Key result
Longitudinal Lp(a) levels increased ≥10 mg/dL in only 2.8% of adults over 5.2 years, predicted by a 5-factor clinical score (AUC 86.4%; 95% CI 84.8%–88.0%).
Why the study?
Although lipoprotein(a) [Lp(a)] concentrations are mainly determined by genetic factors, evidence on their long-term variability and clinical determinants remains limited, particularly among Asian populations.
Cohort (n=17,363)
Yes
While lipoprotein(a) concentrations remain stable over a mean of 5.2 years in most individuals, repeat testing may be warranted in select patients with specific clinical risk factors (higher baseline Lp(a), new statin initiation, diabetes, female sex, higher triglycerides) who are at higher risk for substantial Lp(a) elevation.
Background/Introduction Lipoprotein(a) [Lp(a)] concentrations are mainly determined by genetic factors, yet evidence on their long-term variability and determinants remains limited, particularly among Asian populations. Purpose This study examined temporal changes in Lp(a) concentrations and identified clinical predictors of substantial intra-individual elevation. Methods We conducted a retrospective cohort study using the Chang Gung Research Database from January 2004 through December 2019. Adults with baseline and follow-up Lp(a) measurements at least one year apart were included. Participants were categorized according to temporal changes: increase ≥10 mg/dL, increase <10 mg/dL, or decrease. Multivariable logistic regression was used to identify predictors of Lp(a) increase ≥10 mg/dL. Results Among 17,363 participants (mean age 42.1 years; 73.3% male) with a mean follow-up of 5.2 years, median Lp(a) levels declined from 9.3 mg/dL (interquartile range [IQR] 4.1–17.3) to 7.4 mg/dL (IQR 3.6–16.3). Only 479 participants (2.8%) exhibited an increase of ≥10 mg/dL. Independent predictors of such elevation included higher baseline Lp(a), new statin initiation, diabetes mellitus, female sex, and higher triglyceride levels. By modeling Lp(a) using restricted cubic splines, we identified a baseline threshold of 17.1 mg/dL for predicting an increase in Lp(a) ≥10 mg/dL during follow-up. We constructed a simple score by summing 5 risk factors and evaluated its association with subsequent Lp(a) elevation. The model demonstrated good discrimination (AUC, 86.4%; 95% CI, 84.8%–88.0%). The risk of Lp(a) increase ≥10 mg/dL rose progressively with a greater number of risk factors. Conclusion(s) In this large longitudinal Taiwanese cohort, Lp(a) concentrations were generally stable, with only a small proportion showing substantial increases. However, specific clinical factors predicted Lp(a) elevation, suggesting that repeat Lp(a) measurements may be warranted in selected high-risk individuals to enhance cardiovascular risk stratification.Fig 1.Flowchart for the study participants.
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Chen et al. (2026) conducted a cohort in Lipoprotein(a) temporal variability (n=17,363). Clinical risk factors for Lp(a) elevation (baseline Lp(a), new statin initiation, diabetes mellitus, female sex, higher triglycerides) vs. Absence of risk factors was evaluated on Intra-individual Lp(a) increase ≥10 mg/dL (AUC 86.4%, 95% CI 84.8%–88.0%). Longitudinal Lp(a) levels increased ≥10 mg/dL in only 2.8% of adults over 5.2 years, predicted by a 5-factor clinical score (AUC 86.4%; 95% CI 84.8%–88.0%).
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