The association between Factor V Leiden with the presence and severity of coronary artery disease
The presence of Factor V Leiden (FVL) is proposed to be associated with a higher risk for arterial thrombosis. The aim of this study was to examine a relationship between FVL with the presence and severity of angiographically determined coronary artery disease (CAD). In this case–control study, 1083...
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| Veröffentlicht in: | Clinical biochemistry 2014-04, Vol.47 (6), p.356-360 |
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| container_title | Clinical biochemistry |
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| creator | Boroumand, Mohammadali pourgholi, Leila Ziaee, Shayan Anvari, Maryam Sotoudeh Jalali, Arash Goodarzynejad, Hamidreza |
| description | The presence of Factor V Leiden (FVL) is proposed to be associated with a higher risk for arterial thrombosis. The aim of this study was to examine a relationship between FVL with the presence and severity of angiographically determined coronary artery disease (CAD).
In this case–control study, 1083 patients having angiographic evidence of atherosclerosis with ≥50% luminal stenosis in their epicardial coronary tree were compared with patients with no luminal stenosis (n=320) or with luminal stenosis |
| doi_str_mv | 10.1016/j.clinbiochem.2013.12.006 |
| format | Article |
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In this case–control study, 1083 patients having angiographic evidence of atherosclerosis with ≥50% luminal stenosis in their epicardial coronary tree were compared with patients with no luminal stenosis (n=320) or with luminal stenosis <50% (n=191) at coronary angiography as reference group. The severity of CAD was determined by vessel score and also a semi-quantitative scoring system (Gensini score). The presence of Factor V polymorphisms was analyzed using polymerase chain reaction–based restriction fragment length polymorphism (PCR–RFLP).
FVL was found to be independently associated with the occurrence of CAD (p=0.020). As compared to wild genotype, heterozygote or homozygote mutant genotypes were more likely associated with a trend towards more severe CAD (adjusted OR=1.85, 95% CI=1.26 to 2.72; p=0.002, and adjusted OR=3.70, 95% CI=1.71 to 8.00; p=0.001; respectively). In addition, the median and inter-quartile range for Gensini score were significantly different among the GG (27.8, 3 to 66.5), GA (53.5, 10 to 104.1), and AA (92.8, 48.1 to 125.9) genotypes (p<0.001).
Our results confirmed the hypothesis that FVL mutation is a significant determinant of CAD risk. Furthermore, we observed that FVL is independently associated with increasing CAD severity.
•Factor V Leiden was independently associated with coronary artery disease presence.•Vessel score was more likely severe in mutant genotypes as compared to wild type.•Gensini score was significantly higher in mutant genotypes of Factor V.</description><identifier>ISSN: 0009-9120</identifier><identifier>EISSN: 1873-2933</identifier><identifier>DOI: 10.1016/j.clinbiochem.2013.12.006</identifier><identifier>PMID: 24360889</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Coronary angiography ; Coronary artery disease ; Coronary Artery Disease - genetics ; Factor V - genetics ; Factor V Leiden ; Female ; G1691A variant ; Gene Frequency - genetics ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Logistic Models ; Male ; Middle Aged ; Multivariate Analysis ; Odds Ratio ; Severity of Illness Index</subject><ispartof>Clinical biochemistry, 2014-04, Vol.47 (6), p.356-360</ispartof><rights>2013 The Canadian Society of Clinical Chemists</rights><rights>Copyright © 2013 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c377t-bed038c743c3baccae70dc077b5d90681a8dc88f8ab775f34ba11fe5086afd773</citedby><cites>FETCH-LOGICAL-c377t-bed038c743c3baccae70dc077b5d90681a8dc88f8ab775f34ba11fe5086afd773</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.clinbiochem.2013.12.006$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24360889$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Boroumand, Mohammadali</creatorcontrib><creatorcontrib>pourgholi, Leila</creatorcontrib><creatorcontrib>Ziaee, Shayan</creatorcontrib><creatorcontrib>Anvari, Maryam Sotoudeh</creatorcontrib><creatorcontrib>Jalali, Arash</creatorcontrib><creatorcontrib>Goodarzynejad, Hamidreza</creatorcontrib><title>The association between Factor V Leiden with the presence and severity of coronary artery disease</title><title>Clinical biochemistry</title><addtitle>Clin Biochem</addtitle><description>The presence of Factor V Leiden (FVL) is proposed to be associated with a higher risk for arterial thrombosis. The aim of this study was to examine a relationship between FVL with the presence and severity of angiographically determined coronary artery disease (CAD).
In this case–control study, 1083 patients having angiographic evidence of atherosclerosis with ≥50% luminal stenosis in their epicardial coronary tree were compared with patients with no luminal stenosis (n=320) or with luminal stenosis <50% (n=191) at coronary angiography as reference group. The severity of CAD was determined by vessel score and also a semi-quantitative scoring system (Gensini score). The presence of Factor V polymorphisms was analyzed using polymerase chain reaction–based restriction fragment length polymorphism (PCR–RFLP).
FVL was found to be independently associated with the occurrence of CAD (p=0.020). As compared to wild genotype, heterozygote or homozygote mutant genotypes were more likely associated with a trend towards more severe CAD (adjusted OR=1.85, 95% CI=1.26 to 2.72; p=0.002, and adjusted OR=3.70, 95% CI=1.71 to 8.00; p=0.001; respectively). In addition, the median and inter-quartile range for Gensini score were significantly different among the GG (27.8, 3 to 66.5), GA (53.5, 10 to 104.1), and AA (92.8, 48.1 to 125.9) genotypes (p<0.001).
Our results confirmed the hypothesis that FVL mutation is a significant determinant of CAD risk. Furthermore, we observed that FVL is independently associated with increasing CAD severity.
•Factor V Leiden was independently associated with coronary artery disease presence.•Vessel score was more likely severe in mutant genotypes as compared to wild type.•Gensini score was significantly higher in mutant genotypes of Factor V.</description><subject>Coronary angiography</subject><subject>Coronary artery disease</subject><subject>Coronary Artery Disease - genetics</subject><subject>Factor V - genetics</subject><subject>Factor V Leiden</subject><subject>Female</subject><subject>G1691A variant</subject><subject>Gene Frequency - genetics</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Multivariate Analysis</subject><subject>Odds Ratio</subject><subject>Severity of Illness Index</subject><issn>0009-9120</issn><issn>1873-2933</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkMtKAzEUhoMoWi-vIHHnZsZc2klmKcWqUHCjbkPm5AxNaSc1SRXf3pSquHR1OPD95_IRcsVZzRlvbpY1rPzQ-QALXNeCcVlzUTPWHJAR10pWopXykIwYY23VcsFOyGlKy9KKsW6OyYkYy4Zp3Y6IfV4gtSkF8Db7MNAO8wfiQGcWcoj0lc7Ru9J_-LygucCbiAkHKKnB0YTvGH3-pKGnEGIYbPykNmYsxfmENuE5OertKuHFdz0jL7O75-lDNX-6f5zeziuQSuWqQ8ekBjWWIDsLYFExB0ypbuJa1mhutQOte207pSa9HHeW8x4nTDe2d0rJM3K9n7uJ4W2LKZu1T4CrlR0wbJPhEy6E0LJtC9ruUYghpYi92US_LqcbzszOsFmaP4bNzrDhwhTDJXv5vWbbrdH9Jn-UFmC6B7A8--4xmgR-J8z5iJCNC_4fa74ASP-UaQ</recordid><startdate>20140401</startdate><enddate>20140401</enddate><creator>Boroumand, Mohammadali</creator><creator>pourgholi, Leila</creator><creator>Ziaee, Shayan</creator><creator>Anvari, Maryam Sotoudeh</creator><creator>Jalali, Arash</creator><creator>Goodarzynejad, Hamidreza</creator><general>Elsevier Inc</general><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></search><sort><creationdate>20140401</creationdate><title>The association between Factor V Leiden with the presence and severity of coronary artery disease</title><author>Boroumand, Mohammadali ; pourgholi, Leila ; Ziaee, Shayan ; Anvari, Maryam Sotoudeh ; Jalali, Arash ; Goodarzynejad, Hamidreza</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c377t-bed038c743c3baccae70dc077b5d90681a8dc88f8ab775f34ba11fe5086afd773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Coronary angiography</topic><topic>Coronary artery disease</topic><topic>Coronary Artery Disease - genetics</topic><topic>Factor V - genetics</topic><topic>Factor V Leiden</topic><topic>Female</topic><topic>G1691A variant</topic><topic>Gene Frequency - genetics</topic><topic>Genetic Association Studies</topic><topic>Genetic Predisposition to Disease</topic><topic>Humans</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Multivariate Analysis</topic><topic>Odds Ratio</topic><topic>Severity of Illness Index</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Boroumand, Mohammadali</creatorcontrib><creatorcontrib>pourgholi, Leila</creatorcontrib><creatorcontrib>Ziaee, Shayan</creatorcontrib><creatorcontrib>Anvari, Maryam Sotoudeh</creatorcontrib><creatorcontrib>Jalali, Arash</creatorcontrib><creatorcontrib>Goodarzynejad, Hamidreza</creatorcontrib><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><jtitle>Clinical biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Boroumand, Mohammadali</au><au>pourgholi, Leila</au><au>Ziaee, Shayan</au><au>Anvari, Maryam Sotoudeh</au><au>Jalali, Arash</au><au>Goodarzynejad, Hamidreza</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The association between Factor V Leiden with the presence and severity of coronary artery disease</atitle><jtitle>Clinical biochemistry</jtitle><addtitle>Clin Biochem</addtitle><date>2014-04-01</date><risdate>2014</risdate><volume>47</volume><issue>6</issue><spage>356</spage><epage>360</epage><pages>356-360</pages><issn>0009-9120</issn><eissn>1873-2933</eissn><abstract>The presence of Factor V Leiden (FVL) is proposed to be associated with a higher risk for arterial thrombosis. The aim of this study was to examine a relationship between FVL with the presence and severity of angiographically determined coronary artery disease (CAD).
In this case–control study, 1083 patients having angiographic evidence of atherosclerosis with ≥50% luminal stenosis in their epicardial coronary tree were compared with patients with no luminal stenosis (n=320) or with luminal stenosis <50% (n=191) at coronary angiography as reference group. The severity of CAD was determined by vessel score and also a semi-quantitative scoring system (Gensini score). The presence of Factor V polymorphisms was analyzed using polymerase chain reaction–based restriction fragment length polymorphism (PCR–RFLP).
FVL was found to be independently associated with the occurrence of CAD (p=0.020). As compared to wild genotype, heterozygote or homozygote mutant genotypes were more likely associated with a trend towards more severe CAD (adjusted OR=1.85, 95% CI=1.26 to 2.72; p=0.002, and adjusted OR=3.70, 95% CI=1.71 to 8.00; p=0.001; respectively). In addition, the median and inter-quartile range for Gensini score were significantly different among the GG (27.8, 3 to 66.5), GA (53.5, 10 to 104.1), and AA (92.8, 48.1 to 125.9) genotypes (p<0.001).
Our results confirmed the hypothesis that FVL mutation is a significant determinant of CAD risk. Furthermore, we observed that FVL is independently associated with increasing CAD severity.
•Factor V Leiden was independently associated with coronary artery disease presence.•Vessel score was more likely severe in mutant genotypes as compared to wild type.•Gensini score was significantly higher in mutant genotypes of Factor V.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>24360889</pmid><doi>10.1016/j.clinbiochem.2013.12.006</doi><tpages>5</tpages></addata></record> |
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| ispartof | Clinical biochemistry, 2014-04, Vol.47 (6), p.356-360 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Coronary angiography Coronary artery disease Coronary Artery Disease - genetics Factor V - genetics Factor V Leiden Female G1691A variant Gene Frequency - genetics Genetic Association Studies Genetic Predisposition to Disease Humans Logistic Models Male Middle Aged Multivariate Analysis Odds Ratio Severity of Illness Index |
| title | The association between Factor V Leiden with the presence and severity of coronary artery disease |
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