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. 2024 Jun;52(6):1554-1567.
doi: 10.1007/s10439-024-03462-8. Epub 2024 Apr 8.

Computational Investigation of Vessel Injury Due to Catheter Tracking During Transcatheter Aortic Valve Replacement

Affiliations

Computational Investigation of Vessel Injury Due to Catheter Tracking During Transcatheter Aortic Valve Replacement

David G Symes et al. Ann Biomed Eng. 2024 Jun.

Abstract

Catheter reaction forces during transcatheter valve replacement (TAVR) may result in injury to the vessel or plaque rupture, triggering distal embolization or thrombosis. In vitro test methods represent the arterial wall using synthetic proxies to determine catheter reaction forces during tracking, but whether they can account for reaction forces within the compliant aortic wall tissue in vivo is unknown. Moreover, the role of plaque inclusions is not well understood. Computational approaches have predicted the impact of TAVR positioning, migration, and leaflet distortion, but have not yet been applied to investigate aortic wall reaction forces and stresses during catheter tracking. In this study, we investigate the role that catheter design and aorta and plaque mechanical properties have on the risk of plaque rupture during TAVR catheter delivery. We report that, for trackability testing, a rigid test model provides a reasonable estimation of the peak reaction forces experienced during catheter tracking within compliant vessels. We investigated the risk of rupture of both the aortic tissue and calcified plaques. We report that there was no risk of diseased aortic tissue rupture based on an accepted aortic tissue stress threshold (4.2 MPa). However, we report that both the aortic and plaque tissue exceed a rupture stress threshold (300 kPa) with and without the presence of stiff and soft plaque inclusions. We also highlight the potential risks associated with shorter catheter tips during catheter tracking and demonstrate that increasing the contact surface will reduce peak contact pressures experienced in the tissue.

Keywords: Aorta; Atherosclerosis; Catheter trackability; Finite element analysis; Plaque rupture; Transcatheter aortic valve replacement.

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Conflict of interest statement

David G. Symes, Professor Laoise M. McNamara, and Dr. Claire Conway are collaborating with Medtronic under an Irish Research Council Enterprise Partnership Scheme Postgraduate Scholarship.

Figures

Fig. 1
Fig. 1
a Flowchart linking study objective with aorta model type analysed, b 3D representation and measurements of idealized aortic arch and catheter material shafts identified per Table 1; c Anonymised (outline of morphology—edited per request) benchtop in vitro model during catheter trackability testing
Fig. 2
Fig. 2
2D representation and measurements of varying idealized tip geometries that are used to investigate the impact catheter tip lengths have on reaction forces and contact pressures during tracking
Fig. 3
Fig. 3
Stages of the catheter’s progress while tracking around the a in vitro test anatomy and b in-silico idealized aorta arch. Timepoints signify start point and in vitro test reaction force peaks presented in c Predicted temporal reaction force obtained from the FE simulation compared with in vitro reaction force data. All data are normalised against the first in vitro reaction force peak
Fig. 4
Fig. 4
Predicted temporal reaction forces obtained from the rigid and biomechanically representative model simulations. All data are normalised against the first in vitro reaction force peak (see Fig. 3c)
Fig. 5
Fig. 5
a Cross-section image of idealized aorta arch (pink) with plaques (yellow). Maximum principal stresses were analysed in the histograms at three key displacement time points, based on reaction force-displacement curves: D1 (distal upper arch), D2 (proximal upper arch), and D3 (proximal aorta arch). b Predicted temporal reaction forces obtained from simulations with the biomechanically representative model with no plaques (5 MPa) and the model with stiff and soft plaque inclusions. All data are normalised against the first in vitro reaction force peak (see Fig. 3c). c Histograms of logarithmic max principal stress per logarithmic element volume of the aorta arch wall without plaque inclusions at the displacement points highlighted. The rupture stress threshold, H1 = 0.833˙ Et = 4.1667 MPa
Fig. 6
Fig. 6
a Histograms of logarithmic maximum principal stress per logarithmic element volume of the aorta arch wall with plaque inclusions at the displacement points depicted in Fig. 5a. The rupture stress threshold, H2 = 0.3 MPa; bd Contour plots of max principal stress at key displacement points, see Fig. 5a, for the idealized aorta model with stiff plaques, soft plaques, and no plaques, respectively. The first legend corresponds to the stiff plaques only, the second legend corresponds to both the soft plaques and no plaque models
Fig. 7
Fig. 7
a Contour plots of contact pressure for each tip length (6, 12, 18 & 24 mm), overlaid at key displacement timepoints (D1–D3), see Fig. 5a, during catheter tracking within the idealized rigid aorta model; b Histograms of logarithmic tip contact pressure (CPRESS) per logarithmic element surface area of the rigid aorta wall at the displacement points depicted in Fig. 5a
Fig. 8
Fig. 8
2D representation and tip angle of deflection measurements of varying idealized tip lengths (6–24 mm) during tracking at three key displacement points (D1–D3), see Fig. 5a

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