Repeat Measures of Lipoprotein(a) Molar Concentration and Cardiovascular Risk

Mark Trinder1, Kaavya Paruchuri2, Sara Haidermota3

  • 1Centre for Heart Lung Innovation, University of British Columbia, Vancouver, British Columbia, Canada; Program in Medical and Population Genetics and the Cardiovascular Disease Initiative, Broad Institute of Harvard, Cambridge, Massachusetts, USA. Electronic address: https://twitter.com/marketrinder.

Insights

Repeat lipoprotein(a) measurements show high stability over time. A single measurement of lipoprotein(a) is sufficient for assessing coronary artery disease (CAD) risk, as changes do not independently predict future events.

Area of Science:

  • Cardiovascular Medicine
  • Clinical Chemistry
  • Genetics and Genomics

Background:

  • Lipoprotein(a) [Lp(a)] measurement is recommended for cardiovascular risk assessment.
  • Temporal variability of Lp(a) and its impact on coronary artery disease (CAD) risk prediction are not well understood.

Purpose of the Study:

  • To examine the stability of repeat Lp(a) measurements.
  • To assess the association between Lp(a) instability and incident CAD.

Main Methods:

  • Assessed correlation between baseline and follow-up Lp(a) molar concentration in 16,017 UK Biobank participants.
  • Used Cox proportional hazards models to evaluate the association between Lp(a) changes and incident CAD in 15,432 participants.

Main Results:

  • Baseline and follow-up Lp(a) molar concentrations were highly correlated (Spearman rho = 0.96) over a median of 4.42 years, with stable correlations across different time intervals.
  • Follow-up Lp(a) molar concentration was significantly associated with incident CAD risk (HR per 120 nmol/L: 1.32).
  • Changes in Lp(a) molar concentration were not significantly associated with incident CAD independent of follow-up Lp(a) levels.

Conclusions:

  • A single, accurate Lp(a) molar concentration measurement is an efficient tool for informing CAD risk.
  • Repeat Lp(a) testing is not necessary for refining CAD risk prediction in the absence of therapies that significantly alter Lp(a) levels.
Abstract

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