Effect of low-intensity warfarin anticoagulation on level of activity of the hemostatic system in patients with atrial fibrillation. BAATAF Investigators.
Why the study?
Does low-intensity warfarin anticoagulation reduce plasma levels of prothrombin activation fragment F1+2 in patients with nonvalvular atrial fibrillation?
Population
n=125 patients with nonvalvular atrial fibrillation from the Boston Area Anticoagulation Trial for Atrial…
Comparison
Low-intensity warfarin anticoagulation vs Control group not taking warfarin
Design
Cross-sectional
Authors
Discussion
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Implication
Supports biological plausibility of low-intensity warfarin in nonvalvular AF; hypothesis-generating for F1+2 mediation of stroke reduction.
Key Points
- This research aims to evaluate how low-intensity warfarin affects the hemostatic system in patients with atrial fibrillation.
- 125 patients from the BAATAF trial were included, with 62 receiving warfarin and 63 as controls.
- Plasma levels of prothrombin activation fragment F1+2 were measured to assess in vivo clotting.
- Data compared F1+2 levels between patients on warfarin and those not on anticoagulants.
- The warfarin group exhibited a 71% lower mean F1+2 level (0.46 nmol/L) compared to controls (1.57 nmol/L), P < .001.
- F1+2 levels remained consistently lower in the warfarin group across all ages.
- Aspirin use in control patients did not significantly affect F1+2 levels, maintaining a mean around 1.52 nmol/L.
Structured PICO
Does low-intensity warfarin anticoagulation reduce plasma levels of prothrombin activation fragment F1+2 in patients with nonvalvular atrial fibrillation?
P
Population
n=125 patients with nonvalvular atrial fibrillation from the Boston Area Anticoagulation Trial for Atrial Fibrillation (BAATAF)
I
Intervention
Low-intensity warfarin anticoagulation
C
Comparator
Control group not taking warfarin (52% of which were taking chronic aspirin therapy)
O
Outcome
Plasma level of prothrombin activation fragment F1+2surrogate
Low-intensity warfarin, but not aspirin, significantly suppresses in vivo prothrombin activation (F1+2 levels) in patients with nonvalvular atrial fibrillation, correlating with its clinical efficacy in stroke reduction.
Cite This Study
Kistler et al. (1993) studied this question.