized into high (≥75 nmol/L, n=34) and low (<75 nmol/L, n=112) groups. Clinical profiles, angiographic features, and OCT data were compared between groups. Multivariate logistic regression adjusted for covariates was performed to identify independent associations. The primary endpoint was the presence of in-stent neoatherosclerosis (ISNA). Results: The cohort had a mean age of 62.3±8.9 years, with 73.3% (107/146) males. Elevated Lp(a) (≥75 nmol/L) was observed in 23.3% (34/146) of patients. Compared to the low Lp(a) group, the high Lp(a) group exhibited significantly higher rates of ISNA (91.2% vs. 50.9%, P<0.001), thin-cap fibroatheroma (TCFA) (38.2% vs. 8.0%, P<0.001), macrophage accumulation (82.4% vs. 64.3%, P=0.047). Conversely, homogeneous neointima was more prevalent in the low Lp(a) group (41.1% vs. 4.2%, P<0.001). Multivariate analysis confirmed that elevated Lp(a) independently correlated with ISNA (OR: 1.012, 95% CI: 1.004–1.020; P=0.002) and TCFA (OR: 1.010, 95% CI: 1.005–1.016; P<0.001). Conclusion: In ACS patients with ISR, Lp(a) ≥75 nmol/L is independently associated with increased risks of ISNA and vulnerable plaque phenotypes. These findings highlight the potential role of Lp(a) in ISR pathogenesis and suggest its utility in risk stratification and targeted therapeutic strategies.