Additional information is available at the end of the chapter http://dx.doi.org/10.5772/53613. Introduction "trial fibrillation is the most common sustained cardiac arrhythmia, which is associated with a high risk of stroke and thromboembolism. Increasing evidence suggests that the thrombogenic tendency in atrial fibrillation is related to several underlying pathophysiological mechanisms. Virchow's triad, a time-honored paradigm that offers mechanistic insights for thrombus initiation and development regardless of origin, does indeed apply to atrial fibrillation thrombogenesis [ , ].
. Mechanisms of thrombogenesis in atrial fibrillationMore than years ago, Rudolf Virchow proposed a triad of events needed for thrombus formation ie, abnormal changes of the vessel wall, blood flow, and blood constituents [ ]. In the st century, we now recognize Virchow's triad as endothelial or endocardial damage or dysfunction and related structural abnormal changes abnormal blood stasis and abnormal haemostasis, platelets, and fibrinolysis Figure . Extensive abnormal changes of these variables are clearly evident in atrial fibrillation. Thus, atrial fibrillation could in fact drive a prothrombotic or hypercoagulable state, by virtue of its fulfillment of Virchow's triad for thrombogenesis [ ]."bnormal changes shown in the vessel wall eg, atrial tissue changes, endothelial damage and dysfunction , in fl ow stasis eg, in the left atrial appendage , and in blood constituents eg, haemoconcentration, platelets, coagulation cascade activation, infl ammation all factors contribute to propensity for thrombus formation thrombogenesis in atrial fi brillation. vWf=von Willebrand factor.