Testing
Lp(a) rose significantly 3 months after acute coronary syndrome in all 40 patients studied, challenging single-timepoint measurement (Pol Arch Intern Med 2025)
Original title: Changes in lipoprotein(a) concentrations in patients with acute coronary syndrome
This study enrolled 40 patients with acute coronary syndrome (ACS), split into STEMI and NSTEMI-plus-unstable-angina groups, to compare Lp(a) at the time of ACS versus 3 months later. Elevated Lp(a) (above 75 nmol/L) was present in 9 patients (22.5%) at baseline, more often in STEMI (35%) than NSTEMI/UA (13%). All ACS patients showed significantly higher serum Lp(a) at 3 months than at the acute event, with significant differences in STEMI patients (P = 0.03), the whole ACS group (P = 0.003), and NSTEMI/UA patients specifically (P = 0.003). The authors conclude that measuring Lp(a) during the acute event itself may be insufficient for accurate risk assessment, since its concentration rises over the following months, positioning ACS as another non-genetic factor that can transiently alter Lp(a) levels.
Original abstract
Introduction: Recently, interest has been growing in lipoprotein(a) (Lp[a]) as an independent risk factor for cardiovascular diseases. European Society of Cardiology recommends a single measurement of Lp(a) concentration as a guide to determine cardiovascular risk group and appropriate treatment. Although initially assumed to be genetically determined, a growing number of reports indicate that Lp(a) concentration may change over time.
Objectives: The aim of the study was to compare changes in the concentration of Lp(a) in patients with acute coronary syndrome (ACS) at the moment of ACS and 3 months later.
Patients And Methods: Forty patients with ACS were enrolled and divided into ST‑segment elevation myocardial infarction (STEMI) and non‑STEMI (NSTEMI) + unstable angina (UA) groups. The levels of lipids, C‑reactive protein, high‑sensitivity troponin T, N-terminal pro-B-type natriuretic peptide, and Lp(a) were determined using routine laboratory methods, with interleukin‑33 levels measured using an enzyme‑linked immunosorbent assay.
Results: Among all ACS patients, 9 (22.5%) had elevated Lp(a) levels (>75 nmol/l). This proportion was higher in the STEMI (n = 8; 35%) than NSTEMI+UA (n = 2; 13%) patients. All patients with ACS showed significantly higher serum Lp(a) levels 3 months after ACS. The Lp(a) level at the moment of ACS and 3 months later differed markedly in the STEMI patients (P = 0.03), all patients with ACS (P = 0.003), and NSTEMI+UA individuals (P = 0.003).
Conclusion: Measuring Lp(a) level during ACS may be insufficient for accurate diagnosis and effective treatment, as its concentration increases 3 months post‑ACS. Therefore, ACS may be regarded as another nongenetic factor influencing Lp(a) concentration.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.