Conrado Pedroso Balbo et al. Luciana Paula Seabra Victor Gualda Galoro Guido Caputi … José Honório Palma Ênio Buffolo
Introduction
Aortic Stenosis (AoS) is the valvular pathology most frequently acquired in developed countries, present in 4% of individuals over 85 years of age. Patients with severe AoS may have comorbidities, presenting greater risk of thrombotic and bleeding events.
Heyde’s Syndrome was described in 1958 by E. C. Heyde as he observed the relation between aortic valve stenosis and gastrointestinal bleeding. In 1992, Warkentin et al. observed the loss of the largest Willebrand factor multimers, characterizing the Acquired type 2A, von Willebrand syndrome. Von Willebrand Factor (vWF) is a multimeric protein, secreted by endothelial cells and platelets. It promotes adherence of platelets to vascular lesion sites through glycoprotein Ib-vWF interactions. A change in the shape of vWF occurs in AoS, making such protein more susceptible to proteolytic cleavage. As a consequence, vWF is degraded specifically by protease ADAMTS13, hindering vWF-mediated platelet adhesion, thus generating a lack of these multimers and causing bleeding, especially in pre-existing lesions such as gastrointestinal angiodysplasia.–
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