Lipoprotein lipase gene mutations, plasma lipid levels, progression/regression of coronary atherosclerosis, response to therapy, and future clinical events: Lipoproteins and Coronary Atherosclerosis Study
Mutations in human lipoprotein lipase (LPL) gene are potential risk factors for susceptibility to coronary artery disease (CAD). The objectives of this study were to determine the influence LPL mutations Asn 291Ser and Ser 447Ter on plasma lipid levels, regression and progression of CAD, clinical ev...
Gespeichert in:
| Veröffentlicht in: | Atherosclerosis 1999-06, Vol.144 (2), p.435-442 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 442 |
|---|---|
| container_issue | 2 |
| container_start_page | 435 |
| container_title | Atherosclerosis |
| container_volume | 144 |
| creator | Sing, Karandeep Ballantyne, Christie M Ferlic, Laura Brugada, Ramon Cushman, Ian Dunn, J.Kay Herd, J.Alan Pownall, Henry J Gotto, Antonio M Marian, Ali J |
| description | Mutations in human lipoprotein lipase (LPL) gene are potential risk factors for susceptibility to coronary artery disease (CAD). The objectives of this study were to determine the influence LPL mutations Asn
291Ser and Ser
447Ter on plasma lipid levels, regression and progression of CAD, clinical events rate, and response to fluvastatin therapy in the Lipoprotein and Coronary Atherosclerosis Study (LCAS) population. LCAS is a double blind, randomized, placebo-controlled study designed to test the influence of fluvastatin on progression or regression of CAD. The Asn
291Ser and Ser
447Ter genotypes were determined by polymerase chain reaction (PCR) and restriction enzyme digestion. Fasting plasma lipid profiles were measured and quantitative coronary angiography was performed at baseline and 2.5 years following randomization. Fatal and non-fatal cardiovascular events during the follow-up period were recorded. A total of 4% (14/363) and 18% (62/352) of the subjects had the Asn
291Ser and Ser
447Ter mutations, respectively. Overall, there was no statistically association between the Asn
291Ser and Ser
447Ter mutations and the baseline or final mean plasma levels of lipids, number of coronary lesions, total occlusions, the mean minimal lumen diameter (MLD) stenoses and the clinical events rate. However, patients with the Ser
447Ter variant had a slightly higher baseline high density lipoprotein-cholesterol (HDL-C) level (46.2±12 vs 43.2±11,
P=0.057), less increase in plasma HDL levels in response to fluvastatin therapy (3 vs 11%,
P=0.056) and a higher cardiovascular events rate (23 vs 13%,
P=0.056). Thus, the Ser
447Ter variant had a modest influence on plasma HDL levels and the rate of cardiovascular events. These changes were of borderline statistical significance. Neither the Ser
447Ter nor the Asn
291Ser mutation had a major impact on susceptibility to CAD, progression or regression of CAD, clinical events rate or response to fluvastatin therapy in LCAS population. |
| doi_str_mv | 10.1016/S0021-9150(99)00004-0 |
| format | Article |
| fullrecord | <record><control><sourceid>elsevier_pubme</sourceid><recordid>TN_cdi_pubmed_primary_10407505</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0021915099000040</els_id><sourcerecordid>S0021915099000040</sourcerecordid><originalsourceid>FETCH-LOGICAL-e292t-b1b5d2e2eade694ce076e6eb30b3b8b3fe2178048fba5518dcd8581b1d747a573</originalsourceid><addsrcrecordid>eNpVkctuHCEQRVGUKB47-YRELLKIJbcN_QRvImvkR6SRvHCyRjyqbaIeaAE90vyjP8r02BPbtaAQdbgUdRH6RskpJbQ9uyOkpAWnDfnJ-THJURfkA1pQ1vGC1qz-iBb_kQN0GOO_meko-4wOKKlJ15BmgR5XdvRj8Amsw4MdZQR8Dw7wekoyWe_iCR4HGddyrlqDB9jAMB8Gfx8gxoycBdhvse-x9sE7GbZYpgcIPuphXm2-k6ExKwJOHs81OW5PsHQG91OaAmA9WGe1HHB-w6V4jt80F3fgcq998V4b36XJbL-gT70cInx9yUfo79Xln-VNsbq9_r28WBVQ8jIViqrGlFCCNNDyWgPpWmhBVURViqmqh5J2jNSsV7JpKDPasIZRRU1Xd7LpqiP0_Vl3nNQajBiDXeemxH6sGfjxAsiY_9MH6bSNrxxjVdXyjP16xvJEYWMhiKgtOA3GBtBJGG-zppj9Fju_xWym4Fzs_BakegJyC6M5</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Lipoprotein lipase gene mutations, plasma lipid levels, progression/regression of coronary atherosclerosis, response to therapy, and future clinical events: Lipoproteins and Coronary Atherosclerosis Study</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Sing, Karandeep ; Ballantyne, Christie M ; Ferlic, Laura ; Brugada, Ramon ; Cushman, Ian ; Dunn, J.Kay ; Herd, J.Alan ; Pownall, Henry J ; Gotto, Antonio M ; Marian, Ali J</creator><creatorcontrib>Sing, Karandeep ; Ballantyne, Christie M ; Ferlic, Laura ; Brugada, Ramon ; Cushman, Ian ; Dunn, J.Kay ; Herd, J.Alan ; Pownall, Henry J ; Gotto, Antonio M ; Marian, Ali J</creatorcontrib><description>Mutations in human lipoprotein lipase (LPL) gene are potential risk factors for susceptibility to coronary artery disease (CAD). The objectives of this study were to determine the influence LPL mutations Asn
291Ser and Ser
447Ter on plasma lipid levels, regression and progression of CAD, clinical events rate, and response to fluvastatin therapy in the Lipoprotein and Coronary Atherosclerosis Study (LCAS) population. LCAS is a double blind, randomized, placebo-controlled study designed to test the influence of fluvastatin on progression or regression of CAD. The Asn
291Ser and Ser
447Ter genotypes were determined by polymerase chain reaction (PCR) and restriction enzyme digestion. Fasting plasma lipid profiles were measured and quantitative coronary angiography was performed at baseline and 2.5 years following randomization. Fatal and non-fatal cardiovascular events during the follow-up period were recorded. A total of 4% (14/363) and 18% (62/352) of the subjects had the Asn
291Ser and Ser
447Ter mutations, respectively. Overall, there was no statistically association between the Asn
291Ser and Ser
447Ter mutations and the baseline or final mean plasma levels of lipids, number of coronary lesions, total occlusions, the mean minimal lumen diameter (MLD) stenoses and the clinical events rate. However, patients with the Ser
447Ter variant had a slightly higher baseline high density lipoprotein-cholesterol (HDL-C) level (46.2±12 vs 43.2±11,
P=0.057), less increase in plasma HDL levels in response to fluvastatin therapy (3 vs 11%,
P=0.056) and a higher cardiovascular events rate (23 vs 13%,
P=0.056). Thus, the Ser
447Ter variant had a modest influence on plasma HDL levels and the rate of cardiovascular events. These changes were of borderline statistical significance. Neither the Ser
447Ter nor the Asn
291Ser mutation had a major impact on susceptibility to CAD, progression or regression of CAD, clinical events rate or response to fluvastatin therapy in LCAS population.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/S0021-9150(99)00004-0</identifier><identifier>PMID: 10407505</identifier><language>eng</language><publisher>Amsterdam: Elsevier Ireland Ltd</publisher><subject>Adult ; Aged ; Amino Acids - genetics ; Anticholesteremic Agents - adverse effects ; Anticholesteremic Agents - therapeutic use ; Biological and medical sciences ; Cardiology. Vascular system ; Cholesterol, LDL - blood ; Coronary Angiography ; Coronary artery disease ; Coronary Artery Disease - drug therapy ; Coronary Artery Disease - enzymology ; Coronary Artery Disease - genetics ; Coronary heart disease ; Double-Blind Method ; Fatty Acids, Monounsaturated - adverse effects ; Fatty Acids, Monounsaturated - therapeutic use ; Female ; Fluvastatin ; Genetics ; Genotype ; Heart ; Humans ; Indoles - adverse effects ; Indoles - therapeutic use ; Lipids - blood ; Lipoprotein lipase ; Lipoprotein Lipase - blood ; Lipoprotein Lipase - genetics ; Male ; Medical sciences ; Middle Aged ; Mutation ; Mutation - genetics ; Myocardial infarction ; Myocardial Infarction - drug therapy ; Myocardial Infarction - enzymology ; Myocardial Infarction - genetics ; Polymerase Chain Reaction ; Risk factor ; Treatment Outcome</subject><ispartof>Atherosclerosis, 1999-06, Vol.144 (2), p.435-442</ispartof><rights>1999 Elsevier Science Ireland Ltd</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0021915099000040$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1883369$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10407505$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sing, Karandeep</creatorcontrib><creatorcontrib>Ballantyne, Christie M</creatorcontrib><creatorcontrib>Ferlic, Laura</creatorcontrib><creatorcontrib>Brugada, Ramon</creatorcontrib><creatorcontrib>Cushman, Ian</creatorcontrib><creatorcontrib>Dunn, J.Kay</creatorcontrib><creatorcontrib>Herd, J.Alan</creatorcontrib><creatorcontrib>Pownall, Henry J</creatorcontrib><creatorcontrib>Gotto, Antonio M</creatorcontrib><creatorcontrib>Marian, Ali J</creatorcontrib><title>Lipoprotein lipase gene mutations, plasma lipid levels, progression/regression of coronary atherosclerosis, response to therapy, and future clinical events: Lipoproteins and Coronary Atherosclerosis Study</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>Mutations in human lipoprotein lipase (LPL) gene are potential risk factors for susceptibility to coronary artery disease (CAD). The objectives of this study were to determine the influence LPL mutations Asn
291Ser and Ser
447Ter on plasma lipid levels, regression and progression of CAD, clinical events rate, and response to fluvastatin therapy in the Lipoprotein and Coronary Atherosclerosis Study (LCAS) population. LCAS is a double blind, randomized, placebo-controlled study designed to test the influence of fluvastatin on progression or regression of CAD. The Asn
291Ser and Ser
447Ter genotypes were determined by polymerase chain reaction (PCR) and restriction enzyme digestion. Fasting plasma lipid profiles were measured and quantitative coronary angiography was performed at baseline and 2.5 years following randomization. Fatal and non-fatal cardiovascular events during the follow-up period were recorded. A total of 4% (14/363) and 18% (62/352) of the subjects had the Asn
291Ser and Ser
447Ter mutations, respectively. Overall, there was no statistically association between the Asn
291Ser and Ser
447Ter mutations and the baseline or final mean plasma levels of lipids, number of coronary lesions, total occlusions, the mean minimal lumen diameter (MLD) stenoses and the clinical events rate. However, patients with the Ser
447Ter variant had a slightly higher baseline high density lipoprotein-cholesterol (HDL-C) level (46.2±12 vs 43.2±11,
P=0.057), less increase in plasma HDL levels in response to fluvastatin therapy (3 vs 11%,
P=0.056) and a higher cardiovascular events rate (23 vs 13%,
P=0.056). Thus, the Ser
447Ter variant had a modest influence on plasma HDL levels and the rate of cardiovascular events. These changes were of borderline statistical significance. Neither the Ser
447Ter nor the Asn
291Ser mutation had a major impact on susceptibility to CAD, progression or regression of CAD, clinical events rate or response to fluvastatin therapy in LCAS population.</description><subject>Adult</subject><subject>Aged</subject><subject>Amino Acids - genetics</subject><subject>Anticholesteremic Agents - adverse effects</subject><subject>Anticholesteremic Agents - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cholesterol, LDL - blood</subject><subject>Coronary Angiography</subject><subject>Coronary artery disease</subject><subject>Coronary Artery Disease - drug therapy</subject><subject>Coronary Artery Disease - enzymology</subject><subject>Coronary Artery Disease - genetics</subject><subject>Coronary heart disease</subject><subject>Double-Blind Method</subject><subject>Fatty Acids, Monounsaturated - adverse effects</subject><subject>Fatty Acids, Monounsaturated - therapeutic use</subject><subject>Female</subject><subject>Fluvastatin</subject><subject>Genetics</subject><subject>Genotype</subject><subject>Heart</subject><subject>Humans</subject><subject>Indoles - adverse effects</subject><subject>Indoles - therapeutic use</subject><subject>Lipids - blood</subject><subject>Lipoprotein lipase</subject><subject>Lipoprotein Lipase - blood</subject><subject>Lipoprotein Lipase - genetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Mutation - genetics</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - enzymology</subject><subject>Myocardial Infarction - genetics</subject><subject>Polymerase Chain Reaction</subject><subject>Risk factor</subject><subject>Treatment Outcome</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkctuHCEQRVGUKB47-YRELLKIJbcN_QRvImvkR6SRvHCyRjyqbaIeaAE90vyjP8r02BPbtaAQdbgUdRH6RskpJbQ9uyOkpAWnDfnJ-THJURfkA1pQ1vGC1qz-iBb_kQN0GOO_meko-4wOKKlJ15BmgR5XdvRj8Amsw4MdZQR8Dw7wekoyWe_iCR4HGddyrlqDB9jAMB8Gfx8gxoycBdhvse-x9sE7GbZYpgcIPuphXm2-k6ExKwJOHs81OW5PsHQG91OaAmA9WGe1HHB-w6V4jt80F3fgcq998V4b36XJbL-gT70cInx9yUfo79Xln-VNsbq9_r28WBVQ8jIViqrGlFCCNNDyWgPpWmhBVURViqmqh5J2jNSsV7JpKDPasIZRRU1Xd7LpqiP0_Vl3nNQajBiDXeemxH6sGfjxAsiY_9MH6bSNrxxjVdXyjP16xvJEYWMhiKgtOA3GBtBJGG-zppj9Fju_xWym4Fzs_BakegJyC6M5</recordid><startdate>19990601</startdate><enddate>19990601</enddate><creator>Sing, Karandeep</creator><creator>Ballantyne, Christie M</creator><creator>Ferlic, Laura</creator><creator>Brugada, Ramon</creator><creator>Cushman, Ian</creator><creator>Dunn, J.Kay</creator><creator>Herd, J.Alan</creator><creator>Pownall, Henry J</creator><creator>Gotto, Antonio M</creator><creator>Marian, Ali J</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>19990601</creationdate><title>Lipoprotein lipase gene mutations, plasma lipid levels, progression/regression of coronary atherosclerosis, response to therapy, and future clinical events: Lipoproteins and Coronary Atherosclerosis Study</title><author>Sing, Karandeep ; Ballantyne, Christie M ; Ferlic, Laura ; Brugada, Ramon ; Cushman, Ian ; Dunn, J.Kay ; Herd, J.Alan ; Pownall, Henry J ; Gotto, Antonio M ; Marian, Ali J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e292t-b1b5d2e2eade694ce076e6eb30b3b8b3fe2178048fba5518dcd8581b1d747a573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Amino Acids - genetics</topic><topic>Anticholesteremic Agents - adverse effects</topic><topic>Anticholesteremic Agents - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cholesterol, LDL - blood</topic><topic>Coronary Angiography</topic><topic>Coronary artery disease</topic><topic>Coronary Artery Disease - drug therapy</topic><topic>Coronary Artery Disease - enzymology</topic><topic>Coronary Artery Disease - genetics</topic><topic>Coronary heart disease</topic><topic>Double-Blind Method</topic><topic>Fatty Acids, Monounsaturated - adverse effects</topic><topic>Fatty Acids, Monounsaturated - therapeutic use</topic><topic>Female</topic><topic>Fluvastatin</topic><topic>Genetics</topic><topic>Genotype</topic><topic>Heart</topic><topic>Humans</topic><topic>Indoles - adverse effects</topic><topic>Indoles - therapeutic use</topic><topic>Lipids - blood</topic><topic>Lipoprotein lipase</topic><topic>Lipoprotein Lipase - blood</topic><topic>Lipoprotein Lipase - genetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Mutation - genetics</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - enzymology</topic><topic>Myocardial Infarction - genetics</topic><topic>Polymerase Chain Reaction</topic><topic>Risk factor</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sing, Karandeep</creatorcontrib><creatorcontrib>Ballantyne, Christie M</creatorcontrib><creatorcontrib>Ferlic, Laura</creatorcontrib><creatorcontrib>Brugada, Ramon</creatorcontrib><creatorcontrib>Cushman, Ian</creatorcontrib><creatorcontrib>Dunn, J.Kay</creatorcontrib><creatorcontrib>Herd, J.Alan</creatorcontrib><creatorcontrib>Pownall, Henry J</creatorcontrib><creatorcontrib>Gotto, Antonio M</creatorcontrib><creatorcontrib>Marian, Ali J</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sing, Karandeep</au><au>Ballantyne, Christie M</au><au>Ferlic, Laura</au><au>Brugada, Ramon</au><au>Cushman, Ian</au><au>Dunn, J.Kay</au><au>Herd, J.Alan</au><au>Pownall, Henry J</au><au>Gotto, Antonio M</au><au>Marian, Ali J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lipoprotein lipase gene mutations, plasma lipid levels, progression/regression of coronary atherosclerosis, response to therapy, and future clinical events: Lipoproteins and Coronary Atherosclerosis Study</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>1999-06-01</date><risdate>1999</risdate><volume>144</volume><issue>2</issue><spage>435</spage><epage>442</epage><pages>435-442</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>Mutations in human lipoprotein lipase (LPL) gene are potential risk factors for susceptibility to coronary artery disease (CAD). The objectives of this study were to determine the influence LPL mutations Asn
291Ser and Ser
447Ter on plasma lipid levels, regression and progression of CAD, clinical events rate, and response to fluvastatin therapy in the Lipoprotein and Coronary Atherosclerosis Study (LCAS) population. LCAS is a double blind, randomized, placebo-controlled study designed to test the influence of fluvastatin on progression or regression of CAD. The Asn
291Ser and Ser
447Ter genotypes were determined by polymerase chain reaction (PCR) and restriction enzyme digestion. Fasting plasma lipid profiles were measured and quantitative coronary angiography was performed at baseline and 2.5 years following randomization. Fatal and non-fatal cardiovascular events during the follow-up period were recorded. A total of 4% (14/363) and 18% (62/352) of the subjects had the Asn
291Ser and Ser
447Ter mutations, respectively. Overall, there was no statistically association between the Asn
291Ser and Ser
447Ter mutations and the baseline or final mean plasma levels of lipids, number of coronary lesions, total occlusions, the mean minimal lumen diameter (MLD) stenoses and the clinical events rate. However, patients with the Ser
447Ter variant had a slightly higher baseline high density lipoprotein-cholesterol (HDL-C) level (46.2±12 vs 43.2±11,
P=0.057), less increase in plasma HDL levels in response to fluvastatin therapy (3 vs 11%,
P=0.056) and a higher cardiovascular events rate (23 vs 13%,
P=0.056). Thus, the Ser
447Ter variant had a modest influence on plasma HDL levels and the rate of cardiovascular events. These changes were of borderline statistical significance. Neither the Ser
447Ter nor the Asn
291Ser mutation had a major impact on susceptibility to CAD, progression or regression of CAD, clinical events rate or response to fluvastatin therapy in LCAS population.</abstract><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>10407505</pmid><doi>10.1016/S0021-9150(99)00004-0</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0021-9150 |
| ispartof | Atherosclerosis, 1999-06, Vol.144 (2), p.435-442 |
| issn | 0021-9150 1879-1484 |
| language | eng |
| recordid | cdi_pubmed_primary_10407505 |
| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Adult Aged Amino Acids - genetics Anticholesteremic Agents - adverse effects Anticholesteremic Agents - therapeutic use Biological and medical sciences Cardiology. Vascular system Cholesterol, LDL - blood Coronary Angiography Coronary artery disease Coronary Artery Disease - drug therapy Coronary Artery Disease - enzymology Coronary Artery Disease - genetics Coronary heart disease Double-Blind Method Fatty Acids, Monounsaturated - adverse effects Fatty Acids, Monounsaturated - therapeutic use Female Fluvastatin Genetics Genotype Heart Humans Indoles - adverse effects Indoles - therapeutic use Lipids - blood Lipoprotein lipase Lipoprotein Lipase - blood Lipoprotein Lipase - genetics Male Medical sciences Middle Aged Mutation Mutation - genetics Myocardial infarction Myocardial Infarction - drug therapy Myocardial Infarction - enzymology Myocardial Infarction - genetics Polymerase Chain Reaction Risk factor Treatment Outcome |
| title | Lipoprotein lipase gene mutations, plasma lipid levels, progression/regression of coronary atherosclerosis, response to therapy, and future clinical events: Lipoproteins and Coronary Atherosclerosis Study |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-04T15%3A35%3A22IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-elsevier_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Lipoprotein%20lipase%20gene%20mutations,%20plasma%20lipid%20levels,%20progression/regression%20of%20coronary%20atherosclerosis,%20response%20to%20therapy,%20and%20future%20clinical%20events:%20Lipoproteins%20and%20Coronary%20Atherosclerosis%20Study&rft.jtitle=Atherosclerosis&rft.au=Sing,%20Karandeep&rft.date=1999-06-01&rft.volume=144&rft.issue=2&rft.spage=435&rft.epage=442&rft.pages=435-442&rft.issn=0021-9150&rft.eissn=1879-1484&rft_id=info:doi/10.1016/S0021-9150(99)00004-0&rft_dat=%3Celsevier_pubme%3ES0021915099000040%3C/elsevier_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/10407505&rft_els_id=S0021915099000040&rfr_iscdi=true |