ESC Congress 2026 Abstract · Oct 26, 2026
Lipoprotein(a) levels in patients hospitalized for acute coronary syndrome according to prior statin therapy
By Meseguer Hernandez A, Buendia Santiago F, Andreu Cayuelas JM et al.
Introduction: The persistence of coronary events in statin-treated patients highlights residual risk mechanisms beyond low-density lipoprotein cholesterol (LDL-C), with lipoprotein(a) [Lp(a)] playing a pivotal role. Treatment with statins has been suggested to be associated with an elevation in plasma Lp(a) levels, though the clinical significance remains uncertain. Purpose: This study analyzes Lp(a) levels and their relationship with prior statin therapy, as well as their association with a diagnosis of atherosclerotic cardiovascular disease (ASCVD) prior to admission in patients hospitalized for acute coronary syndrome (ACS). Methods: This observational study included 729 patients admitted for ACS with available Lp(a) measurements. Clinical variables, lipid profile, prior statin therapy, and adherence assessed by the 8-item Morisky Medication Adherence Scale were recorded. The association between prior statin therapy and log-transformed Lp(a) levels was evaluated using multivariable linear regression adjusted for confounding factors. Additionally, propensity score matching (1:1 nearest neighbor, caliper 0.2) was performed as a sensitivity analysis, yielding 117 matched pairs. Sample size was estimated a priori to ensure 80% power (α=0.05) to detect a small effect size (Cohen’s d = 0.20). Based on an estimated standard deviation of 1.33, a minimum of 722 participants was required; thus, the final cohort of 729 patients (361 on statins and 368 statin-naive) provided adequate statistical power. Results: Prior statin therapy was present in 49.5% of patients. These subjects exhibited lower LDL-C and apoB, but higher Lp(a) levels (77 [26–181] vs. 56 [26–133] nmol/L; p = 0.009) (figure). However, this association lost significance after multivariable adjustment (B = 0.025; 95% CI −0.204 to 0.255; p = 0.829) and propensity score adjustment (p = 0.686). Neither statin intensity [84 (29–187) vs. 71 (31–174) nmol/L; p = 0.644] nor treatment adherence [78 (29–192) vs. 79 (31–178) nmol/L; p = 0.749] influenced Lp(a) levels. Female sex was the only independent predictor of Lp(a) levels (table). Conversely, elevated Lp(a) was independently associated with prior ASCVD (OR 1.638; 95% CI 1.115–2.405; p = 0.012), indicating that higher Lp(a) levels are more prevalent in patients with recurrent cardiovascular events. Conclusion: In ACS patients, Lp(a) remains a marker of residual cardiovascular risk independent of statin therapy. The observed association between elevated Lp(a) levels and statin use is primarily driven by confounding by indication, reflecting the patients' higher baseline risk profile rather than a direct biological effect of the medication.FigureTable