Lipoprotein(a) [Lp(a)] is a genetically determined particle composed of apolipoprotein B-100 linked to apolipoprotein(a) by a disulfide bond, enriched with oxidized phospholipids, which increase its atherogenic and pro-inflammatory properties compared to LDL. Elevated Lp(a) levels are independently associated with atherosclerotic cardiovascular disease and calcific aortic valve stenosis according to genetic and epidemiological evidence. There is currently no approved treatment that specifically lowers Lp(a) or shows fewer cardiovascular events. New therapies such as antisense oligonucleotides (eg, pelacarsen), small interfering RNAs (eg, olpasiran, lepodisiran, zerlasiran), and oral inhibitors (eg, muvalaplin) reduce Lp(a) levels by 80%, in some cases almost completely. An absolute reduction in Lp(a) of at least 50 mg/dL is required according to genetic and model evidence for meaningful cardiovascular benefits. Large studies are ongoing to assess effects on cardiovascular and valvular outcomes, with early findings of beneficial effects on oxidized phospholipids and vascular inflammation. Routine measurement of Lp(a) will be important for personalized prevention.