Eduardo Gomes Lima et al. Leticia Neves Solon Carvalho Tatiane Mascarenhas Santiago Emerich Eduardo Ferreira Amorim Fabiana Hanna Rached
The incorporation of lipoprotein(a) [Lp(a)] into contemporary cardiovascular risk assessment has introduced a practical question that is increasingly common in clinical practice: when faced with an elevated result, how should risk be reclassified and what management should be adopted, given that current guidelines recommend measuring Lp(a) at least once in adulthood and recognize it as a risk-modifying factor., However, the cardiovascular risk estimation proposed by these same guidelines — based on prognostic scores such as Predicting Risk of Cardiovascular Disease EVENTs – atherosclerotic cardiovascular disease (PREVENT-ASCVD), developed in 2023 by the American Heart Association — does not, a priori, account for the impact of elevated Lp(a) levels in its calculation. This creates a clinical scenario that is both concrete and challenging: the possibility that an asymptomatic patient, without traditional risk factors, may carry a biologically relevant risk factor that the score simply does not “see.” Thus arises the central question: what should be done when Lp(a) is elevated? In particular, should cardiovascular imaging be used to refine risk stratification?
A reasonable answer to these important questions requires an analysis of the biology and evidence that have propelled Lp(a) to its newly acquired prominence in the field of primary prevention in cardiology. Lp(a) is a particle similar to low-density lipoprotein (LDL), composed by an apolipoprotein B-100 molecule covalently bound to apolipoprotein(a), with levels predominantly determined by the LPA gene and relative stability throughout life., Its association with atherosclerotic cardiovascular disease is supported by epidemiological, genetic, and Mendelian randomization evidence, giving the particle a status stronger than that of a simple associative marker., Data from 450,000 patients demonstrate a strong linear correlation between elevated Lp(a) levels and atherosclerotic disease, with an approximate 11% increase in relative risk for every 50 nmol/L.
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