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dc.contributor.authorRienstra, Michiel
dc.contributor.authorYin, Xiaoyan
dc.contributor.authorLarson, Martin G.
dc.contributor.authorFontes, Joao D.
dc.contributor.authorMagnani, Jared W.
dc.contributor.authorMcManus, David D.
dc.contributor.authorMcCabe, Elizabeth L.
dc.contributor.authorCoglianese, Erin E.
dc.contributor.authorAmponsah, Michael
dc.contributor.authorHo, Jennifer E.
dc.contributor.authorJanuzzi, James L. Jr.
dc.contributor.authorWollert, Kai C.
dc.contributor.authorFradley, Michael G.
dc.contributor.authorVasan, Ramachandran S.
dc.contributor.authorEllinor, Patrick T.
dc.contributor.authorWang, Thomas J.
dc.contributor.authorBenjamin, Emelia J.
dc.date2022-08-11T08:08:29.000
dc.date.accessioned2022-08-23T15:57:02Z
dc.date.available2022-08-23T15:57:02Z
dc.date.issued2014-01-01
dc.date.submitted2014-03-27
dc.identifier.citation<p>Rienstra M, Yin X, Larson MG, Fontes JD, Magnani JW, McManus DD, McCabe EL, Coglianese EE, Amponsah M, Ho JE, Januzzi JL Jr, Wollert KC, Fradley MG, Vasan RS, Ellinor PT, Wang TJ, Benjamin EJ. Relation between soluble ST2, growth differentiation factor-15, and high-sensitivity troponin I and incident atrial fibrillation. Am Heart J. 2014 Jan;167(1):109-115.e2. doi:10.1016/j.ahj.2013.10.003. <a href="http://dx.doi.org/10.1016/j.ahj.2013.10.003" target="_blank">Link to article on publisher's site</a></p>
dc.identifier.issn0002-8703 (Linking)
dc.identifier.doi10.1016/j.ahj.2013.10.003
dc.identifier.pmid24332149
dc.identifier.urihttp://hdl.handle.net/20.500.14038/30101
dc.description.abstractBACKGROUND: We investigated whether circulating concentrations of soluble ST2, growth differentiation factor-15 (GDF-15), and high-sensitivity troponin I (hsTnI) are associated with incident atrial fibrillation (AF) and whether these biomarkers improve current risk prediction models including AF risk factors, B-type natriuretic peptide (BNP), and C-reactive protein (CRP). METHODS: We studied the relation between soluble ST2, GDF-15, and hsTnI and development of AF in Framingham Heart Study participants without prevalent AF. We used Cox proportional hazard regression analysis to examine the relation of incident AF during a 10-year follow-up period with each biomarker. We adjusted for standard AF clinical risk factors, BNP, and CRP. RESULTS: The mean age of the 3,217 participants was 59 +/- 10 years, and 54% were women. During a 10-year follow-up, 242 participants developed AF. In age- and sex-adjusted models, GDF-15 and hsTnI were associated with risk of incident AF; however, after including the AF risk factors and BNP and CRP, only hsTnI was significantly associated with AF (hazard ratio per 1 SD of loge hsTnI, 1.12, 95% CI 1.00-1.26, P = .045). The c statistic of the base model including AF risk factors, BNP, and CRP was 0.803 (95% CI 0.777-0.830) and did not improve by adding individual or all 3 biomarkers. None of the discrimination and reclassification statistics were significant compared with the base model. CONCLUSION: In a community-based cohort, circulating hsTnI concentrations were associated with incident AF. None of the novel biomarkers evaluated improved AF risk discrimination or reclassification beyond standard clinical AF risk factors and biomarkers.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=24332149&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3884900/
dc.subjectAged
dc.subjectAtrial Fibrillation
dc.subjectBiological Markers
dc.subjectC-Reactive Protein
dc.subjectFemale
dc.subjectGrowth Differentiation Factor 15
dc.subjectHumans
dc.subjectMale
dc.subjectMiddle Aged
dc.subjectNatriuretic Peptide, Brain
dc.subjectProportional Hazards Models
dc.subjectReceptors, Cell Surface
dc.subjectRisk Assessment
dc.subjectRisk Factors
dc.subjectUMCCTS funding
dc.subjectCardiology
dc.subjectCardiovascular Diseases
dc.subjectClinical Epidemiology
dc.subjectEpidemiology
dc.titleRelation between soluble ST2, growth differentiation factor-15, and high-sensitivity troponin I and incident atrial fibrillation
dc.typeJournal Article
dc.source.journaltitleAmerican heart journal
dc.source.volume167
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/336
dc.identifier.contextkey5395152
html.description.abstract<p>BACKGROUND: We investigated whether circulating concentrations of soluble ST2, growth differentiation factor-15 (GDF-15), and high-sensitivity troponin I (hsTnI) are associated with incident atrial fibrillation (AF) and whether these biomarkers improve current risk prediction models including AF risk factors, B-type natriuretic peptide (BNP), and C-reactive protein (CRP).</p> <p>METHODS: We studied the relation between soluble ST2, GDF-15, and hsTnI and development of AF in Framingham Heart Study participants without prevalent AF. We used Cox proportional hazard regression analysis to examine the relation of incident AF during a 10-year follow-up period with each biomarker. We adjusted for standard AF clinical risk factors, BNP, and CRP.</p> <p>RESULTS: The mean age of the 3,217 participants was 59 +/- 10 years, and 54% were women. During a 10-year follow-up, 242 participants developed AF. In age- and sex-adjusted models, GDF-15 and hsTnI were associated with risk of incident AF; however, after including the AF risk factors and BNP and CRP, only hsTnI was significantly associated with AF (hazard ratio per 1 SD of loge hsTnI, 1.12, 95% CI 1.00-1.26, P = .045). The c statistic of the base model including AF risk factors, BNP, and CRP was 0.803 (95% CI 0.777-0.830) and did not improve by adding individual or all 3 biomarkers. None of the discrimination and reclassification statistics were significant compared with the base model.</p> <p>CONCLUSION: In a community-based cohort, circulating hsTnI concentrations were associated with incident AF. None of the novel biomarkers evaluated improved AF risk discrimination or reclassification beyond standard clinical AF risk factors and biomarkers.</p>
dc.identifier.submissionpathfaculty_pubs/336
dc.contributor.departmentMeyers Primary Care Institute
dc.contributor.departmentDepartment of Medicine, Division of Cardiovascular Medicine
dc.source.pages109-115.e2


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