Influence of Aortic Valve Stenosis and Wall Shear Stress on Platelets Function

Area of Science:

• Cardiovascular Medicine
• Hematology
• Pathophysiology

Background:

• Aortic valve stenosis (AS) is a prevalent condition in the elderly, characterized by progressive aortic valve leaflet degeneration, fibrosis, and calcification.
• The resulting turbulent blood flow and elevated shear stress significantly impact cardiovascular health and hemostasis.
• Understanding the pathogenesis of AS is crucial for developing effective therapeutic strategies.

Purpose of the Study:

• To review current knowledge on high shear stress-induced hemostatic disorders in the context of AS.
• To explore the influence of AS on platelet function and activation.
• To discuss the implications for antiplatelet therapy in patients with AS.

Main Methods:

• Literature review of existing research on AS, shear stress, and hemostasis.
• Analysis of the mechanisms linking turbulent blood flow to von Willebrand factor degradation and platelet activation.
• Synthesis of information on the role of platelets and their mediators in AS pathogenesis.

Main Results:

• Elevated shear stress in AS can degrade von Willebrand factor, potentially causing mucosal bleeding.
• High shear stress also promotes thrombin release and platelet activation, even in acquired von Willebrand syndrome.
• Turbulent flow activates endothelium and aortic valve surfaces, promoting platelet adhesion and mediator release, including pro-osteogenic factors.

Conclusions:

• AS-induced high shear stress triggers complex hemostatic disorders involving coagulation, fibrinolysis, and platelet dysfunction.
• Platelet activation and mediator release play a significant role in the progression of AS.
• Further research into these mechanisms is essential for optimizing antiplatelet therapy in AS patients.