Mechanisms
IVUS study links elevated Lp(a) to more neoatherosclerosis and a 3.4-fold higher odds of stent edge restenosis after PCI (Int J Gen Med 2025)
Original title: Elevated Lipoprotein(a) Predicts Stent Edge Restenosis and Adverse Two-Year Outcomes After PCI: An Intravascular Ultrasound Study
In 211 patients with stent edge restenosis who underwent intravascular ultrasound (IVUS)-guided percutaneous coronary intervention, those with elevated Lp(a) (50 mg/dL or above, n = 75) were compared with those with non-elevated Lp(a) (below 50 mg/dL, n = 136), despite similar baseline clinical and angiographic characteristics (P > 0.05). The elevated Lp(a) group showed significantly more neoatherosclerosis on IVUS (56.0% vs. 44.1%, P < 0.001) and less neointimal hyperplasia (24.0% vs. 33.8%, P < 0.001). Multivariate analysis identified elevated Lp(a) as an independent predictor of stent edge restenosis (odds ratio 3.391, 95% CI 2.030-5.273, P < 0.001). Over two years of follow-up, the elevated Lp(a) group had higher rates of device-oriented clinical endpoints (16.0% vs. 7.4%, P < 0.001) and target lesion revascularisation (13.3% vs. 5.1%, P = 0.011). The IVUS findings point to a neoatherosclerosis-driven mechanism linking Lp(a) to stent failure, positioning Lp(a) as a potential target for improving long-term stent durability.
Original abstract
Background: Elevated lipoprotein(a) [Lp(a)] is a known contributor to recurrent ischemic events following percutaneous coronary intervention (PCI). Although drug-eluting stents (DES) have significantly advanced coronary revascularization, stent edge restenosis (SER) remains a clinical challenge. However, the relationship between Lp(a) levels and the incidence of SER is not well defined.
Objective: This study aimed to investigate the association between serum Lp(a) levels and the development of SER, and to explore potential pathophysiological mechanisms using intravascular ultrasound (IVUS).
Methods: A total of 211 patients with SER lesions who underwent IVUS-guided PCI were included. Patients were divided into two groups based on their baseline Lp(a) concentrations: elevated Lp(a) (≥50 mg/dL, n=75) and non-elevated Lp(a) (<50 mg/dL, n=136). Clinical characteristics, angiographic features, IVUS findings, and device-oriented clinical endpoints (DoCE) were compared between the two cohorts.
Results: Baseline clinical and angiographic characteristics were similar between the groups (P > 0.05). Neoatherosclerosis was significantly more frequent in the elevated Lp(a) group (56.0% vs 44.1%, P < 0.001), whereas neointimal hyperplasia was less common (24.0% vs 33.8%, P < 0.001). Multivariate analysis identified elevated Lp(a) as an independent predictor of SER (odds ratio: 3.391; 95% confidence interval: 2.030-5.273; P < 0.001). During a two-year follow-up, the elevated Lp(a) group showed higher rates of DoCE (16.0% vs 7.4%, P < 0.001) and target lesion revascularization (13.3% vs 5.1%, P = 0.011).
Conclusion: Elevated Lp(a) is an independent predictor of SER and is associated with adverse two-year clinical outcomes after PCI. These findings underscore the importance of Lp(a) as a potential therapeutic target for improving long-term stent durability.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.