Is Lp(a) ready for prime time use in the clinic? A pros-and-cons debate

Lipoprotein (a) (Lp(a)) is a cholesterol-rich lipoprotein known since 1963. In spite of extensive research on Lp(a), there are still numerous gaps in our knowledge relating to its function, biosynthesis and catabolism. One reason for this might be that apo(a), the characteristic glycoprotein of Lp(a), is expressed only in primates. Results from experiments using transgenic animals therefore may need verification in humans. Studies on Lp(a) are also handicapped by the great number of isoforms of apo(a) and the heterogeneity of apo(a)-containing fractions in plasma. Quantification of Lp(a) in the clinical laboratory for a long time has not been standardized. Starting from its discovery, reports accumulated that Lp(a) contributed to the risk of cardiovascular disease (CVD), myocardial infarction (MI) and stroke. Early reports were based on case control studies but in the last decades a great deal of prospective studies have been published that highlight the increased risk for CVD and MI in patients with elevated Lp(a). Final answers to the question of whether Lp(a) is ready for wider clinical use will come from intervention studies with novel selective Lp(a) lowering medications that are currently underway. This article expounds arguments for and against this proposition from currently available data. •Lipoprotein (a) has been known to be a cardiovascular risk factor for many years but is not routinely measured.•Reasons to measure lipoprotein (a) based on epidemiology, assay methods and future interventions are presented.•Reasons not to measure lipoprotein (a) based on assay methods, and current trial data are presented.