Visceral Debranching for the Treatment of Thoracoabdominal Aortic Aneurysms: Based on a Presentation at the 2013 VEITH Symposium, November 19-23, 2013 (New York, NY, USA).

Surgical repair of thoracoabdominal aortic aneurysms (TAAA) is associated with significant morbidity and mortality. Hybrid approaches that involve visceral debranching and aortic endografting allow for an alternative approach in certain high-risk patients. In most circumstances the visceral vessels can be bypassed in a retrograde manner from the iliac arteries via a midline laparotomy, and the aortic aneurysm subsequently excluded with standard aortic endografts. These procedures avoid the extensive two-cavity exposure, aortic cross-clamping, and mechanical circulatory support that comprise open TAAA repair, and offer the theoretical advantage of being less invasive. Despite this, outcomes have been mixed with reported perioperative mortality rates of 0% and 34% and permanent paraplegia rates of 0% to 13% in most major series. The reported outcomes, as well as the variation between centers, highlight the importance of patient selection in undertaking hybrid repair. In practice, the best outcomes are achieved in patients who have high-risk anatomy, rather than high-risk comorbidities.

The complications of uncomplicated acute type-B dissection: the introduction of the Penn classification.

Uncomplicated acute type-B aortic dissection (ATBAD) is a misnomer because it has subgroups with excessive mortality risk. The Penn classification has designated these ATBAD presentations as class-A because they initially are characterized by the absence of malperfusion and/or aortic rupture. The Penn classification also has designated class-A high-risk subgroups as type I and low-risk subgroups as type II. The risk factors for Penn class-A type-I presentations relate to medical therapy; aortic anatomy, and dissection extent as outlined by the DeBakey classification. Tight medical therapy significantly protects against aortic complications. Beta-blockade, angiotensin inhibition, and calcium channel antagonists may reduce mortality. The details of optimal medical therapy require further research. The aortic risk factors for type-I presentations include false lumen size and patency, ulcer-like projections, aortic diameter >40 mm, and intimal tear characteristics such as size and proximal location. The prognostic role of dissection extent in ATBAD remains unclear, requiring further investigation to determine its effect on natural history. Future trials in Penn class-A ATBAD should focus on type-I presentations. The Penn classification can serve as a clinical framework for trial design, laying the groundwork for future management advances. It also may provide a common language to facilitate standardized definitions, trial design, and management approaches for this high-risk patient cohort.

Increased wall stress of saccular versus fusiform aneurysms of the descending thoracic aorta.

BACKGROUND: Repair of fusiform descending thoracic aortic aneurysms (DTAs) is indicated when aneurysmal diameter exceeds a certain threshold; however, diameter-related indications for repair of saccular DTA are less well established. METHODS: Human subjects with fusiform (n = 17) and saccular (n = 17) DTAs who underwent computed tomographic angiography were identified. Patients with aneurysms related to connective tissue disease were excluded. The thoracic aorta was segmented, reconstructed, and triangulated to create a mesh. Finite element analysis was performed using a pressure load of 120 mm Hg and a uniform aortic wall thickness of 3.2 mm to compare the pressure-induced wall stress of fusiform and saccular DTAs. RESULTS: The mean maximum diameter of the fusiform DTAs (6.0 ± 1.5 cm) was significantly greater (p = 0.006) than that of the saccular DTAs (4.4 ± 1.8 cm). However, mean peak wall stress of the fusiform DTAs (0.33 ± 0.15 MPa) was equivalent to that of the saccular DTAs (0.30 ± 0.14 MPa), as found by using an equivalence threshold of 0.15 MPa. The mean normalized wall stress (peak wall stress divided by maximum aneurysm radius) of the saccular DTAs was greater than that of the fusiform DTAs (0.16 ± 0.09 MPa/cm vs. 0.11 ± 0.03 MPa/cm, p = 0.035). CONCLUSIONS: The normalized wall stress for saccular DTA is greater than that for fusiform DTA, indicating that geometric factors such as aneurysm shape influence wall stress. These results suggest that saccular aneurysms may be more prone to rupture than fusiform aneurysms of similar diameter, provide a theoretical rationale for the repair of saccular DTAs at a smaller diameter, and suggest investigation of the role of biomechanical modeling in surgical decision making is warranted.

Pathogenesis of acute aortic dissection: a finite element stress analysis.

BACKGROUND: Type A and type B aortic dissections typically result from intimal tears above the sinotubular junction and distal to the left subclavian artery (LSA) ostium, respectively. We hypothesized that this pathology results from elevated pressure-induced regional wall stress. METHODS: We identified 47 individuals with normal thoracic aortas by electrocardiogram-gated computed tomography angiography. The thoracic aorta was segmented, reconstructed, and triangulated to create a geometric mesh. Finite element analysis using a systolic pressure load of 120 mm Hg was performed to predict regional thoracic aortic wall stress. RESULTS: There were local maxima of wall stress above the sinotubular junction in the ascending aorta and distal to the ostia of the supraaortic vessels, including the LSA, in the aortic arch. No local maximum of wall stress was found in the descending thoracic aorta. Comparison of the mean peak wall stress above the sinotubular junction (0.43 ± 0.07 MPa), distal to the LSA (0.21 ± 0.07 MPa), and in the descending thoracic aorta (0.06 ± 0.01 MPa) showed a significant effect for wall stress by aortic region (p < 0.001). CONCLUSIONS: In the normal thoracic aorta, there are peaks in wall stress above the sinotubular junction and distal to the LSA ostium. This stress distribution may contribute to the pathogenesis of aortic dissections, given their colocalization. Future investigations to determine the utility of image-derived biomechanical calculations in predicting aortic dissection are warranted, and therapies designed to reduce the pressure load-induced wall stress in the thoracic aorta are rational.