Early Aortic Stiffening after TEVAR: An In Vitro Mock Perfusion Study

C. Mayer; E. Agrafiotis; C. Nebert; P. Regitnig; D. Zimpfer; G. Holzapfel; H. Mächler

doi:10.1055/s-0043-1761776

The Thoracic and Cardiovascular Surgeon, Table of Contents

Thorac Cardiovasc Surg 2023; 71(S 01): S1-S72
DOI: 10.1055/s-0043-1761776

Monday, 13 February

Perioperative Risikoadjustierung

Early Aortic Stiffening after TEVAR: An In Vitro Mock Perfusion Study

Authors

C. Mayer

¹Medical University of Graz, Graz, Austria
E. Agrafiotis

²TU Graz, Graz, Austria
C. Nebert

¹Medical University of Graz, Graz, Austria
P. Regitnig

¹Medical University of Graz, Graz, Austria
D. Zimpfer

¹Medical University of Graz, Graz, Austria
G. Holzapfel

²TU Graz, Graz, Austria
H. Mächler

¹Medical University of Graz, Graz, Austria

Abstract

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Background: Thoracic endovascular repair (TEVAR) stiffens the elastomechanical properties of the aorta from the moment of deployment. Chronically, the stent-wall interaction can lead (cardio)-vascular ramifications that stem from stent-induced biomechanical events. The present experimental study aims to investigate the early biomechanical impact of TEVAR against the aortic wall.

Method: Human cadaver thoracic aortas (n = 10) were exposed to pulsatile perfusion for 8 hours under physiological pressure and volume conditions within a mock circulation loop. The pressure, diameter and compliance variations of the aortas were measured with pressure sensors and a video-extensometer was tracking the cyclic circumferential stretch of the aorta at the proximal landing zone of the stent graft. The compliance variations were visualized and compared by plotting hysteresis loops. After perfusion, biaxial tension tests were conducted to investigate strength and stiffness profiles, respectively, on stented and nonstented samples. Further investigations of possible damage and local alterations caused by the stent or the implantation process were assessed with histological analysis.

Results: In our experiments, there was a significant loss in aortic elasticity (> 25%) indicating global aortic stiffening and compliance mismatch as visualized in the hysteresis loops. Additionally there was a slight increase in systolic blood pressure, revealing reduced energy storage capacities of the stiffer stented aorta. Post-perfusion mechanical analysis reveals tissue stiffening in the stented area compared with the nonstented. That implies elastin loss reflected into the shorter elastic phase of the stress-stretch relationship. Global loss of distensibility and local tissue stiffening occurred already in the first hours post implantation.

Conclusion: For the first time early stiffening after TEVAR has been artificially created and studied. The loss of cyclic distensibility is shown in the hysteresis loops and highlights the compliance mismatch between the stent-graft and aortic wall. The knowledge gained might give a better insight into the etiology of device related problems and provide knowledge on how to refine next-generation stent-grafts meeting a more natural compliance and therefore reducing complications.