File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Genetically deprived vitamin D exposure predisposes to atrial fibrillation

TitleGenetically deprived vitamin D exposure predisposes to atrial fibrillation
Authors
Keywords25-Hydroxyvitamin D
Atrial fibrillation
Genetic polymorphism
Vitamin D-binding protein
Issue Date2017
Citation
EP Europace, 2017, v. 19, p. iv25-iv31 How to Cite?
AbstractAims: Low vitamin D level is associated with atrial fibrillation (AF) and may be implicated in its pathogenesis. Methods and results: We studied single nucleotide polymorphisms (SNPs) of vitamin D mechanistic pathways and serum 25-hydroxyvitamin D [25(OH)D] levels in an age- and gender-matched case–control study (controls without AF: mean age 68.6 ± 8.7 years, female 25%; n = 1019; with AF: mean age 69.7 ± 9.5 years, female 30%; n = 156) recruited from a Chinese clinical cohort of patients with stable coronary artery disease. Twelve SNPs involved in the vitamin D mechanistic pathways were studied [biosynthetic: rs4646536, rs10877012, rs3829251, rs1790349; activation: rs2060793, rs1993116; vitamin D-binding protein (VBP)/group-specific component (GC): rs4588, rs7041, rs2282679, rs1155563; and vitamin D receptor: rs1544410, rs10735810]. A genetic risk score (GRS) (0–8) was constructed from SNPs associated with serum 25(OH)D as a proxy to lifelong vitamin D-deficient state. All 4 SNPs involved in the VBP/GC were significantly associated with serum 25(OH)D (rs4588, P < 0.001; rs2282679, P < 0.001; rs7041, P = 0.011; rs1155563, P < 0.001; all other SNPs, P > 0.05). Vitamin D GRS (points 0–8) generated from these 4 SNPs was independently predictive of serum 25(OH)D [B = 0.54, 95% confidence interval (CI) 0.30–0.79; P < 0.001]. Genetically deprived vitamin D status as denoted by a low GRS (0–3) independently predicted an increased risk of AF, compared to a high GRS (4–8) (odds ratio = 1.848, 95% CI 1.217–2.805; P = 0.004). Conclusion: Genetically deprived vitamin D exposure predisposes to increased AF among patients with coronary artery disease. Whether VBP/GC may alter the risk of AF via alternative mechanisms warrants further studies.
Persistent Identifierhttp://hdl.handle.net/10722/250521
ISSN
2021 Impact Factor: 5.486
2020 SCImago Journal Rankings: 2.119
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, YH-
dc.contributor.authorYiu, KH-
dc.contributor.authorHai, SHJJ-
dc.contributor.authorChan, PHM-
dc.contributor.authorLam, TH-
dc.contributor.authorCowling, BJ-
dc.contributor.authorSham, PC-
dc.contributor.authorLau, CP-
dc.contributor.authorLam, KSL-
dc.contributor.authorSiu, DCW-
dc.contributor.authorTse, HF-
dc.date.accessioned2018-01-18T04:28:21Z-
dc.date.available2018-01-18T04:28:21Z-
dc.date.issued2017-
dc.identifier.citationEP Europace, 2017, v. 19, p. iv25-iv31-
dc.identifier.issn1099-5129-
dc.identifier.urihttp://hdl.handle.net/10722/250521-
dc.description.abstractAims: Low vitamin D level is associated with atrial fibrillation (AF) and may be implicated in its pathogenesis. Methods and results: We studied single nucleotide polymorphisms (SNPs) of vitamin D mechanistic pathways and serum 25-hydroxyvitamin D [25(OH)D] levels in an age- and gender-matched case–control study (controls without AF: mean age 68.6 ± 8.7 years, female 25%; n = 1019; with AF: mean age 69.7 ± 9.5 years, female 30%; n = 156) recruited from a Chinese clinical cohort of patients with stable coronary artery disease. Twelve SNPs involved in the vitamin D mechanistic pathways were studied [biosynthetic: rs4646536, rs10877012, rs3829251, rs1790349; activation: rs2060793, rs1993116; vitamin D-binding protein (VBP)/group-specific component (GC): rs4588, rs7041, rs2282679, rs1155563; and vitamin D receptor: rs1544410, rs10735810]. A genetic risk score (GRS) (0–8) was constructed from SNPs associated with serum 25(OH)D as a proxy to lifelong vitamin D-deficient state. All 4 SNPs involved in the VBP/GC were significantly associated with serum 25(OH)D (rs4588, P < 0.001; rs2282679, P < 0.001; rs7041, P = 0.011; rs1155563, P < 0.001; all other SNPs, P > 0.05). Vitamin D GRS (points 0–8) generated from these 4 SNPs was independently predictive of serum 25(OH)D [B = 0.54, 95% confidence interval (CI) 0.30–0.79; P < 0.001]. Genetically deprived vitamin D status as denoted by a low GRS (0–3) independently predicted an increased risk of AF, compared to a high GRS (4–8) (odds ratio = 1.848, 95% CI 1.217–2.805; P = 0.004). Conclusion: Genetically deprived vitamin D exposure predisposes to increased AF among patients with coronary artery disease. Whether VBP/GC may alter the risk of AF via alternative mechanisms warrants further studies.-
dc.languageeng-
dc.relation.ispartofEP Europace-
dc.subject25-Hydroxyvitamin D-
dc.subjectAtrial fibrillation-
dc.subjectGenetic polymorphism-
dc.subjectVitamin D-binding protein-
dc.titleGenetically deprived vitamin D exposure predisposes to atrial fibrillation-
dc.typeArticle-
dc.identifier.emailYiu, KH: khkyiu@hku.hk-
dc.identifier.emailHai, SHJJ: haishjj@hku.hk-
dc.identifier.emailChan, PHM: phmchan@hku.hk-
dc.identifier.emailLam, TH: hrmrlth@hkucc.hku.hk-
dc.identifier.emailCowling, BJ: bcowling@hku.hk-
dc.identifier.emailSham, PC: pcsham@hku.hk-
dc.identifier.emailLau, CP: cplau@hkucc.hku.hk-
dc.identifier.emailLam, KSL: ksllam@hku.hk-
dc.identifier.emailSiu, DCW: cwdsiu@hkucc.hku.hk-
dc.identifier.emailTse, HF: hftse@hkucc.hku.hk-
dc.identifier.authorityYiu, KH=rp01490-
dc.identifier.authorityHai, SHJJ=rp02047-
dc.identifier.authorityChan, PHM=rp01864-
dc.identifier.authorityLam, TH=rp00326-
dc.identifier.authorityCowling, BJ=rp01326-
dc.identifier.authoritySham, PC=rp00459-
dc.identifier.authorityLam, KSL=rp00343-
dc.identifier.authoritySiu, DCW=rp00534-
dc.identifier.authorityTse, HF=rp00428-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/europace/eux312-
dc.identifier.scopuseid_2-s2.0-85040073298-
dc.identifier.hkuros284003-
dc.identifier.volume19-
dc.identifier.spageiv25-
dc.identifier.epageiv31-
dc.identifier.eissn1532-2092-
dc.identifier.isiWOS:000417738300004-
dc.identifier.issnl1099-5129-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats