Plasma lipid composition and risk of developing cardiovascular disease
We tested whether characteristic changes of the plasma lipidome in individuals with comparable total lipids level associate with future cardiovascular disease (CVD) outcome and whether 23 validated gene variants associated with coronary artery disease (CAD) affect CVD associated lipid species. Scree...
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| Veröffentlicht in: | PloS one 2013-08, Vol.8 (8), p.e71846-e71846 |
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| creator | Fernandez, Celine Sandin, Marianne Sampaio, Julio L Almgren, Peter Narkiewicz, Krzysztof Hoffmann, Michal Hedner, Thomas Wahlstrand, Björn Simons, Kai Shevchenko, Andrej James, Peter Melander, Olle |
| description | We tested whether characteristic changes of the plasma lipidome in individuals with comparable total lipids level associate with future cardiovascular disease (CVD) outcome and whether 23 validated gene variants associated with coronary artery disease (CAD) affect CVD associated lipid species.
Screening of the fasted plasma lipidome was performed by top-down shotgun analysis and lipidome compositions compared between incident CVD cases (n = 211) and controls (n = 216) from the prospective population-based MDC study using logistic regression adjusting for Framingham risk factors. Associations with incident CVD were seen for eight lipid species (0.21≤q≤0.23). Each standard deviation unit higher baseline levels of two lysophosphatidylcholine species (LPC), LPC16∶0 and LPC20∶4, was associated with a decreased risk for CVD (P = 0.024-0.028). Sphingomyelin (SM) 38∶2 was associated with increased odds of CVD (P = 0.057). Five triglyceride (TAG) species were associated with protection (P = 0.031-0.049). LPC16∶0 was negatively correlated with the carotid intima-media thickness (P = 0.010) and with HbA1c (P = 0.012) whereas SM38∶2 was positively correlated with LDL-cholesterol (P = 0.0*10(-6)) and the q-values were good (q≤0.03). The risk allele of 8 CAD-associated gene variants showed significant association with the plasma level of several lipid species. However, the q-values were high for many of the associations (0.015≤q≤0.75). Risk allele carriers of 3 CAD-loci had reduced level of LPC16∶0 and/or LPC 20∶4 (P≤0.056).
Our study suggests that CVD development is preceded by reduced levels of LPC16∶0, LPC20∶4 and some specific TAG species and by increased levels of SM38∶2. It also indicates that certain lipid species are intermediate phenotypes between genetic susceptibility and overt CVD. But it is a preliminary study that awaits replication in a larger population because statistical significance was lost for the associations between lipid species and future cardiovascular events when correcting for multiple testing. |
| doi_str_mv | 10.1371/journal.pone.0071846 |
| format | Article |
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Screening of the fasted plasma lipidome was performed by top-down shotgun analysis and lipidome compositions compared between incident CVD cases (n = 211) and controls (n = 216) from the prospective population-based MDC study using logistic regression adjusting for Framingham risk factors. Associations with incident CVD were seen for eight lipid species (0.21≤q≤0.23). Each standard deviation unit higher baseline levels of two lysophosphatidylcholine species (LPC), LPC16∶0 and LPC20∶4, was associated with a decreased risk for CVD (P = 0.024-0.028). Sphingomyelin (SM) 38∶2 was associated with increased odds of CVD (P = 0.057). Five triglyceride (TAG) species were associated with protection (P = 0.031-0.049). LPC16∶0 was negatively correlated with the carotid intima-media thickness (P = 0.010) and with HbA1c (P = 0.012) whereas SM38∶2 was positively correlated with LDL-cholesterol (P = 0.0*10(-6)) and the q-values were good (q≤0.03). The risk allele of 8 CAD-associated gene variants showed significant association with the plasma level of several lipid species. However, the q-values were high for many of the associations (0.015≤q≤0.75). Risk allele carriers of 3 CAD-loci had reduced level of LPC16∶0 and/or LPC 20∶4 (P≤0.056).
Our study suggests that CVD development is preceded by reduced levels of LPC16∶0, LPC20∶4 and some specific TAG species and by increased levels of SM38∶2. It also indicates that certain lipid species are intermediate phenotypes between genetic susceptibility and overt CVD. But it is a preliminary study that awaits replication in a larger population because statistical significance was lost for the associations between lipid species and future cardiovascular events when correcting for multiple testing.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0071846</identifier><identifier>PMID: 23967253</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Aged ; Alleles ; ARTERY-DISEASE ; ASSOCIATION ; Biology ; BIOMARKERS ; Blood cholesterol ; BLOOD-PLASMA ; Cancer ; Cardiac and Cardiovascular Systems ; Cardiology and Cardiovascular Disease ; Cardiovascular disease ; Cardiovascular diseases ; Cardiovascular Diseases - blood ; Cardiovascular Diseases - epidemiology ; Cardiovascular Diseases - genetics ; Case-Control Studies ; CHOLESTEROL ; Chromatography ; Clinical Medicine ; Cluster Analysis ; Coronary artery ; Coronary artery disease ; Coronary Artery Disease - blood ; Coronary Artery Disease - epidemiology ; Coronary Artery Disease - genetics ; Coronary vessels ; CORONARY-HEART-DISEASE ; Disease susceptibility ; Endocrinology and Diabetes ; Endokrinologi och diabetes ; EVENTS ; Family medical history ; Fatalities ; Female ; Gene Expression Profiling ; Genetic aspects ; Genetic Predisposition to Disease ; Genetics ; Genomes ; Health risk assessment ; Health risks ; Heart attacks ; Heart diseases ; Humans ; Hypertension ; Kardiologi ; Kardiologi och kardiovaskulära sjukdomar ; Klinisk medicin ; Lipid composition ; Lipids ; Lipids - blood ; Lipoproteins (low density) ; Low density lipoprotein ; Low density lipoproteins ; Lysophosphatidylcholine ; Male ; Medical and Health Sciences ; Medical research ; Medicin och hälsovetenskap ; Medicine ; Metabolome ; Middle Aged ; Patient Outcome Assessment ; Plasma ; POLYMORPHISMS ; Population (statistical) ; Population studies ; PREDICTION ; Public Health Surveillance ; Regression analysis ; Risk ; Risk analysis ; Risk Factors ; SHOTGUN LIPIDOMICS ; Species ; Sphingomyelin ; Statistical analysis ; Triglycerides ; Wildlife conservation</subject><ispartof>PloS one, 2013-08, Vol.8 (8), p.e71846-e71846</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Fernandez et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Fernandez et al 2013 Fernandez et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c865t-f2950e497ddddea1af62e2a5cf6d314d094f9fc96a770cf59c8e98680c80053e3</citedby><cites>FETCH-LOGICAL-c865t-f2950e497ddddea1af62e2a5cf6d314d094f9fc96a770cf59c8e98680c80053e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3744469/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3744469/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,550,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23967253$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://gup.ub.gu.se/publication/184250$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttps://lup.lub.lu.se/record/4005404$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Fernandez, Celine</creatorcontrib><creatorcontrib>Sandin, Marianne</creatorcontrib><creatorcontrib>Sampaio, Julio L</creatorcontrib><creatorcontrib>Almgren, Peter</creatorcontrib><creatorcontrib>Narkiewicz, Krzysztof</creatorcontrib><creatorcontrib>Hoffmann, Michal</creatorcontrib><creatorcontrib>Hedner, Thomas</creatorcontrib><creatorcontrib>Wahlstrand, Björn</creatorcontrib><creatorcontrib>Simons, Kai</creatorcontrib><creatorcontrib>Shevchenko, Andrej</creatorcontrib><creatorcontrib>James, Peter</creatorcontrib><creatorcontrib>Melander, Olle</creatorcontrib><title>Plasma lipid composition and risk of developing cardiovascular disease</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>We tested whether characteristic changes of the plasma lipidome in individuals with comparable total lipids level associate with future cardiovascular disease (CVD) outcome and whether 23 validated gene variants associated with coronary artery disease (CAD) affect CVD associated lipid species.
Screening of the fasted plasma lipidome was performed by top-down shotgun analysis and lipidome compositions compared between incident CVD cases (n = 211) and controls (n = 216) from the prospective population-based MDC study using logistic regression adjusting for Framingham risk factors. Associations with incident CVD were seen for eight lipid species (0.21≤q≤0.23). Each standard deviation unit higher baseline levels of two lysophosphatidylcholine species (LPC), LPC16∶0 and LPC20∶4, was associated with a decreased risk for CVD (P = 0.024-0.028). Sphingomyelin (SM) 38∶2 was associated with increased odds of CVD (P = 0.057). Five triglyceride (TAG) species were associated with protection (P = 0.031-0.049). LPC16∶0 was negatively correlated with the carotid intima-media thickness (P = 0.010) and with HbA1c (P = 0.012) whereas SM38∶2 was positively correlated with LDL-cholesterol (P = 0.0*10(-6)) and the q-values were good (q≤0.03). The risk allele of 8 CAD-associated gene variants showed significant association with the plasma level of several lipid species. However, the q-values were high for many of the associations (0.015≤q≤0.75). Risk allele carriers of 3 CAD-loci had reduced level of LPC16∶0 and/or LPC 20∶4 (P≤0.056).
Our study suggests that CVD development is preceded by reduced levels of LPC16∶0, LPC20∶4 and some specific TAG species and by increased levels of SM38∶2. It also indicates that certain lipid species are intermediate phenotypes between genetic susceptibility and overt CVD. But it is a preliminary study that awaits replication in a larger population because statistical significance was lost for the associations between lipid species and future cardiovascular events when correcting for multiple testing.</description><subject>Aged</subject><subject>Alleles</subject><subject>ARTERY-DISEASE</subject><subject>ASSOCIATION</subject><subject>Biology</subject><subject>BIOMARKERS</subject><subject>Blood cholesterol</subject><subject>BLOOD-PLASMA</subject><subject>Cancer</subject><subject>Cardiac and Cardiovascular Systems</subject><subject>Cardiology and Cardiovascular Disease</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cardiovascular Diseases - blood</subject><subject>Cardiovascular Diseases - epidemiology</subject><subject>Cardiovascular Diseases - genetics</subject><subject>Case-Control Studies</subject><subject>CHOLESTEROL</subject><subject>Chromatography</subject><subject>Clinical Medicine</subject><subject>Cluster Analysis</subject><subject>Coronary artery</subject><subject>Coronary artery disease</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - epidemiology</subject><subject>Coronary Artery Disease - genetics</subject><subject>Coronary vessels</subject><subject>CORONARY-HEART-DISEASE</subject><subject>Disease susceptibility</subject><subject>Endocrinology and Diabetes</subject><subject>Endokrinologi och diabetes</subject><subject>EVENTS</subject><subject>Family medical history</subject><subject>Fatalities</subject><subject>Female</subject><subject>Gene Expression Profiling</subject><subject>Genetic aspects</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetics</subject><subject>Genomes</subject><subject>Health risk assessment</subject><subject>Health risks</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Kardiologi</subject><subject>Kardiologi och kardiovaskulära sjukdomar</subject><subject>Klinisk medicin</subject><subject>Lipid composition</subject><subject>Lipids</subject><subject>Lipids - blood</subject><subject>Lipoproteins (low density)</subject><subject>Low density lipoprotein</subject><subject>Low density lipoproteins</subject><subject>Lysophosphatidylcholine</subject><subject>Male</subject><subject>Medical and Health Sciences</subject><subject>Medical research</subject><subject>Medicin och hälsovetenskap</subject><subject>Medicine</subject><subject>Metabolome</subject><subject>Middle Aged</subject><subject>Patient Outcome Assessment</subject><subject>Plasma</subject><subject>POLYMORPHISMS</subject><subject>Population (statistical)</subject><subject>Population studies</subject><subject>PREDICTION</subject><subject>Public Health Surveillance</subject><subject>Regression analysis</subject><subject>Risk</subject><subject>Risk analysis</subject><subject>Risk Factors</subject><subject>SHOTGUN LIPIDOMICS</subject><subject>Species</subject><subject>Sphingomyelin</subject><subject>Statistical analysis</subject><subject>Triglycerides</subject><subject>Wildlife 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lipid composition and risk of developing cardiovascular disease</title><author>Fernandez, Celine ; Sandin, Marianne ; Sampaio, Julio L ; Almgren, Peter ; Narkiewicz, Krzysztof ; Hoffmann, Michal ; Hedner, Thomas ; Wahlstrand, Björn ; Simons, Kai ; Shevchenko, Andrej ; James, Peter ; Melander, Olle</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c865t-f2950e497ddddea1af62e2a5cf6d314d094f9fc96a770cf59c8e98680c80053e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Aged</topic><topic>Alleles</topic><topic>ARTERY-DISEASE</topic><topic>ASSOCIATION</topic><topic>Biology</topic><topic>BIOMARKERS</topic><topic>Blood cholesterol</topic><topic>BLOOD-PLASMA</topic><topic>Cancer</topic><topic>Cardiac and Cardiovascular Systems</topic><topic>Cardiology and Cardiovascular Disease</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Cardiovascular Diseases - blood</topic><topic>Cardiovascular Diseases - epidemiology</topic><topic>Cardiovascular Diseases - genetics</topic><topic>Case-Control Studies</topic><topic>CHOLESTEROL</topic><topic>Chromatography</topic><topic>Clinical Medicine</topic><topic>Cluster Analysis</topic><topic>Coronary artery</topic><topic>Coronary artery disease</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - epidemiology</topic><topic>Coronary Artery Disease - genetics</topic><topic>Coronary vessels</topic><topic>CORONARY-HEART-DISEASE</topic><topic>Disease susceptibility</topic><topic>Endocrinology and Diabetes</topic><topic>Endokrinologi och diabetes</topic><topic>EVENTS</topic><topic>Family medical history</topic><topic>Fatalities</topic><topic>Female</topic><topic>Gene Expression Profiling</topic><topic>Genetic aspects</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetics</topic><topic>Genomes</topic><topic>Health risk assessment</topic><topic>Health 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Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Göteborgs universitet</collection><collection>SWEPUB Lunds universitet full text</collection><collection>SWEPUB Freely available online</collection><collection>SWEPUB Lunds universitet</collection><collection>SwePub Articles full text</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fernandez, Celine</au><au>Sandin, Marianne</au><au>Sampaio, Julio L</au><au>Almgren, Peter</au><au>Narkiewicz, Krzysztof</au><au>Hoffmann, Michal</au><au>Hedner, Thomas</au><au>Wahlstrand, Björn</au><au>Simons, Kai</au><au>Shevchenko, Andrej</au><au>James, Peter</au><au>Melander, Olle</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plasma lipid composition and risk of developing cardiovascular disease</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-08-15</date><risdate>2013</risdate><volume>8</volume><issue>8</issue><spage>e71846</spage><epage>e71846</epage><pages>e71846-e71846</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>We tested whether characteristic changes of the plasma lipidome in individuals with comparable total lipids level associate with future cardiovascular disease (CVD) outcome and whether 23 validated gene variants associated with coronary artery disease (CAD) affect CVD associated lipid species.
Screening of the fasted plasma lipidome was performed by top-down shotgun analysis and lipidome compositions compared between incident CVD cases (n = 211) and controls (n = 216) from the prospective population-based MDC study using logistic regression adjusting for Framingham risk factors. Associations with incident CVD were seen for eight lipid species (0.21≤q≤0.23). Each standard deviation unit higher baseline levels of two lysophosphatidylcholine species (LPC), LPC16∶0 and LPC20∶4, was associated with a decreased risk for CVD (P = 0.024-0.028). Sphingomyelin (SM) 38∶2 was associated with increased odds of CVD (P = 0.057). Five triglyceride (TAG) species were associated with protection (P = 0.031-0.049). LPC16∶0 was negatively correlated with the carotid intima-media thickness (P = 0.010) and with HbA1c (P = 0.012) whereas SM38∶2 was positively correlated with LDL-cholesterol (P = 0.0*10(-6)) and the q-values were good (q≤0.03). The risk allele of 8 CAD-associated gene variants showed significant association with the plasma level of several lipid species. However, the q-values were high for many of the associations (0.015≤q≤0.75). Risk allele carriers of 3 CAD-loci had reduced level of LPC16∶0 and/or LPC 20∶4 (P≤0.056).
Our study suggests that CVD development is preceded by reduced levels of LPC16∶0, LPC20∶4 and some specific TAG species and by increased levels of SM38∶2. It also indicates that certain lipid species are intermediate phenotypes between genetic susceptibility and overt CVD. But it is a preliminary study that awaits replication in a larger population because statistical significance was lost for the associations between lipid species and future cardiovascular events when correcting for multiple testing.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23967253</pmid><doi>10.1371/journal.pone.0071846</doi><tpages>e71846</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-08, Vol.8 (8), p.e71846-e71846 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1430437663 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; SWEPUB Freely available online; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Aged Alleles ARTERY-DISEASE ASSOCIATION Biology BIOMARKERS Blood cholesterol BLOOD-PLASMA Cancer Cardiac and Cardiovascular Systems Cardiology and Cardiovascular Disease Cardiovascular disease Cardiovascular diseases Cardiovascular Diseases - blood Cardiovascular Diseases - epidemiology Cardiovascular Diseases - genetics Case-Control Studies CHOLESTEROL Chromatography Clinical Medicine Cluster Analysis Coronary artery Coronary artery disease Coronary Artery Disease - blood Coronary Artery Disease - epidemiology Coronary Artery Disease - genetics Coronary vessels CORONARY-HEART-DISEASE Disease susceptibility Endocrinology and Diabetes Endokrinologi och diabetes EVENTS Family medical history Fatalities Female Gene Expression Profiling Genetic aspects Genetic Predisposition to Disease Genetics Genomes Health risk assessment Health risks Heart attacks Heart diseases Humans Hypertension Kardiologi Kardiologi och kardiovaskulära sjukdomar Klinisk medicin Lipid composition Lipids Lipids - blood Lipoproteins (low density) Low density lipoprotein Low density lipoproteins Lysophosphatidylcholine Male Medical and Health Sciences Medical research Medicin och hälsovetenskap Medicine Metabolome Middle Aged Patient Outcome Assessment Plasma POLYMORPHISMS Population (statistical) Population studies PREDICTION Public Health Surveillance Regression analysis Risk Risk analysis Risk Factors SHOTGUN LIPIDOMICS Species Sphingomyelin Statistical analysis Triglycerides Wildlife conservation |
| title | Plasma lipid composition and risk of developing cardiovascular disease |
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