Testing
A single Lp(a) measurement suffices for CAD risk prediction, since repeat levels stay 96% correlated over years, in 16,017 UK Biobank participants (J Am Coll Cardiol 2022)
Original title: Repeat Measures of Lipoprotein(a) Molar Concentration and Cardiovascular Risk
In the UK Biobank, baseline and follow-up Lp(a) molar concentration (measured a median 4.42 years apart, IQR 3.69-4.93) were highly correlated in 16,017 unrelated individuals (Spearman rho 0.96, P<0.0001), with similarly strong correlations regardless of whether the interval between measurements was under 3 years (rho 0.96), 3-4 years (rho 0.97), 4-5 years (rho 0.96), or over 5 years (rho 0.96). Statin use was associated with a significant Lp(a) increase only among those with baseline Lp(a) >=70 nmol/L. Among 15,432 participants, follow-up Lp(a) significantly predicted incident coronary artery disease (HR per 120 nmol/L 1.32, 95% CI 1.16-1.50, P=0.0002), but the change in Lp(a) between baseline and follow-up added no independent predictive value beyond the follow-up value itself (P=0.98). The findings support that, absent Lp(a)-lowering therapy, a single accurate Lp(a) measurement is sufficient to inform coronary artery disease risk.
Original abstract
Background: When indicated, guidelines recommend measurement of lipoprotein(a) for cardiovascular risk assessment. However, temporal variability in lipoprotein(a) is not well understood, and it is unclear if repeat testing may help refine risk prediction of coronary artery disease (CAD).
Objectives: The authors examined the stability of repeat lipoprotein(a) measurements and the association between instability in lipoprotein(a) molar concentration with incident CAD.
Methods: The authors assessed the correlation between baseline and first follow-up measurements of lipoprotein(a) in the UK Biobank (n = 16,017 unrelated individuals). The association between change in lipoprotein(a) molar concentration and incident CAD was assessed among 15,432 participants using Cox proportional hazards models.
Results: Baseline and follow-up lipoprotein(a) molar concentration were significantly correlated over a median of 4.42 years (IQR: 3.69-4.93 years; Spearman rho = 0.96; P < 0.0001). The correlation between baseline and follow-up lipoprotein(a) molar concentration were stable across time between measurements of <3 (rho = 0.96), 3-4 (rho = 0.97), 4-5 (rho = 0.96), and >5 years (rho = 0.96). Although there were negligible-to-modest associations between statin use and changes in lipoprotein(a) molar concentration, statin usage was associated with a significant increase in lipoprotein(a) among individuals with baseline levels ≥70 nmol/L. Follow-up lipoprotein(a) molar concentration was significantly associated with risk of incident CAD (HR per 120 nmol/L: 1.32 [95% CI: 1.16-1.50]; P = 0.0002). However, the delta between follow-up and baseline lipoprotein(a) molar concentration was not significantly associated with incident CAD independent of follow-up lipoprotein(a) (P = 0.98).
Conclusions: These findings suggest that, in the absence of therapies substantially altering lipoprotein(a), a single accurate measurement of lipoprotein(a) molar concentration is an efficient method to inform CAD risk.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.