{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T15:58:59Z","timestamp":1790697539248,"version":"4.1.0"},"reference-count":47,"publisher":"IMR Press","issue":"9","license":[{"start":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T00:00:00Z","timestamp":1787875200000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Rev. Cardiovasc. Med."],"abstract":"<jats:p>Lipoprotein(a) [Lp(a)] is a genetically determined, apolipoprotein B-containing lipoprotein that contributes to cardiovascular risk through atherogenic, proinflammatory, and potentially antifibrinolytic mechanisms. Genetic, epidemiological, and mechanistic evidence supports a causal role for elevated Lp(a) in atherosclerotic cardiovascular disease and calcific aortic valve disease. In contrast, associations with other cardiovascular phenotypes are less consistent. Since circulating concentrations are largely inherited and only modestly affected by lifestyle measures and conventional lipid-lowering therapies, Lp(a) represents an important component of residual cardiovascular risk. This review summarizes the structural, genetic, and pathogenic characteristics of Lp(a), examines the strength of evidence across coronary artery disease, ischemic stroke, peripheral artery disease, abdominal aortic aneurysm, calcific aortic valve disease, and heart failure, and discusses measurement, clinical interpretation, and potential biomarkers. The therapeutic landscape has expanded rapidly. Antisense oligonucleotides and small interfering RNA agents substantially suppress hepatic apolipoprotein(a) synthesis, oral small-molecule inhibitors prevent Lp(a) particle assembly, and in vivo gene-editing strategies aim to provide highly durable reductions. Early-phase trials have demonstrated marked lowering of circulating Lp(a); however, most were not designed to assess cardiovascular outcomes, so direct comparisons among agents are limited by differences in study populations, assays, dosing schedules, and follow-up. Ongoing cardiovascular outcome trials will determine whether selective Lp(a) lowering reduces clinical events and which patients are most likely to benefit. Until these results are available, Lp(a) measurement can refine risk stratification and support intensive management of modifiable risk factors, whereas biomarker reduction alone should not be equated with proven clinical benefit.<\/jats:p>","DOI":"10.31083\/rcm55004","type":"journal-article","created":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T14:57:11Z","timestamp":1790693831000},"source":"Crossref","is-referenced-by-count":0,"title":["Lipoprotein(a) Inhibition: Current Evidence, Therapeutic Landscape, and Future Directions"],"prefix":"10.31083","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0243-3673","authenticated-orcid":true,"given":"Pierre","family":"Sabouret","sequence":"first","affiliation":[{"name":"ACTION Study Group, Inserm UMRS1166, Heart Institute, Piti\u00e9-Salpetriere Hospital, Sorbonne University, 75013 Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-2161-3066","authenticated-orcid":true,"given":"Domenico Mario","family":"Giamundo","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Policlinico Casilino, 00169 Rome, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9108-8391","authenticated-orcid":true,"given":"Joanna","family":"Popiolek-Kalisz","sequence":"additional","affiliation":[{"name":"Clinical Dietetics Unit, Department of Bioanalytics, Medical University of Lublin, 20-059 Lublin, Poland"},{"name":"Department of Cardiology, Cardinal Wyszynski Hospital in Lublin, 20-718 Lublin, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6443-4121","authenticated-orcid":true,"given":"Luigi","family":"Spadafora","sequence":"additional","affiliation":[{"name":"Department of Clinical, Internal Medicine, Anesthesiology and Cardiovascular Sciences, Sapienza University of Rome, 00185 Rome, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9269-8829","authenticated-orcid":true,"given":"Marco","family":"Bernardi","sequence":"additional","affiliation":[{"name":"Department of Clinical, Internal Medicine, Anesthesiology and Cardiovascular Sciences, Sapienza University of Rome, 00185 Rome, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3381-605X","authenticated-orcid":true,"given":"Elad","family":"Asher","sequence":"additional","affiliation":[{"name":"Jesselson Heart Center, Shaare Zedek Medical Center, The Eisenberg R&D Authority, and Faculty of Medicine, Hebrew University of Jerusalem, 9103102 Jerusalem, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9241-8890","authenticated-orcid":true,"given":"Mamas A","family":"Mamas","sequence":"additional","affiliation":[{"name":"Keele Cardiac Research Group, Centre for Prognosis Research, Keele University, ST5 5BG Stoke-on-Trent, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1513-8793","authenticated-orcid":true,"given":"Dan","family":"Atar","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Oslo University Hospital, 0450 Oslo, Norway"},{"name":"Institute of Clinical Medicine, University of Oslo, 0372 Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5552-6382","authenticated-orcid":true,"given":"Giuseppe","family":"And\u00f2","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, University of Messina and Azienda Ospedaliera Universitaria Policlinico \u201cGaetano Martino\u201d, 98125 Messina, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"16242","published-online":{"date-parts":[[2026,8,28]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","unstructured":"Tsimikas S. 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Medical Center). 2025; 38: 783\u2013786.","DOI":"10.1080\/08998280.2025.2524791"},{"key":"ref28","doi-asserted-by":"publisher","unstructured":"Nicholls SJ, Nelson AJ, Ditmarsch M, Kastelein JJP, Ballantyne CM, Ray KK, et al. Obicetrapib in patients with heterozygous familial hypercholesterolemia: the BROOKLYN randomized clinical trial. Nature Medicine. 2026; 32: 1052\u20131060.","DOI":"10.1038\/s41591-025-04179-4"},{"key":"ref29","doi-asserted-by":"publisher","unstructured":"Parhofer KG, Julius U, Herzog AL, Kr\u00fcger T, Weinmann-Menke J, Heine GH, et al. Pelacarsen and lipoprotein(a) apheresis in secondary prevention: the Lp(a)FRONTIERS APHERESIS trial. European Heart Journal. 2026; 47: 3284\u20133294.","DOI":"10.1093\/eurheartj\/ehag073"},{"key":"ref30","doi-asserted-by":"publisher","unstructured":"Cho L, Nicholls SJ, Nordestgaard BG, Landmesser U, Tsimikas S, Blaha MJ, et al. 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A focused update to the 2019 NLA scientific statement on use of lipoprotein(a) in clinical practice. Journal of Clinical Lipidology. 2024; 18: e308\u2013e319.","DOI":"10.1016\/j.jacl.2024.03.001"},{"key":"ref45","doi-asserted-by":"publisher","unstructured":"Gilliland TC, Liu Y, Mohebi R, Miksenas H, Haidermota S, Wong M, et al. Lipoprotein(a), Oxidized Phospholipids, and Coronary Artery Disease Severity and Outcomes. Journal of the American College of Cardiology. 2023; 81: 1780\u20131792.","DOI":"10.1016\/j.jacc.2023.02.050"},{"key":"ref46","doi-asserted-by":"publisher","unstructured":"Mehta A, Vasquez N, Ayers CR, Patel J, Hooda A, Khera A, et al. Independent Association of Lipoprotein(a) and Coronary Artery Calcification With Atherosclerotic Cardiovascular Risk. 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