Revista medica de Chile · 2002
[Hypercoagulability in atrial fibrillation and its relationship with risk factors for systemic embolism].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Pérez Luis A, Corbalán Ramón, Acevedo Mónica, Pereira Jaime, Braun Sandra, Tapia Jorge, Kramer Albrecht, Lira M Teresa, Huete Isidro, Sepúlveda Gonzalo, Springmüller Daniel
Аннотация
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.
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.