Mechanisms
A larger early drop in Lp(a) after emergency PCI paradoxically predicts worse outcomes in acute coronary syndrome (World J Cardiol 2024)
Original title: Initial decrease in the lipoprotein(a) level is a novel prognostic biomarker in patients with acute coronary syndrome
In 249 patients with acute coronary syndrome who underwent emergency percutaneous coronary intervention (PCI) and completed at least 1,000 days of follow-up, Lp(a) was measured serially from before PCI to 48 hours after using an isoform-independent assay. Mean Lp(a) fell significantly from pre-PCI (19.0 mg/dL) to 12 hours after (17.8 mg/dL, P < 0.001), then rose again to 19.3 mg/dL by 48 hours (P < 0.001). The magnitude of this early drop (Lp(a) change from 0 to 12 hours) correlated with baseline creatinine and baseline Lp(a). Patients in the lowest tertile of this early Lp(a) change (the largest drop) had significantly more major adverse cardiac events (MACE) than the other two tertiles combined (66.2% vs. 53.6%, P = 0.034). Multivariate analysis confirmed the early Lp(a) change (hazard ratio 0.96, 95% CI 0.92-0.99) and baseline creatinine (hazard ratio 1.13, 95% CI 1.05-1.22) as independent predictors of subsequent MACE. A greater early drop in circulating Lp(a) after emergency PCI, seemingly counterintuitive, independently predicts a worse cardiovascular prognosis.
Original abstract
Background: Lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular diseases; however, its role in acute coronary syndrome (ACS) remains unclear.
Aim: To investigate the hypothesis that the Lp(a) levels are altered by various conditions during the acute phase of ACS, resulting in subsequent cardiovascular events.
Methods: From September 2009 to May 2016, 377 patients with ACS who underwent emergent coronary angiography, and 249 who completed ≥ 1000 d of follow-up were enrolled. Lp(a) levels were measured using an isoform-independent assay at each time point from before percutaneous coronary intervention (PCI) to 48 h after PCI. The primary endpoint was the occurrence of major adverse cardiac events (MACE; cardiac death, other vascular death, ACS, and non-cardiac vascular events).
Results: The mean circulating Lp(a) level decreased significantly from pre-PCI (0 h) to 12 h after (19.0 mg/dL to 17.8 mg/dL, P < 0.001), and then increased significantly up to 48 h after (19.3 mg/dL, P < 0.001). The changes from 0 to 12 h [Lp(a)Δ0-12] significantly correlated with the basal levels of creatinine [Spearman's rank correlation coefficient (SRCC): -0.181, P < 0.01] and Lp(a) (SRCC: -0.306, P < 0.05). Among the tertiles classified according to Lp(a)Δ0-12, MACE was significantly more frequent in the lowest Lp(a)Δ0-12 group than in the remaining two tertile groups (66.2% vs 53.6%, P = 0.034). A multivariate analysis revealed that Lp(a)Δ0-12 [hazard ratio (HR): 0.96, 95% confidence interval (95%CI): 0.92-0.99] and basal creatinine (HR: 1.13, 95%CI: 1.05-1.22) were independent determinants of subsequent MACE.
Conclusion: Circulating Lp(a) levels in patients with ACS decreased significantly after emergent PCI, and a greater decrease was independently associated with a worse prognosis.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.