Key result
False-lumen intercostal arteries reduce thrombosis-promoting hemodynamics vs true-lumen origins, inhibiting stable false-lumen thrombosis.
Why the study?
The hemodynamic influence of intercostal artery origin on long-term false lumen thrombosis in patients with type B aortic dissection after TEVAR required clarification.
Does intercostal artery origin from the false lumen compared to the true lumen impair false lumen thrombosis propensity in post-TEVAR type B aortic dissection models?
Does intercostal artery origin from the false lumen compared to the true lumen impair false lumen thrombosis propensity in post-TEVAR type B aortic dissection models?
Computational fluid dynamics simulations indicate that intercostal arteries originating from the false lumen alter local hemodynamics and may inhibit stable false lumen thrombosis after TEVAR in type B aortic dissection, suggesting a potential anatomical marker for risk stratification.
Answers are grounded in this paper and cite their sources.
False-lumen intercostal origin was associated with lower SAR-TAWSS/OSI; leaves open predictive role for FL thrombosis after TEVAR.
Objective This study aimed to investigate the influence of intercostal artery origin on long-term FL thrombosis in TBAD patients after TEVAR using the computational fluid dynamics. Methods Patient-specific three-dimensional models of post-operative type B aortic dissection (TBAD) were reconstructed from preoperative computed tomography angiography (CTA) images. Intercostal arteries were segmented separately and virtually repositioned to originate from either the true or false lumen. Numerical simulations were performed to investigate the hemodynamic impact of intercostal arteries origin(IAO) on false lumen thrombosis propensity. Results Hemodynamic analysis demonstrated that the site of origin of intercostal arteries modulated the flow pattern within the false lumen. When arising from the true lumen (M-T), streamlines in the false lumen remained smooth and orderly, with no evident vortices; in contrast, origin from the false lumen (M-F) induced marked flow separation and complex vortex structures in the distal false lumen, accompanied by substantially greater streamline disturbance. Pressure analysis showed that in all models, true lumen pressure exceeded false lumen pressure and decreased along the aortic course, whereas false lumen pressure remained relatively steady. The pressure-difference curves overlapped extensively across origin groups, indicating a negligible influence of IAO on transmural pressure load. Furthermore, compared with M-T, M-F exhibited lower SAR-TAWSS (M1–M3: 73.75% vs. 80.24%, 47.09% vs. 63.64%, 71.04% vs. 77.46%), lower SAR-OSI (70.05% vs. 82.65%, 37.72% vs. 67.72%, 56.30% vs. 61.99%), and lower SAR-RRT (65.35% vs. 77.40%, 36.55% vs. 57.33%, 52.09% vs. 61.40%). Conclusion Based on CFD analysis, this study elucidates the correlation between the presence of intercostal arteries and the potential for thrombus formation within the FL in patients with TBAD following TEVAR. Specifically, intercostal arteries originating from the false lumen can inhibit stable thrombus formation within the FL by altering the local hemodynamic environment after TEVAR, thereby exerting an adverse effect on favorable false lumen remodeling. These findings suggest that incorporating the anatomical characteristics of the intercostal arteries into the predictive evaluation system for long-term clinical outcomes after TEVAR holds considerable clinical significance and may serve as a potential reference indicator for risk stratification and individualized follow-up management.
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Wang et al. (2026) studied Post-operative type B aortic dissection (TBAD) after thoracic endovascular aortic repair (TEVAR) (n=3). Intercostal arteries originating from the false lumen (M-F) vs. Intercostal arteries originating from the true lumen (M-T) was evaluated on False lumen thrombosis propensity and hemodynamic parameters (SAR-TAWSS, SAR-OSI, SAR-RRT). Intercostal arteries originating from the false lumen vs true lumen exhibited lower SAR-TAWSS (e.g., M1: 73.75% vs 80.24%), SAR-OSI, and SAR-RRT, inhibiting stable thrombus formation.
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