ESC Congress 2026 Abstract · Oct 26, 2026
Changes in lipoprotein(a) levels in younger patients following ST-elevation myocardial infarction
By Yoon J, Atefi N, Hosseini F et al.
Background: Lipoprotein(a) [Lp(a)] is a well-established, genetically determined risk factor for atherosclerotic cardiovascular disease. Contemporary consensus guidelines from the ESC and ACC/AHA recommend at least one lifetime Lp(a) measurement; however, interpretation of Lp(a) in the setting of acute ST-elevation myocardial infarction (STEMI) remains challenging. Prior studies suggest that acute myocardial infarction may transiently alter Lp(a) levels, and as a result, a single Lp(a) measurement obtained at the time of STEMI may underestimate a patient’s baseline Lp(a)-related risk. It also remains uncertain whether post-STEMI Lp(a) elevations reflect true biological change or rebound from acute-phase suppression. Purpose: We aimed to evaluate longitudinal changes in Lp(a) levels after STEMI in younger patients and to assess whether specific LLTs were associated with changes in Lp(a) at time of follow-up visit. Methods: We conducted a retrospective analysis among STEMI patients aged ≤65 years from 13 regional hospitals between January 2016 and December 2022. The primary objective was to determine changes in Lp(a) levels: the inclusion criteria included those with Lp(a) values measured at or shortly following STEMI hospitalization and at follow-up visit (defined as Lp(a) level obtained greater than at least 6 months following baseline measurement). A significant Lp(a) rise was defined as ≥40 nmol/L, based on prior studies (1). The secondary objective was to determine any association in Lp(a) change with LLTs, such as statins, ezetimibe, and PCSK9 inhibitors. Results: Among 1262 STEMI patients, 110 patients had two or more Lp(a) values and 78 met inclusion criteria. The baseline Lp(a) was measured during STEMI hospitalization in 15/78 (19%) and shortly after discharge in 63/78 (81%; median 3 [IQR: 1,7] months). The average change in Lp(a) was 7.3 ± 44 nmol/L with median time to follow-up of 13 (IQR 10, 20) months (Figure 1). Compared to baseline Lp(a) at time of STEMI, at median time of 13 months (IQR 10, 20) follow-up, 8/78 patients (10%) experienced Lp(a) increase ≥40 nmol/L (median 73 [IQR: 46, 177]), while 41/78 (53%) had an increase 0-39 nmol/L and 29/78 (37%) had a lower Lp(a) (median -13 [IQR: -20, -7]) (Figure 2). Among this cohort, 76/78 (97%) were on a statin, 16/78 (21%) were on ezetimibe, and 1/78 (1%) were on a PCSK9 inhibitor at time of follow-up measurement. There were no association in changes of Lp(a) levels with specific LLTs, though this was likely underpowered. Conclusion: Lp(a) trends following STEMI in younger patients demonstrate substantial heterogeneity, with a small proportion experiencing a significant rise over time. These findings may reflect variable recovery from acute-phase Lp(a) perturbation and/or true longitudinal biological variation. Larger studies are needed to identify determinants of significant Lp(a) changes and to establish their prognostic implications after STEMI.Figure 1Figure 2