Aortic stenosis interacts dynamically with the haemostatic system at each pathophysiological stage, potentially leading to microthrombosis and impacting valve function after replacement.
Understanding the interaction between aortic stenosis and the haemostatic system is crucial for developing prophylactic treatments, particularly to address microthrombosis following transcatheter aortic valve replacement.
Aortic stenosis (AS) affects more than 10% of the population over 80 years of age and constitutes a major risk factor for heart failure, thromboembolic stroke, and death. A better understanding of the disease, including its interaction with the haemostatic system, is a prerequisite to develop prophylactic treatments. AS pathogenesis is a dynamic process involving endothelial dysfunction, inflammation, fibrosis, and calcification. Several studies support the interplay between the components of the haemostatic system such as platelets, the coagulation system, von Willebrand factor, and extracellular micro-particles at each pathophysiological stage of AS. Previous reports have evidenced persistent biological activity of the native valve after transcatheter aortic valve replacement and the subsequent development of microthrombosis that may impact the function of the newly implanted valve. Here, we review the current evidence on the interplay between AS and prothrombotic activity, and we emphasize the clinical consequences of these interactions after aortic valve replacement.
Trimaille et al. (Tue,) conducted a review in Aortic stenosis. Aortic stenosis interacts dynamically with the haemostatic system at each pathophysiological stage, potentially leading to microthrombosis and impacting valve function after replacement.
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