Neosinus and Valve Thrombosis After Transcatheter Aortic Valve Replacement

Figures

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  Figure 1. Neosinus and Anatomic sinus after transcatheter aortic valve replacement.

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  Figure 2. Mechanism of leaflet thrombosis after TAVR based on Virchow's triad. Schematic illustration of thrombus formation on transcatheter heart valves leaflets, as explained through the lens of Virchow's triad. The left panel shows a cross‐sectional view of a deployed transcatheter heart valves within the neosinus, depicting the metallic stent frame, the transcatheter valve leaflet, and the native leaflet. Aggregates of red blood cells indicate sites of thrombus development. The right panel (A–D) outlines the key sequential stages of the thrombotic process: (A) Normal laminar flow condition shortly after valve implantation. B, Initiation phase, characterized by endothelial injury and blood flow stasis, leading to initial platelet adhesion. C, Propagation phase, featuring progressive platelet aggregation and mass expansion. D, Formation of a macroscopic, non‐obstructive thrombus within the neosinus cavity. TAVR indicates transcatheter aortic valve replacement.

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  Figure 3. Key determinants influencing neosinus hemodynamics following transcatheter aortic valve replacement. The factors are categorized into 2 main groups: (i) Patient‐specific anatomical characteristics (green segment), including coronary artery flow, cardiac output, and native aortic root geometry; and (ii) Prosthesis‐related characteristics (pink segment), encompassing prosthesis type (eg, self‐expanding vs balloon‐expandable), leaflet length, implantation depth, degree of prosthesis expansion and shape of deformation, and intentional leaflet laceration (various techniques). The interplay of these factors collectively determines blood flow patterns within the neosinus, which is critical for assessing risks of flow stasis and subsequent leaflet thrombosis.