Elevated Lipoprotein(a) Predicts Stent Edge Restenosis and Adverse Two-Year Outcomes After PCI: An Intravascular...

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.

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).

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.

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).

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.