Fibrinolytic activity in atrial fibrillation

Atrial fibrillation (AF) is one of the most common causes of thromboembolic cerebrovascular accidents. This is a prerequisite for the significant scientific and clinical interest in hemostatic disorders in AF. Despite the large number of studies on the topic, the exact mechanisms of thrombosis remain unclear. A well established fact is the significant activation of the coagulation cascade, therefore AF is often defined as a hypercoagulable state. The presence of a genetically determined link between coagulation and fibrinolysis inevitably raises the question of fibrinolytic activity in the disease. Our review of fibrinolysis in AF showed that compared to studies on the coagulation system, data are significantly smaller in number. Components of fibrinolysis, its functionality in general, as well as its relationship with the arrhythmia itself and associated thromboembolic disorders, have been studied in both experimental and clinical models. However, single indicators have been examined and the obtained results are absolutely contradictory, presenting the system in both end states - from hypofunction to hyperfunction. One of the main weaknesses of the studies is the heterogeneity of the populations in terms of demographic and clinical characteristics, which in itself is a prerequisite for compromising the results. Most often, the fibrinolytic process is studied independently, without comparison with coagulation activity, which complicates the interpretation of the results. The question of causal relationship between changes in coagulation and fibrinolytic system in AF, as well as their contribution to the clinical manifestation of the disease and related thromboembolic complications, remains open