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Review
. 2021 Nov;18(184):20210599.
doi: 10.1098/rsif.2021.0599. Epub 2021 Nov 24.

Transcatheter aortic valve thrombosis: a review of potential mechanisms

Affiliations
Review

Transcatheter aortic valve thrombosis: a review of potential mechanisms

Vrishank Raghav et al. J R Soc Interface. 2021 Nov.

Abstract

Transcatheter aortic valve (TAV) thrombosis has been recognized as a significant problem that sometimes occurs as early as within 30 days after valve implantation, leading to increased concerns of stroke and long-term valve durability. In this article, a critical summary of the relevant literature on identifying potential mechanisms of TAV thrombosis from the perspective of the well-known Virchow's triad, which comprises blood flow, foreign materials and blood biochemistry, is presented. Blood flow mechanisms have been the primary focus thus far, with a general consensus on the flow mechanisms with respect to haemodynamic conditions, the influence of TAV placement and expansion and the influence of coronary flow. Less attention has been paid to the influence of blood biochemistry and foreign materials (and related endothelial damage), with little consensus among studies with regards to platelet and/or microparticle levels post-TAV implantation. Finally, we discuss the future outlook for research with unanswered scientific questions.

Keywords: mechanisms; thrombosis; transcatheter aortic valve.

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Figures

Figure 1.
Figure 1.
Explanted TAV with thrombus on two cusps [12]. Reproduced with permission from Lippincott Williams & Wilkins.
Figure 2.
Figure 2.
Depiction of the anatomic sinus (1) and the neo-sinus (2) [24]. Reproduced with permission from Lippincott Williams & Wilkins.
Figure 3.
Figure 3.
Virchow's triad describes three primary factors that are widely believed to contribute to thrombosis.
Figure 4.
Figure 4.
Sub- (IAD) versus supra-annular (SAD) deployment of TAVs [39]. Reproduced with permission from Springer.
Figure 5.
Figure 5.
Top view of time evolution of BRT contours on valve leaflets during a cardiac cycle for the (a) 100% expanded TAV, (b) 90% expanded TAV and (c) 80% expanded TAV. From left to right column: early systole, mid-acceleration, peak systole, mid-deceleration, end-systole, mid-diastole and end-diastole. BRT: blood residence time was computed using methods described in the Data analysis and metrics section [42]. Reproduced with permission from Oxford University Press.
Figure 6.
Figure 6.
Flow streamlines and velocity fields for (a) intra-annular deployment and (b) supra-annular deployment. A comparison between the neo-sinus adjacent to the left coronary cusp (LCC; experimental case) and the neo-sinus adjacent to the non-coronary cusp (NCC; control case) illustrates the increase in coronary flow. The different rows indicate different time points during diastole, shown by the red lines on the aortic and coronary flow curves [39]. Reproduced with permission from Springer.
Figure 7.
Figure 7.
Change in (a) serum D-dimer concentration and (b) TAT concentration with the introduction of a foreign material (SAPIEN XT: stent-with-skirt versus entire valve) illustrating the influence on thrombosis markers when compared with a control group indicating the significance of blood–stent and blood–skirt interactions in TAV thrombosis [58]. Reproduced with permission from Springer.

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