K-X Qing1, Y-C Chan2, A C W Ting2, S W K Cheng3. 1. Department of Vascular Surgery, The First Hospital Affiliated to Kunming Medical University, Kunming Medical University, Kunming, Yunnan, PR China. 2. Division of Vascular Surgery, Department of Surgery, The University of Hong Kong, Queen Mary Hospital, Hong Kong, Hong Kong Special Administrative Region. 3. Division of Vascular Surgery, Department of Surgery, The University of Hong Kong, Queen Mary Hospital, Hong Kong, Hong Kong Special Administrative Region. Electronic address: wkcheng@hku.hk.
Abstract
OBJECTIVES: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.
OBJECTIVES: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.
Authors: David Marlevi; Julio A Sotelo; Ross Grogan-Kaylor; Yunus Ahmed; Sergio Uribe; Himanshu J Patel; Elazer R Edelman; David A Nordsletten; Nicholas S Burris Journal: J Cardiovasc Magn Reson Date: 2021-05-13 Impact factor: 5.364
Authors: Aashish Ahuja; Xiaomei Guo; Jillian N Noblet; Joshua F Krieger; Blayne Roeder; Stephan Haulon; Sean Chambers; Ghassan S Kassab Journal: Front Physiol Date: 2018-05-09 Impact factor: 4.566