Jose Javier Gomez-Barrado, Miguel Turegano-Yedro, Miguel Angel Silva-Cerpa, Elias Emilio Majluf, Carla Guillem-Ferrer, Rafael Cantisán-Campillos, Marcos García-Jambrina, Estrella Martínez-Bermúdez, Rocio Soledad González-Garay, Ana Macarro-Soto, Celia González-Peramato, Roberto Pallavera-Sánchez, María Sosa-Sánchez, Paula Gómez-Turégano
In this historical prospective cohort, plasma Lp(a) concentrations remained stable during the first 48 hours after ACS, increased significantly around day 7, and subsequently declined by day 30. These findings suggest that Lp(a) undergoes transient changes during the early post-ACS period and that measurements obtained during the first weeks after the index event should be interpreted with caution. Larger contemporary studies are warranted to determine the optimal timing for Lp(a) assessment following ACS.
BACKGROUND: Lipoprotein(a) [Lp(a)] is an independent causal risk factor for atherosclerotic cardiovascular disease, with plasma concentrations largely determined by genetic factors. Despite its relative stability under basal conditions, its behaviour during acute inflammatory states such as acute coronary syndrome (ACS) remains controversial. This exploratory study evaluated serial changes in plasma Lp(a) concentrations during the first month after ACS using the original patient-level data from a historical prospective cohort with high-frequency serial sampling.
METHODS: Thirty-three men with ACS were prospectively enrolled. Blood samples were collected at hospital admission (≤3 h after symptom onset), and at 12, 24, and 48 hours, as well as on days 7 and 30. Plasma Lp(a) concentrations were measured by immunoturbidimetry. Because Lp(a) values were not normally distributed, results are presented as mean ± standard deviation (SD) and median (interquartile range [IQR]). Overall temporal differences were assessed using the Friedman test, and prespecified pairwise comparisons were performed using the Wilcoxon signed-rank test.
RESULTS: Twenty-nine patients completed all six scheduled assessments. Plasma Lp(a) concentrations showed a significant overall change over time (Friedman χ²(5) = 33.5, p < 0.001). No statistically significant differences were observed between admission and 12 hours (p = 0.473), 24 hours (p = 0.621), or 48 hours (p = 0.630). Median (IQR) Lp(a) concentrations at these respective time points were 21.0 (36.5), 19.0 (30.5), 16.0 (32.5), and 20.0 (29.5) mg/dL. Lp(a) concentrations increased significantly on day 7 (median 39.0 [54.0] mg/dL; p < 0.001 vs. admission) and subsequently declined by day 30 (median 23.0 [46.0] mg/dL; p = 0.023 vs. day 7).
CONCLUSIONS: In this historical prospective cohort, plasma Lp(a) concentrations remained stable during the first 48 hours after ACS, increased significantly around day 7, and subsequently declined by day 30. These findings suggest that Lp(a) undergoes transient changes during the early post-ACS period and that measurements obtained during the first weeks after the index event should be interpreted with caution. Larger contemporary studies are warranted to determine the optimal timing for Lp(a) assessment following ACS.