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[Hypercoagulability in atrial fibrillation and its relationship with risk factors for systemic embolism]
Luis A Pérez1, Ramón Corbalán, Mónica Acevedo
1Departamentos de Enfermedades Cardiovasculares, Hospital Clínico de la Pontificia Universidad Católica de Chile.
Insights
Atrial fibrillation activates the coagulation cascade, increasing embolism risk. However, this activation did not correlate with known risk factors, though antiplatelet agents showed a protective effect.
Area of Science:
- Cardiology
- Hematology
- Thrombosis Research
Context:
- Atrial fibrillation (AF) is a common arrhythmia linked to a high risk of systemic embolism due to hypercoagulability.
- Understanding the mechanisms of hypercoagulability in AF is crucial for developing effective preventative strategies.
Purpose:
- To assess coagulation cascade activation in AF patients by measuring thrombin-antithrombin complex levels.
- To investigate the correlation between coagulation activation and established clinical/echocardiographic risk factors for systemic embolism in AF.
Summary:
- Plasma thrombin-antithrombin complex levels were significantly elevated in 53 AF patients compared to healthy controls.
- No significant association was found between basal thrombin-antithrombin levels and traditional risk factors like age, hypertension, or left atrial diameter.
- Patients on antiplatelet agents exhibited lower thrombin-antithrombin values, suggesting a preventive effect.
Impact:
- Confirms heightened coagulation cascade activity in AF patients.
- Challenges the direct link between known risk factors and hypercoagulability in AF.
- Highlights the potential role of antiplatelet therapy in mitigating coagulation activation in AF.
Background:
Atrial fibrillation is associated to a high risk of systemic embolism and to hypercoagulability.
Aim:
To evaluate the activation of the coagulation cascade through determinations of the thrombin-antithrombin complex in patients with atrial fibrillation and to correlate this data with the clinical and echocardiographic risk factors for systemic embolism.
Patients And Methods:
In 53 patients with atrial fibrillation plasma levels of the thrombin-antithrombin complex were determined on admission to a coronary care unit and 30 days later. Using a univariate and multiple regression analysis, the association basal thrombin-antithrombin with the duration of the arrhythmia, age over 70 years, previous use of antiplatelet agents, history of hypertension, mitral valve disease, diabetes, heart failure, previous systemic embolism, left atrial diameter and the presence of spontaneous contrast echo or thrombus in the left atrial appendage, was studied.
Results:
Basal thrombin-antithrombin values were 40.1 +/- 69 mg/L (Median 8.34 [3.0-47.5]) compared to 2.7 +/- 3.3 mg/L in healthy controls (p < 0.001). No significant correlation was found between activation of the coagulation cascade and risk factors for systemic embolism. There were no significant differences in thrombin-antithrombin values between patients with chronic or paroxysmal atrial fibrillation (29.5 +/- 43 mg/L and 49.4 +/- 83 mg/L respectively). Mean thrombin-antithrombin values in patients under antiplatelet agents were lower than in those without treatment (17.3 +/- 43 vs 66.8 +/- 127 mg/L; p = 0.018).
Conclusions:
The activation of the coagulation cascade in patients with atrial fibrillation was confirmed. However, no association of this activation with well known clinical and echocardiographic risk factors for systemic embolism, was found. Previous antiplatelet treatment prevented a higher activation of the coagulation cascade.