Wesley T O'Neal1, Elsayed Z Soliman2, George Howard3, Virginia J Howard4, Monika M Safford5, Mary Cushman6, Neil A Zakai6. 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.
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.
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