Abstract Background Lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular disease (ASCVD = myocardial infarction, ischemic stroke, peripheral artery disease) and aortic valve stenosis. Plasma concentrations of Lp(a) are >90% genetically determined. Multiple drugs in development reduce lipoprotein(a) by 80% to 98%. While the recently announced topline results, the phase 3 Lp(a)HORIZON trial of pelacarsen did not meet its primary cardiovascular endpoint despite lowering Lp(a), and 3 other cardiovascular outcomes trials remain ongoing. Lipoprotein(a) testing is currently increasing rapidly in many countries. Content Most guidelines on dyslipidemia and prevention of cardiovascular disease worldwide now advise that Lp(a) should be measured once in all adults, ideally jointly with the first lipid profile ordered. If previous lipid profiles were taken, then Lp(a) should be included in the next lipid profile. Lipoprotein(a) should ideally be measured in nmol/L, and repeat measurements are relevant if drugs are given to lower Lp(a) concentrations, initially at suspected acute coronary syndrome or stroke and again after 1 month, and sometimes in women after menopause. Measuring Lp(a) levels alongside a standard lipid profile provides a more comprehensive initial assessment of a patient's overall cardiovascular risk. Clinical chemistry laboratories that measure lipid profiles should therefore also offer Lp(a) testing. This is easily done as Lp(a) assays can be run on most major clinical chemistry platforms. High Lp(a) is >105 nmol/L (>50 mg/dL). Summary As use of Lp(a) testing is increasing rapidly worldwide, more clinical chemistry laboratories will likely offer this test locally. Measuring Lp(a) levels alongside a standard lipid profile provides a more comprehensive initial lipid assessment of a patient's cardiovascular risk.
