Recent studies have clarified the role of lipoprotein(a) [Lp(a)], relative to other lipoproteins, in atherogenesis.1 This JAMA Insights article discusses several clinical aspects of Lp(a), including the association with cardiovascular disease risk, considerations regarding measurement, guideline recommendations, and emerging therapies.
Lp(a) is a low-density lipoprotein (LDL)–like lipoprotein with apolipoprotein(a) [apo(a)] covalently linked to apolipoprotein B through 1 disulfide bond. Conventional lipid assays are unable to measure or estimate Lp(a), requiring a separate assay for its measurement. Lp(a) is a risk factor for atherosclerotic cardiovascular disease (ASCVD), including myocardial infarction and ischemic stroke, in both primary and secondary prevention populations, as well as for incident calcific aortic stenosis.2 The increased risk associated with Lp(a) is attributed to a dyad of heightened procoagulant effects of apo(a), with atherogenic and proinflammatory effects attributed to its oxidized apolipoprotein B–related phospholipids (Figure).2
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Miksenas H, Januzzi JL, Natarajan P. Lipoprotein(a) and Cardiovascular Diseases. JAMA. 2021;326(4):352–353. doi:10.1001/jama.2021.3632
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