Changes in lipoprotein(a) levels in younger patients following ST-elevation myocardial infarction
J Yoon, N Atefi, F Hosseini, T Lee, L Brunham, G B J Mancini, T Roston, I Iatan, G Wong, C FordyceAbstract
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