Platelets plug a breached vessel wall, but may support the activation of coagulation under AF-conditions.

Under normal physiological conditions, platelets support the integrity of the endothelial cell monolayer. Furthermore, when the vessel wall is breached, normal platelets adhere to the exposed extracellular matrix and form the first line of defence, thus preventing excessive blood loss. In patients with atrial fibrillation, systemic activation of platelets coincides with hypercoagulability. Our data show that once the coagulation is activated, the ability of the platelets to support the integrity of the monolayer is overruled, because the platelets themselves potentiate the activation of coagulation. This causes loss of endothelial barrier function, vascular leakage and loss of the microvasculature, eventually leading to tissue fibrosis.