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Atherosclerosis. 2015 Nov;243(1):192-7. doi: 10.1016/j.atherosclerosis.2015.09.009. Epub 2015 Sep 8.

Inflammation and hemostasis in atrial fibrillation and coronary heart disease: The REasons for Geographic And Racial Differences in Stroke study.

Author information

1
Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA. Electronic address: woneal@wakehealth.edu.
2
Department of Internal Medicine, Section on Cardiology, Wake Forest School of Medicine, Winston-Salem, NC, USA; Epidemiological Cardiology Research Center (EPICARE), Department of Epidemiology and Prevention, Wake Forest School of Medicine, Winston-Salem, NC, USA.
3
Department of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.
4
Department of Epidemiology, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.
5
Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
6
Departments of Medicine and Pathology, University of Vermont College of Medicine, Burlington, VT, USA.

Abstract

BACKGROUND:

Recent studies suggest atrial fibrillation (AF) is an independent risk factor for coronary heart disease (CHD).

AIMS:

To determine if alterations in hemostasis or inflammation explain the association between AF and CHD.

METHODS:

C-reactive protein (CRP), D-dimer, factor VIII, and fibrinogen were measured in incident CHD cases (n = 647) and a stratified cohort random sample (CRS, n = 1104) between 2003 and 2007 from the REasons for Geographic And Racial Differences in Stroke (REGARDS) study. Using a case-cohort approach, Cox models examined whether inflammation or hemostasis biomarkers explained the association between AF and CHD.

RESULTS:

In participants free of CHD at baseline, 12.2% of CHD cases and 7.1% of the CRS had AF. Over a median follow-up of 4.4 years, all biomarkers were associated with an increased risk of CHD in those with and those without AF after adjusting for CHD risk factors. The association of D-dimer with CHD was greater in those with AF (HR 2.52, 95% CI = 1.49, 4.26) than those without AF (HR 1.34, 95% CI = 1.12, 1.61) (p-interaction = 0.02). Similar interactions were not observed for the other biomarkers.

CONCLUSIONS:

Our results suggest that alterations in D-dimer, a marker of hemostasis, explain the association between AF and CHD. Potentially, D-dimer is a useful biomarker to assess CHD risk in persons with AF.

KEYWORDS:

Atrial fibrillation; Biological markers; Coronary disease

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