Persistent Intraluminal Pressure After Endovascular Stent Grafting for Type B Aortic Dissection

Despite technically successful thoracic endovascular stent graft repair (TEVAR) in patients with Stanford Type B aortic dissection (TBAD), long-term follow up studies have shown that the false lumen may continue to dilate. The aim of this study was to analyze the possible mechanisms leading to such changes from a hemodynamic perspective.

Twenty-eight ex vivo fresh porcine TBAD models (Mo A: 10; Model B: 12; Model C: 6) were established to simulate three clinical situations: Model A with patent false lumen (pre-TEVAR); Model B with distal re-entry only (post-TEVAR), and Model C with thrombus filling in the false lumen and a distal re-entry (chronic stage of post-TEVAR). Synchronous pressure waveforms were taken from both the true and the false lumen. True lumen and false lumen pressure differences were calculated for each model as four indices: systolic index (SI), diastolic index (DI), mean pressure index (MPI) and area under curve index (AUCI). These indices were compared between the three models.

False lumen pressure and corresponding pressure-accumulating effects were significantly higher in Model A than in Model C: SI (99.9% vs. 189.4%; p < .001); MPI and AUCI (99.5% vs. 128.2%; 99.5% vs. 128%; p < .001). The SI, MPI, and AUCI were significantly higher in Model B compared with Model C. The differences between the four indices were not significant between Model A and B. The false lumen area under curve (AUC) in Model C was merely lowered by 20% compared with its true lumen (67.5 mmHg vs. 85.2 mmHg).

The false lumen pressure remained unchanged in the non-thrombosed segment with patent blood flow after the primary entry tear sealed. Intraluminal pressure reduction in the thrombosed false lumen was significant. However, nearly 80% of the pressure remained in the thrombosed false lumen. If this high intra-thrombus pressure persists, it may contribute to delayed aneurysmal formation after endovascular treatment.