Lp(a): a New Pathway to Target?
Purpose of Review Over the past decades, genetic and observational evidence has positioned lipoprotein(a) as novel important and independent risk factor for cardiovascular disease (ASCVD) and aortic valve stenosis. Recent Findings As Lp(a) levels are determined genetically, lifestyle interventions h...
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| Veröffentlicht in: | Current atherosclerosis reports 2022-11, Vol.24 (11), p.831-838 |
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| container_title | Current atherosclerosis reports |
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| creator | Nurmohamed, Nick S. Kraaijenhof, Jordan M. Stroes, Erik S. G. |
| description | Purpose of Review
Over the past decades, genetic and observational evidence has positioned lipoprotein(a) as novel important and independent risk factor for cardiovascular disease (ASCVD) and aortic valve stenosis.
Recent Findings
As Lp(a) levels are determined genetically, lifestyle interventions have no effect on Lp(a)-mediated ASCVD risk. While traditional low-density lipoprotein cholesterol (LDL-C) can now be effectively lowered in the vast majority of patients, current lipid lowering therapies have no clinically relevant Lp(a) lowering effect.
Summary
There are multiple Lp(a)-directed therapies in clinical development targeting
LPA
mRNA that have shown to lower Lp(a) plasma levels for up to 90%: pelacarsen, olpasiran, and SLN360. Pelacarsen is currently investigated in a phase 3 cardiovascular outcome trial expected to finish in 2024, while olpasiran is about to proceed to phase 3 and SLN360’s phase 1 outcomes were recently published. If proven efficacious, Lp(a) will soon become the next pathway to target in ASCVD risk management. |
| doi_str_mv | 10.1007/s11883-022-01060-4 |
| format | Article |
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Over the past decades, genetic and observational evidence has positioned lipoprotein(a) as novel important and independent risk factor for cardiovascular disease (ASCVD) and aortic valve stenosis.
Recent Findings
As Lp(a) levels are determined genetically, lifestyle interventions have no effect on Lp(a)-mediated ASCVD risk. While traditional low-density lipoprotein cholesterol (LDL-C) can now be effectively lowered in the vast majority of patients, current lipid lowering therapies have no clinically relevant Lp(a) lowering effect.
Summary
There are multiple Lp(a)-directed therapies in clinical development targeting
LPA
mRNA that have shown to lower Lp(a) plasma levels for up to 90%: pelacarsen, olpasiran, and SLN360. Pelacarsen is currently investigated in a phase 3 cardiovascular outcome trial expected to finish in 2024, while olpasiran is about to proceed to phase 3 and SLN360’s phase 1 outcomes were recently published. If proven efficacious, Lp(a) will soon become the next pathway to target in ASCVD risk management.</description><identifier>ISSN: 1523-3804</identifier><identifier>EISSN: 1534-6242</identifier><identifier>DOI: 10.1007/s11883-022-01060-4</identifier><identifier>PMID: 36066785</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Angiology ; Aortic Valve Stenosis ; Cardiology ; Cardiovascular Diseases - drug therapy ; Cholesterol, LDL ; Humans ; Lipoprotein(a) - genetics ; Medicine ; Medicine & Public Health ; Nonstatin Drugs (L. Tokgozoglu and A.L. Catapano ; Nonstatin Drugs (L. Tokgozoglu and A.L. Catapano, Section Editors) ; Oligonucleotides, Antisense - therapeutic use ; Risk Factors ; RNA, Messenger ; Section Editors ; Topical Collection on Nonstatin Drugs</subject><ispartof>Current atherosclerosis reports, 2022-11, Vol.24 (11), p.831-838</ispartof><rights>The Author(s) 2022</rights><rights>2022. The Author(s).</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c446t-acd5a1b09c963b00cf78e9ff10a509882258b7c2c81dc84eb63e3007293391a53</citedby><cites>FETCH-LOGICAL-c446t-acd5a1b09c963b00cf78e9ff10a509882258b7c2c81dc84eb63e3007293391a53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11883-022-01060-4$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11883-022-01060-4$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,777,781,882,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36066785$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nurmohamed, Nick S.</creatorcontrib><creatorcontrib>Kraaijenhof, Jordan M.</creatorcontrib><creatorcontrib>Stroes, Erik S. G.</creatorcontrib><title>Lp(a): a New Pathway to Target?</title><title>Current atherosclerosis reports</title><addtitle>Curr Atheroscler Rep</addtitle><addtitle>Curr Atheroscler Rep</addtitle><description>Purpose of Review
Over the past decades, genetic and observational evidence has positioned lipoprotein(a) as novel important and independent risk factor for cardiovascular disease (ASCVD) and aortic valve stenosis.
Recent Findings
As Lp(a) levels are determined genetically, lifestyle interventions have no effect on Lp(a)-mediated ASCVD risk. While traditional low-density lipoprotein cholesterol (LDL-C) can now be effectively lowered in the vast majority of patients, current lipid lowering therapies have no clinically relevant Lp(a) lowering effect.
Summary
There are multiple Lp(a)-directed therapies in clinical development targeting
LPA
mRNA that have shown to lower Lp(a) plasma levels for up to 90%: pelacarsen, olpasiran, and SLN360. Pelacarsen is currently investigated in a phase 3 cardiovascular outcome trial expected to finish in 2024, while olpasiran is about to proceed to phase 3 and SLN360’s phase 1 outcomes were recently published. If proven efficacious, Lp(a) will soon become the next pathway to target in ASCVD risk management.</description><subject>Angiology</subject><subject>Aortic Valve Stenosis</subject><subject>Cardiology</subject><subject>Cardiovascular Diseases - drug therapy</subject><subject>Cholesterol, LDL</subject><subject>Humans</subject><subject>Lipoprotein(a) - genetics</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Nonstatin Drugs (L. Tokgozoglu and A.L. Catapano</subject><subject>Nonstatin Drugs (L. Tokgozoglu and A.L. Catapano, Section Editors)</subject><subject>Oligonucleotides, Antisense - therapeutic use</subject><subject>Risk Factors</subject><subject>RNA, Messenger</subject><subject>Section Editors</subject><subject>Topical Collection on Nonstatin Drugs</subject><issn>1523-3804</issn><issn>1534-6242</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><recordid>eNp9kD9PwzAQxS0EoqXwBRggYxkMZztxbAYQqvgnVcBQZstxnTZVmxQ7oeq3xyWlgoXpTrp37-79EDolcEkA0itPiBAMA6UYCHDA8R7qkoTFmNOY7m96yjATEHfQkfczAAqCk0PUYRw4T0XSRefDZV9fXEc6erGr6E3X05VeR3UVjbSb2Pr2GB3keu7tybb20PvD_WjwhIevj8-DuyE2ccxrrM040SQDaSRnGYDJU2FlnhPQCUghKE1ElhpqBBkbEduMM8tCBioZk0QnrIduWt9lky3s2Niydnqulq5YaLdWlS7U30lZTNWk-lQy5BWwMehvDVz10Vhfq0XhjZ3PdWmrxiuaEpBc0lQEKW2lxlXeO5vvzhBQG7KqJasCWfVNVsVh6ez3g7uVH5RBwFqBD6NyYp2aVY0rA7T_bL8AOLGBaA</recordid><startdate>20221101</startdate><enddate>20221101</enddate><creator>Nurmohamed, Nick S.</creator><creator>Kraaijenhof, Jordan M.</creator><creator>Stroes, Erik S. G.</creator><general>Springer US</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20221101</creationdate><title>Lp(a): a New Pathway to Target?</title><author>Nurmohamed, Nick S. ; Kraaijenhof, Jordan M. ; Stroes, Erik S. G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c446t-acd5a1b09c963b00cf78e9ff10a509882258b7c2c81dc84eb63e3007293391a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Angiology</topic><topic>Aortic Valve Stenosis</topic><topic>Cardiology</topic><topic>Cardiovascular Diseases - drug therapy</topic><topic>Cholesterol, LDL</topic><topic>Humans</topic><topic>Lipoprotein(a) - genetics</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Nonstatin Drugs (L. Tokgozoglu and A.L. Catapano</topic><topic>Nonstatin Drugs (L. Tokgozoglu and A.L. Catapano, Section Editors)</topic><topic>Oligonucleotides, Antisense - therapeutic use</topic><topic>Risk Factors</topic><topic>RNA, Messenger</topic><topic>Section Editors</topic><topic>Topical Collection on Nonstatin Drugs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nurmohamed, Nick S.</creatorcontrib><creatorcontrib>Kraaijenhof, Jordan M.</creatorcontrib><creatorcontrib>Stroes, Erik S. G.</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Current atherosclerosis reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nurmohamed, Nick S.</au><au>Kraaijenhof, Jordan M.</au><au>Stroes, Erik S. G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lp(a): a New Pathway to Target?</atitle><jtitle>Current atherosclerosis reports</jtitle><stitle>Curr Atheroscler Rep</stitle><addtitle>Curr Atheroscler Rep</addtitle><date>2022-11-01</date><risdate>2022</risdate><volume>24</volume><issue>11</issue><spage>831</spage><epage>838</epage><pages>831-838</pages><issn>1523-3804</issn><eissn>1534-6242</eissn><abstract>Purpose of Review
Over the past decades, genetic and observational evidence has positioned lipoprotein(a) as novel important and independent risk factor for cardiovascular disease (ASCVD) and aortic valve stenosis.
Recent Findings
As Lp(a) levels are determined genetically, lifestyle interventions have no effect on Lp(a)-mediated ASCVD risk. While traditional low-density lipoprotein cholesterol (LDL-C) can now be effectively lowered in the vast majority of patients, current lipid lowering therapies have no clinically relevant Lp(a) lowering effect.
Summary
There are multiple Lp(a)-directed therapies in clinical development targeting
LPA
mRNA that have shown to lower Lp(a) plasma levels for up to 90%: pelacarsen, olpasiran, and SLN360. Pelacarsen is currently investigated in a phase 3 cardiovascular outcome trial expected to finish in 2024, while olpasiran is about to proceed to phase 3 and SLN360’s phase 1 outcomes were recently published. If proven efficacious, Lp(a) will soon become the next pathway to target in ASCVD risk management.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>36066785</pmid><doi>10.1007/s11883-022-01060-4</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Current atherosclerosis reports, 2022-11, Vol.24 (11), p.831-838 |
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| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Angiology Aortic Valve Stenosis Cardiology Cardiovascular Diseases - drug therapy Cholesterol, LDL Humans Lipoprotein(a) - genetics Medicine Medicine & Public Health Nonstatin Drugs (L. Tokgozoglu and A.L. Catapano Nonstatin Drugs (L. Tokgozoglu and A.L. Catapano, Section Editors) Oligonucleotides, Antisense - therapeutic use Risk Factors RNA, Messenger Section Editors Topical Collection on Nonstatin Drugs |
| title | Lp(a): a New Pathway to Target? |
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