Resumen de Hipercoagulabilidad en fibrilación auricular y su relación con factores de riesgo para embolia sistémica
Luis A Pérez P, Ramón Corbalán H, Mónica Acevedo B, Jaime Pereira, Sandra Braun J, Jorge Tapia I, Albrecht Krämer SCH., María Teresa Lira Correa, Isidro Huete, Eduardo Sepúlveda S., Daniel Springmüller
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 (Rev Méd Chile 2002; 130: 1087-94)
