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Proteomics and Risk of Atrial Fibrillation in Older Adults (From the Atherosclerosis Risk in Communities [ARIC] Study).
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- Additional Information
- Source:
Publisher: Excerpta Medica Country of Publication: United States NLM ID: 0207277 Publication Model: Print Cited Medium: Internet ISSN: 1879-1913 (Electronic) Linking ISSN: 00029149 NLM ISO Abbreviation: Am J Cardiol Subsets: MEDLINE
- Publication Information:
Original Publication: New York, NY : Excerpta Medica
- Subject Terms:
- Abstract:
Plasma proteomic profiling may aid in the discovery of novel biomarkers upstream of the development of atrial fibrillation (AF). We used data from the Atherosclerosis Risk in Communities study to examine the relation between large-scale proteomics and incident AF in a cohort of older-aged adults in the United States. We quantified 4,877 plasma proteins in Atherosclerosis Risk in Communities participants at visit 5 (2011-2013) using an aptamer-based proteomic profiling platform. We used Cox proportional hazards models to assess the association between protein levels and incident AF, and explored relation of selected protein biomarkers using annotated pathway analysis. Our study included 4,668 AF-free participants (mean age 75 ± 5 years; 59% female; 20% Black race) with proteomic measures. A total of 585 participants developed AF over a mean follow-up of 5.7 ± 1.7 years. After adjustment for clinical factors associated with AF, N-terminal pro-B-type natriuretic peptide (NT-proBNP) was associated with the risk of incident AF (hazard ratio, 1.82; 95% CI, 1.68 to 1.98; p, 2.91 × 10 -45 per doubling of NT-proBNP). In addition, 36 other proteins were also significantly associated with incident AF after Bonferroni correction. We further adjusted for medication use and estimated glomerular filtration rate and found 17 proteins, including angiopoietin-2 and transgelin, that remained significantly associated with incident AF. Pathway analyses implicated the inhibition of matrix metalloproteases as the top canonical pathway in AF pathogenesis. In conclusion, using a large-scale proteomic platform, we identified both novel and established proteins associated with incident AF and explored mechanistic pathways of AF development.
Competing Interests: Disclosures The authors have no conflicts of interest to declare.
(Copyright © 2021 Elsevier Inc. All rights reserved.)
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- Grant Information:
16EIA26410001 United States AHA American Heart Association-American Stroke Association; HHSN268201700002C United States HL NHLBI NIH HHS; HHSN268201700001I United States HL NHLBI NIH HHS; HHSN268201700004C United States HL NHLBI NIH HHS; HHSN268201700003I United States HL NHLBI NIH HHS; R01 HL126637 United States HL NHLBI NIH HHS; K24 HL148521 United States HL NHLBI NIH HHS; HHSN268201700004I United States HL NHLBI NIH HHS; HHSN268201700005C United States HL NHLBI NIH HHS; HHSN268201700001C United States HL NHLBI NIH HHS; HHSN268201700003C United States HL NHLBI NIH HHS; R01 HL141288 United States HL NHLBI NIH HHS; HHSN268201700002I United States HL NHLBI NIH HHS; HHSN268201700005I United States HL NHLBI NIH HHS
- Accession Number:
0 (Biomarkers)
0 (Peptide Fragments)
0 (Protein Precursors)
0 (pro-brain natriuretic peptide (1-76))
114471-18-0 (Natriuretic Peptide, Brain)
- Publication Date:
Date Created: 20211119 Date Completed: 20211130 Latest Revision: 20240923
- Publication Date:
20240923
- Accession Number:
PMC8608272
- Accession Number:
10.1016/j.amjcard.2021.08.064
- Accession Number:
34794617
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