Dementia in subjects with atrial fibrillation: hemostatic function and the role of anticoagulation
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Published on: February 26, 2013
1University Section of Clinical Gerontology and Vascular Medicine and Department of Haematology, Royal Infirmary, Glasgow, UK. m.barber@clinmed.gla.ac.uk
Insights
Atrial fibrillation (AF) patients with dementia show higher levels of thrombin generation and fibrin turnover. Long-term warfarin use may offer protection against dementia development in AF patients.
Area of Science:
- Cardiology
- Neurology
- Hematology
Background:
- Atrial fibrillation (AF) is linked to cognitive decline and dementia.
- This association may stem from a prothrombotic state and cardioembolism.
- Investigating hemostatic alterations in AF with dementia is crucial.
Purpose of the Study:
- To determine if hemostatic function differs in AF patients who develop dementia.
- To assess if long-term warfarin anticoagulation protects against dementia in AF.
- To explore the relationship between coagulation markers and cognitive decline in AF.
Main Methods:
- Observational cohort study of atrial fibrillation (AF) patients.
- Baseline measurements included plasma fibrinogen, D-dimer, prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complexes (TAT), von Willebrand factor, and tissue plasminogen activator.
- Cognitive function was assessed at 3 years using TICSm and IQCODE.
Main Results:
- Higher D-dimer, F1+2, and TAT levels were observed in AF subjects with dementia.
- These findings showed borderline statistical significance after age adjustment.
- A trend suggested warfarin use was independently associated with reduced dementia prevalence (OR 0.52, P=0.08).
Conclusions:
- Evidence indicates increased thrombin generation and fibrin turnover in AF patients with dementia.
- Long-term warfarin therapy may be a protective factor against dementia in individuals with AF.
Background:
Atrial fibrillation (AF) is associated with cognitive impairment and dementia, perhaps through encouraging a prothrombotic state and cardioembolism.
Objectives:
We wished to test the hypotheses that hemostatic function is altered in subjects with AF who develop dementia, and that long-term warfarin anticoagulation is protective against this complication.
Patients And Methods:
Recruitment was from an observational cohort study of AF. Baseline assessment included measurement of plasma fibrinogen, fibrin D-dimer, prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complexes (TAT), von Willebrand factor and tissue plasminogen activator. We assessed cognitive function after 3 years' follow-up using the 13-item modified Telephone Interview for Cognitive Status (TICSm) and the short form of the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE).
Results:
Of the 218 subjects assessed, 145 (66%) were prescribed warfarin. Forty-nine (22%) met TICSm/IQCODE criteria for dementia. D-dimer, F1+2 and TAT levels were higher in AF subjects with dementia compared with those without (medians 81 vs. 60 ng mL(-1), P = 0.008; 0.76 vs. 0.49 nmol L(-1), P = 0.006; and 1.78 vs. 1.44 microg L(-1), P = 0.003, respectively). These associations became of borderline statistical significance following adjustment for age. Logistic regression showed a trend towards warfarin use being independently associated with reduced prevalence of dementia (odds ratio 0.52, P = 0.08).
Conclusions:
We found evidence of increased thrombin generation and fibrin turnover in subjects with AF and dementia compared with those without dementia. Long-term warfarin use may be protective against the development of dementia in subjects with AF.
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