Transcatheter aortic valves produce unphysiological flows which may contribute to thromboembolic events: An in-vitro study

Abstract

PurposeTranscatheter aortic valve implantation (TAVI) has been associated with large incidence of ischemic events, whose sources are still unclear. In fact, sub-acute complications cannot be directly related to the severity of the calcification in the host tissues, nor with catheter manipulation during the implant. A potential cause could be local flow perturbations introduced by the implantation approach, resulting in thrombo-embolic consequences. In particular, contrary to the surgical approach, TAVI preserves the presence of the native leaflets, which are expanded in the paravalvular space inside the Valsalva sinuses. The purpose of this study is to verify if this configuration can determine hemodynamic variations which may promote blood cell aggregation and thrombus formation.MethodsThe study was performed in vitro, on idealized models of the patient anatomy before and after TAVI, reproducing a range of physiological operating conditions on a pulse duplicator. The fluid dynamics in the Valsalva sinuses was analyzed and characterized using phase resolved Particle Image Velocimetry.ResultsComparison of the flow downstream the valve clearly indicated major alterations in the fluid mechanics after TAVI, characterized by unphysiological conditions associated with extended stagnation zones at the base of the sinuses.ConclusionThe prolonged stasis observed in the Valsalva sinuses for the configuration modelling the presence of transcatheter aortic valves provides a fluid dynamic environment favourable for red blood cell aggregation and thrombus formation, which may justify some of the recently reported thromboembolic and ischemic events. This suggests the adoption of anticoagulation therapies following TAVI, and some caution in the patients׳ selection.

Bioprosthetic aortic valve durability in the era of transcatheter aortic valve implantation

“…Lesions at the surface of leaflets during the TAVI procedure, abnormal transvalvular flow pattern due to deformed stent and impaired leaflet kinetics, as well as areas of flow stasis within the stent or between the stent and the native aortic valve leaflets or aortic root may promote leaflet thrombosis 55. In turn, valve thrombosis, even if treated successfully with warfarin, may subsequently cause inflammation and fibrocalcific remodelling of leaflets (figure 1).…”

Hemodynamic durability of transcatheter aortic valves using the updated Valve Academic Research Consortium‐2 criteria

“…Although, a previous case report showed that patients who developed self‐expandable bioprosthetic valve thrombosis after TAVR had deep valve implantation depth (8 mm), our study is the first to show the association between valve implantation depth and worsening transprosthetic mean gradients after TAVR. On pathologic review, valve thrombosis occurs in the NCC or RCC more commonly and in vitro experiments suggest that the presence of TAV and the native AV in the paravalvular space produces non‐physiological flow in the aortic root that leads to stagnation at the aortic sinuses . After TAVR, native valve leaflets are expanded by the valve frame and formulate the cylindrical wall .…”

“…29 After TAVR, native valve leaflets are expanded by the valve frame and formulate the cylindrical wall. 29,30 When valves were implanted in a deeper position within the LVOT, it is possible that a neo-sinus created between the native valve and the artificial AV can be a nidus for thrombosis ( Figure 6). This may also increase the exposed area of the native valve and exaggerate the non-physiological flow in aortic root.…”

Importance of the valve durability-life expectancy ratio in selection of a prosthetic aortic valve

“…During the TAVI procedure, the native valve leaflets are compressed between the prosthetic valve and aortic wall. This environment is associated with an extended zone of flow stagnation zone at the base of the sinus that may promote thrombus formation resulting in valve leaflet thrombosis and/or embolic events 19. Whether thrombus formation might lead to further progressive leaflet structural changes and eventually SVD is yet unknown.…”