With the worldwide use of the frozen elephant trunk (FET) procedure, consideration of distal stent graft-induced new entry (dSINE), a major FET complication, has become essential (1). Herein, we investigated wall shear stress (WSS) using computational fluid dynamics (CFD) analysis before and after dSINE occurrence following acute type A aortic dissection (TAAD) repair using the FET procedure. We consider that true lumen (TL) stenosis with poor aortic remodelling contributes to dSINE occurrence.

A 46-year-old man with no previous cardiovascular risk factors or medical history suffered from acute type A aortic dissection and underwent total arch replacement using a 26-mm 4-branched prosthetic graft (J Graft: Japan Lifeline, Tokyo, Japan) by the FET procedure using a 27–90 mm Frozenix (Japan Lifeline, Tokyo, Japan). During follow-up, the man suffered from back pain and contrast-enhanced computed tomography (CT) revealed dSINE at the FET. We performed additional extended thoracic endovascular aortic repair (TEVAR) for this pathology. The time between TAAD repair and TEVAR was 2 months. The patient was discharged on postoperative day 4 without any complications.

We investigated dSINE hydrodynamically using CFD analysis as we had CT data before and after dSINE. Postoperative computed tomography angiography (CTA) after TAAD repair revealed poor aortic remodelling with severe TL stenosis (Figure 1A). CTA after dSINE continued to show poor aortic remodelling and residual TL stenosis (Figure 1B). CFD analysis revealed a marked increase in WSS coinciding with the TL stenosis site of the descending aorta (Supplementary Video 1), which was thought to have caused a pressure gradient before and after this stenotic site. This pressure gradient may have affected the repetitive stimulation between the fragile dissected septum and the FET, causing dSINE (Supplementary Video 2). CFD analysis after additional extended TEVAR showed a WSS decrease at the descending and downstream aorta (Figure 2).

dSINE, a major FET complication, reportedly occurs up to 25% after 3 years (2). When a prosthesis harder than the fragile dissected aorta is inserted, dSINE has been reported even when a graft elephant trunk was used, the so-called (soft-graft)-induced new entry (3).

Herein, we focused on addressing the possible risk factor of postoperative narrowed TL by analyzing the CFD streamline. An increased WSS just before the blood passes through the stenosis site has been shown in blood flow simulations involving patients with coarctation of the aorta (4). Similarly in this case, CFD analysis 7 days after the FET procedure showed a marked increase in WSS in the TL stenosis proximal site. This was an aortic stenosis-like condition, and repetitive heartbeat stimulation and mechanical stress on the solid FET and vulnerable dissected aorta in the distal arch caused dSINE. Osswald et al. retrospectively investigated WSS in dSINE development using CFD. They reported that elevated WSS may lead to aortic wall weakening which may be considered a risk factor for the progression or development of new dissections sites (5). In their review of 5 cases, they found elevated WSS in the descending aorta, suggesting that residual TL stenosis after the FET procedure may affect dSINE development.

We investigated dSINE hydrodynamically using CFD analysis and considered that the increased WSS due to TL narrowing and the repetitive mechanical contacts between the FET and the dissected and weakened aortic septum could cause dSINE. Poor aortic remodelling with a narrow TL would be a risk factor for dSINE after the FET procedure and TEVAR for type B aortic dissection.