Thoracic aortopathies, including aneurysm and dissection, are complex vascular disorders characterized by structural alterations of the aortic wall that disrupt normal haemodynamics. Altered shear stress, turbulent flow, and endothelial dysfunction promote thrombus formation and modulate systemic hemostasis via platelet activation and the von Willebrand factor–ADAMTS13 axis. The Total Thrombus-Formation Analysis System (T-TAS) is a microfluidic, flow-dependent assay that quantitatively evaluates thrombus formation under physiological shear conditions. Although studied in various cardiovascular contexts, its application in aortopathies remains largely unexplored, and no prospective studies have validated its clinical utility. Integrating T-TAS with computational haemodynamic approaches, such as two-way fluid–structure interaction simulations, enables assessment of the interplay between blood flow, vessel wall mechanics, pulse wave propagation, and local shear patterns. Patient-specific modelling, including individualized flow profiles, pressure distributions, and wall properties, may enhance mechanistic insights. Genetic variants in Fibrillin-1 gene (FBN1), Transforming Growth Factor Beta Receptor 1/2 (TGFBR1/2), Actin Alpha 2 (ACTA 2), and Myosin Heavy Chain 11 (MYH11) further contribute to structural vascular heterogeneity and diverse systemic haemostatic phenotypes, highlighting the need for personalized assessment. T-TAS should currently be considered an exploratory research tool rather than a validated diagnostic or prognostic method. This narrative review proposes a hypothesis-generating framework integrating structural, haemodynamic, molecular, and functional perspectives. Combining flow-based thrombosis assays with advanced modelling may inform future translational studies, improve mechanistic understanding of thrombus formation, and support personalized risk stratification and management in patients with thoracic aortopathies.
Krych et al. (Mon,) studied this question.