Key result
Higher Lp(a) is linked to ~51% greater cardiovascular death risk after successful CTO PCI.
Why the study?
Does elevated Lipoprotein(a) increase the risk of cardiovascular death and MACEs in patients who underwent successful percutaneous coronary intervention for chronic total occlusion?
Cohort (n=1,509)
No
Does elevated Lipoprotein(a) increase the risk of cardiovascular death and MACEs in patients who underwent successful percutaneous coronary intervention for chronic total occlusion?
Hazard Ratio: 1.51 (95% CI 1.11–2.05)
p-value: p=0.008
Elevated Lipoprotein(a) is independently and linearly associated with an increased risk of cardiovascular death and MACEs in patients following successful PCI for chronic total occlusion, suggesting its utility for risk stratification.
Background: Lipoprotein(a) [Lp(a)] is a genetically determined, atherogenic, and prothrombotic lipoprotein. However, its prognostic value in patients who undergo successful chronic total occlusion (CTO) percutaneous coronary intervention (PCI) remains undefined. Methods: This single-center retrospective cohort study included 1509 patients who underwent successful CTO PCI. The primary outcome was cardiovascular death; secondary outcome was major adverse cardiovascular events (MACEs, cardiovascular death or nonfatal myocardial infarction). Multivariable Cox regression and restricted cubic splines (RCS) assessed the association between Lp(a) and outcomes. Results: Over median follow-up of 810 days, 53 (3.5%) cardiovascular deaths and 62 (4.1%) MACEs occurred. Each 1-SD increase in log-transformed Lp(a) was associated with a 51% higher risk of cardiovascular death (aHR 1.51, 95% CI 1.11–2.05, p = 0.008) and a 44% higher risk of MACEs (aHR 1.44, 95% CI 1.09–1.91, p = 0.011). Compared with Lp(a) < 30 mg/dL, Lp(a) ≥ 50 mg/dL conferred a 2.07-fold higher risk of cardiovascular death (95% CI 1.07–4.00, p = 0.029) and a 1.94-fold higher risk of MACEs (95% CI 1.07–3.53, p = 0.030). RCS analysis demonstrated a linear dose–response relationship between log-transformed Lp(a) and both cardiovascular death (p for nonlinearity = 0.653) and MACEs (p for nonlinearity = 0.562). The association was modified by age, hypertension, and left ventricular ejection fraction and remained robust in sensitivity analyses. Conclusions: In patients undergoing successful CTO PCI, elevated Lp(a) was independently and linearly associated with higher risks of cardiovascular death and MACEs. These findings suggest that Lp(a) may serve as a useful prognostic marker to enhance risk stratification in this high-risk population. Large-scale prospective cohorts are needed to validate these findings before clinical translation can be considered.
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Wang et al. (2026) conducted a cohort in Chronic Total Occlusion (CTO) (n=1,509). Lipoprotein(a) vs. Lower Lipoprotein(a) levels was evaluated on Cardiovascular death (aHR 1.51, 95% CI 1.11-2.05, p=0.008). In patients undergoing successful CTO PCI, each 1-SD increase in log-transformed Lipoprotein(a) was associated with a 51% higher risk of cardiovascular death (aHR 1.51; 95% CI 1.11-2.05; p=0.008).
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