When Should We Measure Lipoprotein(a)?

Abstract

Lp(a) belongs to the cholesterol ester-rich, apoB-containing lipoproteins, yet its metabolism is distinct from that of LDL (low-density lipoprotein). Evidence from large epidemiological, observational and Mendelian randomisation studies leave little doubt on the causality of lipoprotein(a) [Lp(a)] as one of the strongest risk factors for cardiovascular disease (CVD). Levels above 50 mg/dL are considered elevated and seen in up to 20% of the population. It is likely but currently not proven whether lowering of Lp(a) reduces cardiovascular events. Most lipidologists and clinicians recommend decreasing LDL cholesterol more aggressively in high-risk patients with elevated Lp(a) levels, even though hard evidence for this is lacking while large, randomised intervention studies with Lp(a)-lowering therapies are ongoing. Scientific societies are still prudent in recommending the measurement of Lp(a) routinely for assessing CVD risk. This is mainly due to the lack of definite intervention studies demonstrating that lowering Lp(a) reduces CV events, a lack of available therapies to lower Lp(a), the highly variable Lp(a) concentrations among different ethnic groups and the challenges associated with Lp(a) measurement. Herein, I present my view on when to measure Lp(a).