Multiple biomarkers and atrial fibrillation in the general population.
BACKGROUND
Different biological pathways have been related to atrial fibrillation (AF). Novel biomarkers capturing inflammation, oxidative stress, and neurohumoral activation have not been investigated comprehensively in AF.


RESULTS
In the population-based Gutenberg Health Study (n = 5000), mean age 56 ± 11 years, 51% males, we measured ten biomarkers representing inflammation (C-reactive protein, fibrinogen), cardiac and vascular function (midregional pro adrenomedullin [MR-proADM], midregional pro atrial natriuretic peptide [MR-proANP], N-terminal pro-B-type natriuretic peptide [Nt-proBNP], sensitive troponin I ultra [TnI ultra], copeptin, and C-terminal pro endothelin-1), and oxidative stress (glutathioneperoxidase-1, myeloperoxidase) in relation to manifest AF (n = 161 cases). Individuals with AF were older, mean age 64.9 ± 8.3, and more often males, 71.4%. In Bonferroni-adjusted multivariable regression analyses strongest associations per standard deviation increase in biomarker concentrations were observed for the natriuretic peptides Nt-proBNP (odds ratio [OR] 2.89, 99.5% confidence interval [CI] 2.14-3.90; P<0.0001), MR-proANP (OR 2.45, 99.5% CI 1.91-3.14; P<0.0001), the vascular function marker MR-proADM (OR 1.54, 99.5% CI 1.20-1.99; P<0.0001), TnI ultra (OR 1.50, 99.5% CI 1.19-1.90; P<0.0001) and. fibrinogen (OR 1.44, 99.5% CI 1.19-1.75; P<0.0001). Based on a model comprising known clinical risk factors for AF, all biomarkers combined resulted in a net reclassification improvement of 0.665 (99.3% CI 0.441-0.888) and an integrated discrimination improvement of >13%.


CONCLUSIONS
In conclusion, in our large, population-based study, we identified novel biomarkers reflecting vascular function, MR-proADM, inflammation, and myocardial damage, TnI ultra, as related to AF; the strong association of natriuretic peptides was confirmed. Prospective studies need to examine whether risk prediction of AF can be enhanced beyond clinical risk factors using these biomarkers.
Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Germany.
Renate B
RB
Schnabel
Department of Medicine 2, University Medical Center of the Johannes Gutenberg-University Mainz, Germany; Center of Thrombosis and Hemostasis University Medical Center of the Johannes Gutenberg-University Mainz, Germany.
Philipp S
PS
Wild
Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Germany.
Sandra
S
Wilde
Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Germany.
Francisco M
FM
Ojeda
Department of Medicine 2, University Medical Center of the Johannes Gutenberg-University Mainz, Germany.
Andreas
A
Schulz
Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Germany.
Tanja
T
Zeller
Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Germany.
Christoph R
CR
Sinning
BRAHMS GmbH, Hennigsdorf/Germany.
Jan
J
Kunde
Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Germany.
Karl J
KJ
Lackner
Department of Medicine 2, University Medical Center of the Johannes Gutenberg-University Mainz, Germany.
Thomas
T
Munzel
Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Germany.
Stefan
S
Blankenberg
D000368:Aged; D001281:Atrial Fibrillation / Q000453:epidemiology* / Q000378:metabolism*; D015415:Biomarkers; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015233:Models, Statistical; D011159:Population Surveillance; D012307:Risk Factors
D015415:Biomarkers