Valérie Deplano

Background: Long-term follow-up after endovascular aortic repair (TEVAR) is crucial to detect adverse aortic remodeling, even with modern stent grafts offering enhanced flexibility and durability. Conventional imaging, based on diameter measurements, may fail to identify complications such as endograft migration. Methods: We conducted a longitudinal 3D geometric analysis of thoracic aortic and stent-graft evolution over 10 years in a patient treated for descending thoracic aortic aneurysm (DTAA) by endovascular treatment. A three-dimensional morphological analysis (length, tortuosity, angulation, and diameter) was carried out using advanced imaging software (EndoSize, MATLAB) to track aortic geometry and stent-graft behavior over time. A focused review of the literature on stent-graft migration, its risk factors, complications, and surveillance strategies was also performed. Results: This case illustrates how progressive geometric remodeling—including aortic elongation and increased tortuosity—can lead to delayed stent-graft migration and late type III endoleaks, with an elevated risk of rupture. The 3D analysis revealed early morphological changes that were undetectable using standard diameter-based follow-up. These observations are consistent with published data showing higher migration rates over time, particularly in tortuous anatomies. The literature review further emphasizes the clinical relevance of geometric surveillance, given the high rates of reintervention, morbidity, and mortality associated with stent-graft migration. Conclusions: This study underlines the importance of personalized and geometry-based surveillance after TEVAR. Advanced morphological assessment tools provide valuable insights for the early detection of complications and tailored patient management. Their integration into routine follow-up could help optimize long-term outcomes and prevent life-threatening events such as rupture.

Clinical monitoring of thoracic aortic aneurysms (TAA) to determine therapeutic intervention is based on morphological indicators, mainly the maximum diameter and its annual growth rate, which are not sufficiently discriminating. It is therefore necessary to propose studies to predict the evolution of this pathology at an early stage, to make the best decision on the timing of therapeutic intervention. Biomimetic numerical modeling of patients with TAA, coupled with longitudinal studies, would allow to analyse the relevance of certain hemodynamic markers in predicting adverse outcomes. The aim of this study is to develop such biomimetic modeling. To this end, i) the displacement of TAA is determined from magnetic resonance imaging (MRI) images with appropriate spatio-temporal resolutions, ii) then implemented in an advanced numerical model, the results of which iii) are compared with 4D flow MRI data. The results obtained show that i) the 3D patient-specific displacement of pathological aorta can be captured within the limits of the best available medical image spatial and temporal resolution, ii) the use of imposed displacements as boundary conditions allows the aortic heterogeneity of displacements and movements of the aortic root to be accounted while reducing the computational time compared to fluid-structure interaction modeling.

Post-TEVAR (thoracic endovascular aortic repair) follow-up is essential to monitor adverse aortic remodeling, despite technological advancements in stent grafts regarding their flexibility and durability. This article, along with the study of a clinical case over 10 years, explores the use of 3D morphological analysis and shows how type III endoleaks can drastically alter the morphology of the aorta. The literature review was to report the cumulative incidence of endograft migration as well as the morbidity, reintervention rates, and mortality related to endograft migration, to justify the importance of close standardized surveillance after TEVAR.

Aim: Blood flow-induced mechanical forces, particularly wall shear stress (WSS), play a fundamental role in aortic valve remodeling and maturation. Dysregulation of these processes contributes to age-related valve diseases, such as aortic stenosis and regurgitation. While epidermal growth factor receptor (EGFR) signaling has been implicated in valve development, its role in mechanotransduction remains unclear. This study aims to investigate how EGFR regulates WSS-induced signaling in valvular cells and explore its interaction with the mechanosensitive ion channel PIEZO1. Methods and Results: To investigate the role of EGFR in valvular cell mechanotransduction, we used conditional Egfr ^flox allele to selectively delete Egfr in valvular cells. Histological analysis revealed increased valve leaflet thickness and hyperproliferation of mesenchymal cells when Egfr was deleted both endothelial (Tie2-Cre lineage) and mesenchymal (Sm22α-Cre lineage) cells. This was accompanied by a reduction in maturation-related genes ( Egr1, Nos3, Tgf-β ) and extracellular matrix (ECM) components. We previously demonstrated that Egr1 expression is regulated by WSS in valvular endothelial cells, prompting further exploration of Egr1’s role in valvular cells. In vitro, Egr1 overexpression and shRNA-mediated knockdown confirmed its role in regulating Nos3, Col1a1, and Tgf-β , key mediators of valve remodeling. Using a pulsatile WSS-mimicking device, we found that WSS induces Erk1/2 phosphorylation and Egr1 expression in valvular cells, both of which were abolished by EGFR inhibition. However, direct EGFR activation via EGF failed to replicate WSS-induced Egr1 expression, suggesting the involvement of additional mechanosensitive pathways. Pharmacological studies further revealed that PIEZO1 inhibition impaired WSS-induced Egr1 expression, while PIEZO1 activation (via YODA) mimicked WSS effects on Erk1/2 phosphorylation and Egr1 expression. These findings suggest a functional interaction between EGFR and PIEZO1 in mechanotransduction, linking mechanical forces to key molecular pathways in valve remodeling. Conclusion: Our findings establish EGFR as a critical mediator of WSS-induced mechanotransduction in valve remodeling, working in synergy with PIEZO1 to regulate flow-sensitive transcription factors such as Egr1. This study provides new insights into the molecular mechanisms governing valve maturation and highlights potential therapeutic targets for age-related valve pathologies linked to abnormal WSS responses. Translational Perspective: Our study highlights the pivotal role of EGFR and the mechanosensitive ion channel PIEZO1 in aortic valve cell responses to wall shear stress (WSS), offering new insights into valve remodeling. The findings suggest that dysregulated EGFR signaling contributes to valve thickening and stenosis, key factors in age-related valvular heart disease. By identifying EGFR-PIEZO1 as a critical mechanotransduction pathway, our work provides a potential therapeutic target for early intervention in aortic valve disease. Modulating EGFR or PIEZO1 activity could help mitigate pathological valve remodeling, presenting novel strategies for treating or preventing degenerative valve disorders.

Objectives: To assess the ability of the aortic aneurysm volume (AAV), aneurysmal lumen volume (ALV), and aneurysmal thrombus volume (ATV) to predict the need for aortic reintervention when using the maximal aortic diameter as a reference. Methods: This monocentric retrospective study included 31 consecutive patients who underwent successful thoracic endovascular aortic repair (TEVAR) to treat an atheromatous thoracic aortic aneurysm. All patients underwent clinical and computed tomography angiography (CTA) for 3 years after TEVAR. The patients were categorized into group 0 if no aortic reintervention was required during the follow-up period and categorized into group 1 if they experienced a type I or III endoleak or aneurysm diameter increase requiring intervention. The maximum aneurysm sac diameter and the AAV, ALV, and ATV were calculated using CTA images obtained preoperatively (T0) and at 6–12 months (T1), 24 months (T2), and 36 months (T3) postoperatively, and their changes over time were analyzed. Correlations between diameter and changes in AAV, ALV, and ATV were assessed, and the association between diameter and volume changes and reintervetion was examined. The cutoff values for predicting the need for reintervention was determined using a receiver operating characteristic (ROC) curve. The accuracy of volume change versus diameter change for predicting the need for reintervention was analyzed. Results: There were no significant differences in terms of the mean aneurysm diameter or AAV, ALV or ATV between the groups at preoperative CTA or after one year of follow-up imaging. The mean ATV was higher in group 1 than in group 0 at 2 years (187.6 ± 86.3 mL vs. 114.7 ± 64.7 mL; p = 0.057) and after 3 years (195.0 ± 86.7 mL vs. 82.1 ± 39.9 mL; p = 0.013). The maximal diameter was greater in group 1 than in group 0 at 3 years (67.3 ± 9.5 mm vs. 55.3 ± 12.6 mm; p = 0.044). The rate of AAV change between T0 and T1 was significantly higher in group 1 (7 ± 4.5%) than in group 0 (−6 ± 6.8%; p < 0.001). The rate of ATV change between T1-T3 was significantly higher in group 1 than in group 0 (34 ± 40.9% vs. −13 ± 14.4% (p = 0.041)); similar results were observed for the rate of ATV change between T2 and T3 (27 ± 50.1% for group 1 vs. −8 ± 49.5% in group 0 (p < 0.001)). According to our multivariate analysis, the annual growth rate for AAV between T0 and T1 was the only independent factor that was significantly associated with aortic reintervention (area under the curve (AUC) = 0.84, OR = 1.57, p = 0.025; optimal cutoff +0.4%). An increase in the annual growth rate of the ATV between T0 and T3 was independently associated with the need for aortic reintervention (area under the curve (AUC) = 0.90, OR = 1.11, p = 0.0347; optimal cutoff +10.1%). Conclusions: Aortic volume analysis can predict the need for aortic reintervention more accurately and earlier than maximal aortic diameter.

Background: The aim of this study was to evaluate the aortic diameter and volume during the first year after a type A repair to predict the long-term prognosis of a residual aortic dissection (RAD). Methods: All patients treated in our center for an acute type A dissection with a RAD and follow-up > 3 years were included. We defined two groups: group 1 with dissection-related events (defined as an aneurysmal evolution, distal reintervention, or aortic-related death) and group 2 without dissection-related events. The aortic diameters and volume analysis were evaluated on three postoperative CT scans: pre-discharge (T1), 3–6 months (T2) and 1 year (T3). Results: Between 2009 and 2016, 54 patients were included. Following a mean follow-up of 75.4 months (SD 31.5), the rate of dissection-related events was 62.9% (34/54). The total aortic diameters of the descending thoracic aorta were greater in group 1 at T1, T2 and T3, with greater diameters in the FL (p < 0.01). The aortic diameter evolution at 3 months was not predictive of long-term dissection-related events. The total thoracic aortic volume was significantly greater in group 1 at T1 (p < 0.01), T2 (p < 0.01), and T3 (p < 0.01). At 3 months, the increase in the FL volume was significantly greater in group 1 (p < 0.01) and was predictive for long-term dissection-related events. Conclusion: This study shows that an initial CT scan volume analysis coupled with another at 3 months is predictive for the long-term evolution in a RAD. Based on this finding, more aggressive treatment could be given at an earlier stage.

Residual type B aortic dissection was numerically investigated to highlight the contribution of biomechanical parameters to the pathology’s evolution. Patient-specific geometries from cases involving both favorable and unfavorable evolution were modeled to assess their hemodynamic features. This original approach was supported by a longitudinal study confirming the association between morphological changes, hemodynamic features, adverse clinical outcomes, and CT-angioscan observations on the same patient. Comparing one patient with unfavorable evolution with one with favorable one, we identify potential biomechanical indicators predictive of unfavorable evolution: (i) a patent false lumen with a flow rate above 50% of inlet flow rate; (ii) high wall shear stress above 18 Pa at entry tears, and above 10 Pa at some regions of the false lumen wall; (iii) low time-averaged wall shear stress in distal false lumen below 0.5 Pa; (iv) vortical structure dynamics. Although these comparisons could only be conducted on 2 patients and need to be confirmed by a larger number of cases, our findings point to these hemodynamic markers as possible candidates for early evaluation of the pathology’s evolution towards an unfavorable scenario. Correlation between hemodynamics index and thrombus initiation for unfavorable case. ET₂ and ET₃ are entry tear numbers 2 and 3 respectively. WSS is wall shear stress. TAWSS is time average shear stress