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Impact of polymorphism rs7041 and rs4588 of Vitamin D Binding Protein on the extent of coronary artery disease
25-hydroxyvitamin D deficiency represents a widespread social problem but also an emerging risk factor for cardiovascular disease. Genetic variants of the Vitamin D Binding Protein (VDBP), the main transporter of vitamin D in the bloodstream, have been shown to account for a significant variability...
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| Published in: | Nutrition, metabolism, and cardiovascular diseases metabolism, and cardiovascular diseases, 2017-09, Vol.27 (9), p.775-783 |
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| creator | Daffara, V. Verdoia, M. Rolla, R. Nardin, M. Marino, P. Bellomo, G. Carriero, A. De Luca, G. |
| description | 25-hydroxyvitamin D deficiency represents a widespread social problem but also an emerging risk factor for cardiovascular disease. Genetic variants of the Vitamin D Binding Protein (VDBP), the main transporter of vitamin D in the bloodstream, have been shown to account for a significant variability in the levels and systemic effects of vitamin D. We investigated whether the single nucleotide polymorphisms, rs7041 and rs4588, of VDBP are associated to the prevalence and extent of coronary artery disease.
A consecutive cohort of patients undergoing coronary angiography in a single centre were included. Significant CAD was defined as at least 1 stenosis >50%, severe CAD for as left main and/or three-vessel disease. VDBP genetic status was assessed by polymerase chain reaction and restriction fragment length polymorphism technique.
We included 1080 patients, 57% carried the mutated G allele of rs7041, whereas 22% carried the A allele of rs4588. Higher levels of C- reactive protein were observed in the carriers of G allele of rs7041 (p = 0.02), whereas 25-hydroxyvitamin D levels were similar across groups. A higher prevalence of lesions in the left anterior descending artery and a longer lesion length were observed in “A” carriers for rs4588 (p = 0.04 and p = 0.03, respectively). On the contrary, a higher prevalence of bifurcation lesions and chronic occlusions was observed in G carriers (p = 0.002 and p = 0.01 respectively). Both polymorphisms of VDBP did not affect the prevalence of CAD (rs7041: 79.1% TT vs 80.3% TG vs 78.5% GG, p = 0.81; rs4588 = 80.3% CC vs 78.5% AC + AA, p = 0.49) and severe CAD, (rs7041: 31.1% TT % vs 31.3% TG vs 30.6% GG, p = 0.88; rs4588: 32.2% CC vs 29.3% AC + AA, p = 0.31). Results were confirmed at multivariate analysis, for both rs7041 and rs4588. However, when including the levels of 25-hydroxyvitamin D in the multivariate model, we observed that 25(OH)D status and not genetic variants of VDBP were significantly associated with CAD (25-hydroxyvitamin D OR [95% CI] = 0.99 [0.97–1.0], p = 0.05; rs7041 TG: OR [95% CI] = 1.26 [0.73–2.19], p = 0.41; rs7041 GG: OR [95% CI] = 1.25 [0.82–1.91], p = 0.30; rs4588 AC + AA: OR [95% CI] = 0.76 [0.51–1.13], p = 0.18).
This study showed in a large cohort of patients undergoing coronary angiography, that the polymorphisms rs7041 and rs4588 of VDBP are not associated with the levels of 25-hydroxyvitamin D nor with the prevalence and extent of CAD. In fact, 25-hydroxyvitamin D levels but not VDBP ge |
| doi_str_mv | 10.1016/j.numecd.2017.06.002 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1926981233</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0939475317301230</els_id><sourcerecordid>1926981233</sourcerecordid><originalsourceid>FETCH-LOGICAL-c362t-6e0b7c7fd0df57c5dd2796aad6d1d01b0c5ff094b15db470e5375cc415f881d23</originalsourceid><addsrcrecordid>eNp9kE1v1DAQQC0EokvLP0DIRy4J4ziO4wsSFGgrVaKH0qvl2BPq1cYOthe1_x4vWzhymtHozdcj5A2DlgEb3m_bsF_QurYDJlsYWoDuGdkwoaDhslPPyQYUV00vBT8hr3LeAnAJvH9JTrpRSqXGcUPC1bIaW2ic6Rp3j0tM673PC01ZQs-oCa6mvRjHA3Hni1l8oJ_pJx-cDz_oTYoFayUGWu6R4kPB8GeYjSkGkx6pSQVrcD6jyXhGXsxml_H1Uzwl379-uT2_bK6_XVydf7xuLB-60gwIk7RyduBmIa1wrpNqMMYNjjlgE1gxz6D6iQk39RJQcCms7ZmYx5G5jp-Sd8e5a4o_95iLXny2uNuZgHGfNVPdoEbWcV7R_ojaFHNOOOs1-aWerhnog2m91UfT-mBaw6Cr6dr29mnDflrQ_Wv6q7YCH44A1j9_eUw6W4_BovMJbdEu-v9v-A1QapEw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1926981233</pqid></control><display><type>article</type><title>Impact of polymorphism rs7041 and rs4588 of Vitamin D Binding Protein on the extent of coronary artery disease</title><source>ScienceDirect Journals</source><creator>Daffara, V. ; Verdoia, M. ; Rolla, R. ; Nardin, M. ; Marino, P. ; Bellomo, G. ; Carriero, A. ; De Luca, G.</creator><creatorcontrib>Daffara, V. ; Verdoia, M. ; Rolla, R. ; Nardin, M. ; Marino, P. ; Bellomo, G. ; Carriero, A. ; De Luca, G. ; the Novara Atherosclerosis Study Group (NAS) ; Novara Atherosclerosis Study Group (NAS)</creatorcontrib><description>25-hydroxyvitamin D deficiency represents a widespread social problem but also an emerging risk factor for cardiovascular disease. Genetic variants of the Vitamin D Binding Protein (VDBP), the main transporter of vitamin D in the bloodstream, have been shown to account for a significant variability in the levels and systemic effects of vitamin D. We investigated whether the single nucleotide polymorphisms, rs7041 and rs4588, of VDBP are associated to the prevalence and extent of coronary artery disease.
A consecutive cohort of patients undergoing coronary angiography in a single centre were included. Significant CAD was defined as at least 1 stenosis >50%, severe CAD for as left main and/or three-vessel disease. VDBP genetic status was assessed by polymerase chain reaction and restriction fragment length polymorphism technique.
We included 1080 patients, 57% carried the mutated G allele of rs7041, whereas 22% carried the A allele of rs4588. Higher levels of C- reactive protein were observed in the carriers of G allele of rs7041 (p = 0.02), whereas 25-hydroxyvitamin D levels were similar across groups. A higher prevalence of lesions in the left anterior descending artery and a longer lesion length were observed in “A” carriers for rs4588 (p = 0.04 and p = 0.03, respectively). On the contrary, a higher prevalence of bifurcation lesions and chronic occlusions was observed in G carriers (p = 0.002 and p = 0.01 respectively). Both polymorphisms of VDBP did not affect the prevalence of CAD (rs7041: 79.1% TT vs 80.3% TG vs 78.5% GG, p = 0.81; rs4588 = 80.3% CC vs 78.5% AC + AA, p = 0.49) and severe CAD, (rs7041: 31.1% TT % vs 31.3% TG vs 30.6% GG, p = 0.88; rs4588: 32.2% CC vs 29.3% AC + AA, p = 0.31). Results were confirmed at multivariate analysis, for both rs7041 and rs4588. However, when including the levels of 25-hydroxyvitamin D in the multivariate model, we observed that 25(OH)D status and not genetic variants of VDBP were significantly associated with CAD (25-hydroxyvitamin D OR [95% CI] = 0.99 [0.97–1.0], p = 0.05; rs7041 TG: OR [95% CI] = 1.26 [0.73–2.19], p = 0.41; rs7041 GG: OR [95% CI] = 1.25 [0.82–1.91], p = 0.30; rs4588 AC + AA: OR [95% CI] = 0.76 [0.51–1.13], p = 0.18).
This study showed in a large cohort of patients undergoing coronary angiography, that the polymorphisms rs7041 and rs4588 of VDBP are not associated with the levels of 25-hydroxyvitamin D nor with the prevalence and extent of CAD. In fact, 25-hydroxyvitamin D levels but not VDBP genetic status independently predicted the occurrence of coronary lesions at angiography.
•Genetic variants of Vitamin D Binding Protein (VDBP) could explain the variability of levels and effects of vitamin D.•We studied whether the SNPs rs7041 and rs4588 of VDBP are associated to the prevalence and extent of coronary artery disease (CAD).•In a cohort of 1080 consecutive patients, neither polymorphisms affected the prevalence of CAD and severe CAD.•Only vitamin D status, but not genetic variants of VDBP, was associated to CAD in our study.</description><identifier>ISSN: 0939-4753</identifier><identifier>EISSN: 1590-3729</identifier><identifier>DOI: 10.1016/j.numecd.2017.06.002</identifier><identifier>PMID: 28779988</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Aged ; Atherosclerosis ; Biomarkers - blood ; Chi-Square Distribution ; Coronary Angiography ; Coronary Artery Disease - blood ; Coronary Artery Disease - diagnostic imaging ; Coronary Artery Disease - epidemiology ; Coronary Artery Disease - genetics ; Coronary Stenosis - blood ; Coronary Stenosis - diagnostic imaging ; Coronary Stenosis - epidemiology ; Coronary Stenosis - genetics ; Female ; Gene Frequency ; Genetic Association Studies ; Genetic Markers ; Genetic Predisposition to Disease ; Heterozygote ; Homozygote ; Humans ; Italy - epidemiology ; Logistic Models ; Male ; Middle Aged ; Multivariate Analysis ; Mutation ; Odds Ratio ; Phenotype ; Polymorphism, Single Nucleotide ; Polymorphisms ; Prevalence ; Risk Factors ; Severity of Illness Index ; VDBP ; Vitamin D ; Vitamin D - analogs & derivatives ; Vitamin D - blood ; Vitamin D-Binding Protein - genetics</subject><ispartof>Nutrition, metabolism, and cardiovascular diseases, 2017-09, Vol.27 (9), p.775-783</ispartof><rights>2017 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University</rights><rights>Copyright © 2017 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-6e0b7c7fd0df57c5dd2796aad6d1d01b0c5ff094b15db470e5375cc415f881d23</citedby><cites>FETCH-LOGICAL-c362t-6e0b7c7fd0df57c5dd2796aad6d1d01b0c5ff094b15db470e5375cc415f881d23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28779988$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Daffara, V.</creatorcontrib><creatorcontrib>Verdoia, M.</creatorcontrib><creatorcontrib>Rolla, R.</creatorcontrib><creatorcontrib>Nardin, M.</creatorcontrib><creatorcontrib>Marino, P.</creatorcontrib><creatorcontrib>Bellomo, G.</creatorcontrib><creatorcontrib>Carriero, A.</creatorcontrib><creatorcontrib>De Luca, G.</creatorcontrib><creatorcontrib>the Novara Atherosclerosis Study Group (NAS)</creatorcontrib><creatorcontrib>Novara Atherosclerosis Study Group (NAS)</creatorcontrib><title>Impact of polymorphism rs7041 and rs4588 of Vitamin D Binding Protein on the extent of coronary artery disease</title><title>Nutrition, metabolism, and cardiovascular diseases</title><addtitle>Nutr Metab Cardiovasc Dis</addtitle><description>25-hydroxyvitamin D deficiency represents a widespread social problem but also an emerging risk factor for cardiovascular disease. Genetic variants of the Vitamin D Binding Protein (VDBP), the main transporter of vitamin D in the bloodstream, have been shown to account for a significant variability in the levels and systemic effects of vitamin D. We investigated whether the single nucleotide polymorphisms, rs7041 and rs4588, of VDBP are associated to the prevalence and extent of coronary artery disease.
A consecutive cohort of patients undergoing coronary angiography in a single centre were included. Significant CAD was defined as at least 1 stenosis >50%, severe CAD for as left main and/or three-vessel disease. VDBP genetic status was assessed by polymerase chain reaction and restriction fragment length polymorphism technique.
We included 1080 patients, 57% carried the mutated G allele of rs7041, whereas 22% carried the A allele of rs4588. Higher levels of C- reactive protein were observed in the carriers of G allele of rs7041 (p = 0.02), whereas 25-hydroxyvitamin D levels were similar across groups. A higher prevalence of lesions in the left anterior descending artery and a longer lesion length were observed in “A” carriers for rs4588 (p = 0.04 and p = 0.03, respectively). On the contrary, a higher prevalence of bifurcation lesions and chronic occlusions was observed in G carriers (p = 0.002 and p = 0.01 respectively). Both polymorphisms of VDBP did not affect the prevalence of CAD (rs7041: 79.1% TT vs 80.3% TG vs 78.5% GG, p = 0.81; rs4588 = 80.3% CC vs 78.5% AC + AA, p = 0.49) and severe CAD, (rs7041: 31.1% TT % vs 31.3% TG vs 30.6% GG, p = 0.88; rs4588: 32.2% CC vs 29.3% AC + AA, p = 0.31). Results were confirmed at multivariate analysis, for both rs7041 and rs4588. However, when including the levels of 25-hydroxyvitamin D in the multivariate model, we observed that 25(OH)D status and not genetic variants of VDBP were significantly associated with CAD (25-hydroxyvitamin D OR [95% CI] = 0.99 [0.97–1.0], p = 0.05; rs7041 TG: OR [95% CI] = 1.26 [0.73–2.19], p = 0.41; rs7041 GG: OR [95% CI] = 1.25 [0.82–1.91], p = 0.30; rs4588 AC + AA: OR [95% CI] = 0.76 [0.51–1.13], p = 0.18).
This study showed in a large cohort of patients undergoing coronary angiography, that the polymorphisms rs7041 and rs4588 of VDBP are not associated with the levels of 25-hydroxyvitamin D nor with the prevalence and extent of CAD. In fact, 25-hydroxyvitamin D levels but not VDBP genetic status independently predicted the occurrence of coronary lesions at angiography.
•Genetic variants of Vitamin D Binding Protein (VDBP) could explain the variability of levels and effects of vitamin D.•We studied whether the SNPs rs7041 and rs4588 of VDBP are associated to the prevalence and extent of coronary artery disease (CAD).•In a cohort of 1080 consecutive patients, neither polymorphisms affected the prevalence of CAD and severe CAD.•Only vitamin D status, but not genetic variants of VDBP, was associated to CAD in our study.</description><subject>Aged</subject><subject>Atherosclerosis</subject><subject>Biomarkers - blood</subject><subject>Chi-Square Distribution</subject><subject>Coronary Angiography</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - diagnostic imaging</subject><subject>Coronary Artery Disease - epidemiology</subject><subject>Coronary Artery Disease - genetics</subject><subject>Coronary Stenosis - blood</subject><subject>Coronary Stenosis - diagnostic imaging</subject><subject>Coronary Stenosis - epidemiology</subject><subject>Coronary Stenosis - genetics</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Genetic Association Studies</subject><subject>Genetic Markers</subject><subject>Genetic Predisposition to Disease</subject><subject>Heterozygote</subject><subject>Homozygote</subject><subject>Humans</subject><subject>Italy - epidemiology</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Multivariate Analysis</subject><subject>Mutation</subject><subject>Odds Ratio</subject><subject>Phenotype</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Polymorphisms</subject><subject>Prevalence</subject><subject>Risk Factors</subject><subject>Severity of Illness Index</subject><subject>VDBP</subject><subject>Vitamin D</subject><subject>Vitamin D - analogs & derivatives</subject><subject>Vitamin D - blood</subject><subject>Vitamin D-Binding Protein - genetics</subject><issn>0939-4753</issn><issn>1590-3729</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp9kE1v1DAQQC0EokvLP0DIRy4J4ziO4wsSFGgrVaKH0qvl2BPq1cYOthe1_x4vWzhymtHozdcj5A2DlgEb3m_bsF_QurYDJlsYWoDuGdkwoaDhslPPyQYUV00vBT8hr3LeAnAJvH9JTrpRSqXGcUPC1bIaW2ic6Rp3j0tM673PC01ZQs-oCa6mvRjHA3Hni1l8oJ_pJx-cDz_oTYoFayUGWu6R4kPB8GeYjSkGkx6pSQVrcD6jyXhGXsxml_H1Uzwl379-uT2_bK6_XVydf7xuLB-60gwIk7RyduBmIa1wrpNqMMYNjjlgE1gxz6D6iQk39RJQcCms7ZmYx5G5jp-Sd8e5a4o_95iLXny2uNuZgHGfNVPdoEbWcV7R_ojaFHNOOOs1-aWerhnog2m91UfT-mBaw6Cr6dr29mnDflrQ_Wv6q7YCH44A1j9_eUw6W4_BovMJbdEu-v9v-A1QapEw</recordid><startdate>201709</startdate><enddate>201709</enddate><creator>Daffara, V.</creator><creator>Verdoia, M.</creator><creator>Rolla, R.</creator><creator>Nardin, M.</creator><creator>Marino, P.</creator><creator>Bellomo, G.</creator><creator>Carriero, A.</creator><creator>De Luca, G.</creator><general>Elsevier B.V</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>201709</creationdate><title>Impact of polymorphism rs7041 and rs4588 of Vitamin D Binding Protein on the extent of coronary artery disease</title><author>Daffara, V. ; Verdoia, M. ; Rolla, R. ; Nardin, M. ; Marino, P. ; Bellomo, G. ; Carriero, A. ; De Luca, G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-6e0b7c7fd0df57c5dd2796aad6d1d01b0c5ff094b15db470e5375cc415f881d23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Aged</topic><topic>Atherosclerosis</topic><topic>Biomarkers - blood</topic><topic>Chi-Square Distribution</topic><topic>Coronary Angiography</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - diagnostic imaging</topic><topic>Coronary Artery Disease - epidemiology</topic><topic>Coronary Artery Disease - genetics</topic><topic>Coronary Stenosis - blood</topic><topic>Coronary Stenosis - diagnostic imaging</topic><topic>Coronary Stenosis - epidemiology</topic><topic>Coronary Stenosis - genetics</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Genetic Association Studies</topic><topic>Genetic Markers</topic><topic>Genetic Predisposition to Disease</topic><topic>Heterozygote</topic><topic>Homozygote</topic><topic>Humans</topic><topic>Italy - epidemiology</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Multivariate Analysis</topic><topic>Mutation</topic><topic>Odds Ratio</topic><topic>Phenotype</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Polymorphisms</topic><topic>Prevalence</topic><topic>Risk Factors</topic><topic>Severity of Illness Index</topic><topic>VDBP</topic><topic>Vitamin D</topic><topic>Vitamin D - analogs & derivatives</topic><topic>Vitamin D - blood</topic><topic>Vitamin D-Binding Protein - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Daffara, V.</creatorcontrib><creatorcontrib>Verdoia, M.</creatorcontrib><creatorcontrib>Rolla, R.</creatorcontrib><creatorcontrib>Nardin, M.</creatorcontrib><creatorcontrib>Marino, P.</creatorcontrib><creatorcontrib>Bellomo, G.</creatorcontrib><creatorcontrib>Carriero, A.</creatorcontrib><creatorcontrib>De Luca, G.</creatorcontrib><creatorcontrib>the Novara Atherosclerosis Study Group (NAS)</creatorcontrib><creatorcontrib>Novara Atherosclerosis Study Group (NAS)</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>Nutrition, metabolism, and cardiovascular diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Daffara, V.</au><au>Verdoia, M.</au><au>Rolla, R.</au><au>Nardin, M.</au><au>Marino, P.</au><au>Bellomo, G.</au><au>Carriero, A.</au><au>De Luca, G.</au><aucorp>the Novara Atherosclerosis Study Group (NAS)</aucorp><aucorp>Novara Atherosclerosis Study Group (NAS)</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of polymorphism rs7041 and rs4588 of Vitamin D Binding Protein on the extent of coronary artery disease</atitle><jtitle>Nutrition, metabolism, and cardiovascular diseases</jtitle><addtitle>Nutr Metab Cardiovasc Dis</addtitle><date>2017-09</date><risdate>2017</risdate><volume>27</volume><issue>9</issue><spage>775</spage><epage>783</epage><pages>775-783</pages><issn>0939-4753</issn><eissn>1590-3729</eissn><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Undefined-1</notes><notes>ObjectType-Feature-3</notes><notes>content type line 23</notes><abstract>25-hydroxyvitamin D deficiency represents a widespread social problem but also an emerging risk factor for cardiovascular disease. Genetic variants of the Vitamin D Binding Protein (VDBP), the main transporter of vitamin D in the bloodstream, have been shown to account for a significant variability in the levels and systemic effects of vitamin D. We investigated whether the single nucleotide polymorphisms, rs7041 and rs4588, of VDBP are associated to the prevalence and extent of coronary artery disease.
A consecutive cohort of patients undergoing coronary angiography in a single centre were included. Significant CAD was defined as at least 1 stenosis >50%, severe CAD for as left main and/or three-vessel disease. VDBP genetic status was assessed by polymerase chain reaction and restriction fragment length polymorphism technique.
We included 1080 patients, 57% carried the mutated G allele of rs7041, whereas 22% carried the A allele of rs4588. Higher levels of C- reactive protein were observed in the carriers of G allele of rs7041 (p = 0.02), whereas 25-hydroxyvitamin D levels were similar across groups. A higher prevalence of lesions in the left anterior descending artery and a longer lesion length were observed in “A” carriers for rs4588 (p = 0.04 and p = 0.03, respectively). On the contrary, a higher prevalence of bifurcation lesions and chronic occlusions was observed in G carriers (p = 0.002 and p = 0.01 respectively). Both polymorphisms of VDBP did not affect the prevalence of CAD (rs7041: 79.1% TT vs 80.3% TG vs 78.5% GG, p = 0.81; rs4588 = 80.3% CC vs 78.5% AC + AA, p = 0.49) and severe CAD, (rs7041: 31.1% TT % vs 31.3% TG vs 30.6% GG, p = 0.88; rs4588: 32.2% CC vs 29.3% AC + AA, p = 0.31). Results were confirmed at multivariate analysis, for both rs7041 and rs4588. However, when including the levels of 25-hydroxyvitamin D in the multivariate model, we observed that 25(OH)D status and not genetic variants of VDBP were significantly associated with CAD (25-hydroxyvitamin D OR [95% CI] = 0.99 [0.97–1.0], p = 0.05; rs7041 TG: OR [95% CI] = 1.26 [0.73–2.19], p = 0.41; rs7041 GG: OR [95% CI] = 1.25 [0.82–1.91], p = 0.30; rs4588 AC + AA: OR [95% CI] = 0.76 [0.51–1.13], p = 0.18).
This study showed in a large cohort of patients undergoing coronary angiography, that the polymorphisms rs7041 and rs4588 of VDBP are not associated with the levels of 25-hydroxyvitamin D nor with the prevalence and extent of CAD. In fact, 25-hydroxyvitamin D levels but not VDBP genetic status independently predicted the occurrence of coronary lesions at angiography.
•Genetic variants of Vitamin D Binding Protein (VDBP) could explain the variability of levels and effects of vitamin D.•We studied whether the SNPs rs7041 and rs4588 of VDBP are associated to the prevalence and extent of coronary artery disease (CAD).•In a cohort of 1080 consecutive patients, neither polymorphisms affected the prevalence of CAD and severe CAD.•Only vitamin D status, but not genetic variants of VDBP, was associated to CAD in our study.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>28779988</pmid><doi>10.1016/j.numecd.2017.06.002</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0939-4753 |
| ispartof | Nutrition, metabolism, and cardiovascular diseases, 2017-09, Vol.27 (9), p.775-783 |
| issn | 0939-4753 1590-3729 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1926981233 |
| source | ScienceDirect Journals |
| subjects | Aged Atherosclerosis Biomarkers - blood Chi-Square Distribution Coronary Angiography Coronary Artery Disease - blood Coronary Artery Disease - diagnostic imaging Coronary Artery Disease - epidemiology Coronary Artery Disease - genetics Coronary Stenosis - blood Coronary Stenosis - diagnostic imaging Coronary Stenosis - epidemiology Coronary Stenosis - genetics Female Gene Frequency Genetic Association Studies Genetic Markers Genetic Predisposition to Disease Heterozygote Homozygote Humans Italy - epidemiology Logistic Models Male Middle Aged Multivariate Analysis Mutation Odds Ratio Phenotype Polymorphism, Single Nucleotide Polymorphisms Prevalence Risk Factors Severity of Illness Index VDBP Vitamin D Vitamin D - analogs & derivatives Vitamin D - blood Vitamin D-Binding Protein - genetics |
| title | Impact of polymorphism rs7041 and rs4588 of Vitamin D Binding Protein on the extent of coronary artery disease |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-09-21T22%3A46%3A06IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Impact%20of%20polymorphism%20rs7041%20and%20rs4588%20of%20Vitamin%20D%20Binding%20Protein%20on%20the%20extent%20of%20coronary%20artery%20disease&rft.jtitle=Nutrition,%20metabolism,%20and%20cardiovascular%20diseases&rft.au=Daffara,%20V.&rft.aucorp=the%20Novara%20Atherosclerosis%20Study%20Group%20(NAS)&rft.date=2017-09&rft.volume=27&rft.issue=9&rft.spage=775&rft.epage=783&rft.pages=775-783&rft.issn=0939-4753&rft.eissn=1590-3729&rft_id=info:doi/10.1016/j.numecd.2017.06.002&rft_dat=%3Cproquest_cross%3E1926981233%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c362t-6e0b7c7fd0df57c5dd2796aad6d1d01b0c5ff094b15db470e5375cc415f881d23%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1926981233&rft_id=info:pmid/28779988&rfr_iscdi=true |