Dynamic and non-linear changes in lipoprotein(a) during acute coronary syndrome
S Fujioka, K Sakaguchi, H Kusumoto, M Michikura, D shishikura, M Shiba, H MoritaAbstract
Background
Lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerotic cardiovascular disease. Because circulating Lp(a) levels are largely genetically determined by the LPA gene, a single lifetime measurement has traditionally been considered sufficient. However, emerging evidence suggests that Lp(a) may fluctuate during the acute phase of acute coronary syndrome (ACS), with a possible peak around two weeks after onset. We aimed to identify clinical determinants of acute-phase Lp(a) changes and characterize its temporal pattern following ACS.
Methods
This single-center retrospective study included consecutive ACS patients undergoing percutaneous coronary intervention between January 2023 and January 2026. All received intensive statin therapy and had at least two Lp(a) measurements: at admission and within 30 days. Baseline Lp(a) was defined as the value within 72 hours of admission. ΔLp(a) was calculated as follow-up minus baseline Lp(a).Correlations between ΔLp(a) within 14 days and peak creatine kinase-MB (CK-MB), peak C-reactive protein (CRP), peak aspartate aminotransferase (AST), estimated glomerular filtration rate (eGFR), and baseline Lp(a) were assessed. Multivariable linear regression identified independent determinants. Linear and quadratic regression models were applied to evaluate the overall time-course pattern.
Results
Eighty-four patients were analyzed (mean age 69.4 years; 21.4% female). Baseline Lp(a) was 20.8 ± 19.0 mg/dL. Mean ΔLp(a) was 13.3 ± 14.1 mg/dL, with a maximum increase of 72 mg/dL at 12 days.ΔLp(a) within 14 days correlated with baseline Lp(a) (r = 0.42, p < 0.001) and CRP (r = 0.27, p = 0.016), but not with CK-MB or AST. In multivariable analysis adjusting for age, sex, timing, CRP, and baseline Lp(a), CRP (β = 0.64, p = 0.001) and baseline Lp(a) (β = 0.33, p < 0.001) remained independently associated with ΔLp(a). Quadratic regression demonstrated a significant non-linear trajectory (p for non-linearity = 0.012).
Conclusions
Lp(a) shows a transient, non-linear increase during the acute phase of ACS associated with inflammatory response. Early post-ACS Lp(a) measurements may not reflect steady-state levels and should be interpreted cautiously.Lp(a) Changes in the Acute Phase of ACSCorrelation of baseline Lp(a) and CRP