Maurizio Giuseppe Abrignani, Alessandro Maloberti, Stefania Angela Di Fusco, Fabiana Lucà, Arturo Cesaro, Vincenzo Acerbo, Saverio Fabbri, Irene Di Matteo, Antonio F Amico, Pier Luigi Temporelli, Carmine Riccio, Furio Colivicchi, Massimo Grimaldi, Domenico Gabrielli, Fabrizio Oliva
{"title":"[Lipoprotein(a): relationships with atherosclerosis and valvular heart disease, and emerging therapies].","authors":"Maurizio Giuseppe Abrignani, Alessandro Maloberti, Stefania Angela Di Fusco, Fabiana Lucà, Arturo Cesaro, Vincenzo Acerbo, Saverio Fabbri, Irene Di Matteo, Antonio F Amico, Pier Luigi Temporelli, Carmine Riccio, Furio Colivicchi, Massimo Grimaldi, Domenico Gabrielli, Fabrizio Oliva","doi":"10.1714/4187.41756","DOIUrl":null,"url":null,"abstract":"<p><p>Lipoprotein(a) [Lp(a)] is a well-established cardiovascular risk factor, whose relationship with atherosclerotic disease has been confirmed by epidemiological, genome-wide association, Mendelian randomization, and meta-analysis studies. This association is determined by its pro-atherogenic, pro-thrombotic and pro-inflammatory properties. Lp(a) is the most common monogenic risk factor for atherosclerosis, with a prevalence of about 1 in 5 people. Recently, its etiopathogenetic relationship with calcific and degenerative valvular heart diseases, particularly with aortic and mitral stenosis, has been suspected. It has not yet been demonstrated whether its reduction translates into a lower risk of cardiovascular events. Up to now, Lp(a) has been considered a non-modifiable risk factor, as current lipid-lowering drugs have limited effects on its levels. New specific lipid-lowering therapies with high efficacy in reducing circulating Lp(a) levels are being investigated in randomized trials; however, the effects of this reduction on cardiovascular outcomes are still being studied.</p>","PeriodicalId":12510,"journal":{"name":"Giornale italiano di cardiologia","volume":"25 2","pages":"76-87"},"PeriodicalIF":0.7000,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Giornale italiano di cardiologia","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1714/4187.41756","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
Abstract
Lipoprotein(a) [Lp(a)] is a well-established cardiovascular risk factor, whose relationship with atherosclerotic disease has been confirmed by epidemiological, genome-wide association, Mendelian randomization, and meta-analysis studies. This association is determined by its pro-atherogenic, pro-thrombotic and pro-inflammatory properties. Lp(a) is the most common monogenic risk factor for atherosclerosis, with a prevalence of about 1 in 5 people. Recently, its etiopathogenetic relationship with calcific and degenerative valvular heart diseases, particularly with aortic and mitral stenosis, has been suspected. It has not yet been demonstrated whether its reduction translates into a lower risk of cardiovascular events. Up to now, Lp(a) has been considered a non-modifiable risk factor, as current lipid-lowering drugs have limited effects on its levels. New specific lipid-lowering therapies with high efficacy in reducing circulating Lp(a) levels are being investigated in randomized trials; however, the effects of this reduction on cardiovascular outcomes are still being studied.