Repeat Lipoprotein(a) Concentration Measurements and Cardiovascular Risk

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A study was conducted to determine the effect of lipoprotein(a) concentration stability on incident coronary artery disease.

Statin therapy is not associated with significant changes in the molar concentration of lipoprotein(a), and, absent any other therapy significantly altering lipoprotein(a), measuring lipoprotein(a) molar concentration accurately a single time is an efficient way to gauge risk for coronary artery disease (CAD). These findings were published in the Journal of the American College of Cardiology.

Current guidelines recommend cardiovascular risk assessment by measurement of lipoprotein(a). Temporal variability in lipoprotein(a) is not well understood and is difficult to explain. Therefore, it is unclear if repeat testing adds to the refinement of CAD prediction. Researchers sought to examine the stability of repeat lipoprotein(a) measurements and the association between lipoprotein(a) concentration instability and self-reported CAD developing between baseline and follow-up. They also examined if statins have an appreciable effect on lipoprotein(a) molar concentration.

Researchers utilized data from the UK Biobank, a prospective observational study that included 16,017 participants with baseline and repeat lipoprotein(a) measurements, to assess their correlation. Using Cox proportional hazard models, the association between instability in lipoprotein(a) molar concentration and incident CAD was evaluated with 15,432 participants.

Research showed a significant correlation between baseline and follow-up lipoprotein(a) molar concentration (median 4.42 years; IQR: 3.69-4.93 years; Spearman rho =0.96; P <.0001). This correlation was stable across time between measurements of less than 3, 4 to 5, and more than 5 years (rho =0.96), and 3 to 4 years (rho =0.97). Researchers also found a significant association between follow-up lipoprotein(a) molar concentration and incident CAD risk (hazard ratio per 120 nmol/L: 1.32 [95% CI, 1.16-1.50]; P =.0002). Taken independently, the difference between baseline and follow-up lipoprotein(a) was not significantly associated with incident CAD (P =.98).

Noted study limitations included that most participants in the UK Biobank are middle-aged White adults, the volunteer participants in this study tended to be healthier than the general population, statin doses used by participants were unknown, diagnosis and operation codes were used to define cardiovascular events, and there was a relatively low number of events overall.

Based on these study data, there is no significant association between statin therapy and changes in the molar concentration of lipoprotein(a). “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,” the researchers wrote. “Monitoring of lipoprotein(a) levels is unlikely to be clinically useful for understanding an individual patient’s residual risk of an incident cardiovascular event in the context of primary prevention.”

One study author declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.

Reference

Trinder M, Paruchuri K, Haidermota S, et al. Repeat measures of lipoprotein(a) molar concentration and cardiovascular risk. J Am Coll Cardiol. Published online February 22, 2022. doi:10.1016/j.jacc.2021.11.055