Faculty Bibliography

OBJECTIVE:The new Society for Vascular Surgery/Society for Thoracic Surgery reporting standards for type B aortic dissection (TBAD) categorize clinical presentations of aortic dissection into uncomplicated, high-risk features (HRF), and complicated groups. Although it is accepted that complicated dissections require immediate repair, the optimal timing of repair for HRF has yet to be established. This study aims to identify the ideal timing of thoracic endovascular aortic repair (TEVAR) for HRF, as well as outcomes associated with specific HRF. METHODS:The Vascular Quality Initiative was queried for TEVARs performed for acute and subacute TBAD with HRF from 2014 to 2020. Rupture, malperfusion, and uncomplicated patients were excluded. HRF were defined per the guidelines as refractory hypertension, pain, or rapid expansion/aneurysm of more than 40 mm. The primary outcomes were in-hospital/30-day mortality and 1-year survival with primary exposure variables being days from symptoms to repair and number of HRFs. Secondary outcomes were spinal cord ischemia, stroke, and retrograde type A dissection (RTAD). RESULTS:Of the 1100 patients who met inclusion criteria, 811 had one HRF, 249 had two, and 40 had three. There were no significant differences in primary or secondary outcomes based on number of HRFs. There were 309 patients who underwent repair at 0 to 2 days, 262 at 3 to 6 days, 270 at 7 to 14 days, and 259 at 15 days or more. TEVAR performed at 15 days or more was independently associated with lower in-hospital/30-day mortality (odds ratio, 0.38; P = .0388) and improved 1-year survival. Postoperative stroke was associated with earlier repair (0-2 days). There was no association of timing of repair with spinal cord ischemia, retrograde type A dissection or reintervention. CONCLUSIONS:TEVAR for TBAD with HRF delayed at least 15 days from symptom onset is associated with improved survival, supporting the theory that it is best to delay TEVAR until the subacute phase. Additionally, TEVAR delayed at least 3 days is associated with a decrease in stroke. Having more than one HRF was not associated statistically with worse outcomes. Because the classification of HRF is relatively new and without guidelines for repair, this study highlights the risks of early intervention for HRF and suggests that these patients seem to benefit from at least a short stabilization period before TEVAR.

BACKGROUND:Resuscitative endovascular balloon occlusion of the aorta (REBOA) achieves temporary hemorrhage control via aortic occlusion. Existing REBOA literature focuses on blunt trauma without a clearly defined role in penetrating trauma. This study compared clinical/injury data and outcomes after REBOA in penetrating vs blunt trauma. STUDY DESIGN:All patients in the Aortic Occlusion for Resuscitation in Trauma and Acute Care Surgery (AORTA) database, an observational American Association for the Surgery of Trauma dataset of trauma patients requiring aortic occlusion, who underwent REBOA were included (January 2014 through February 2021). Study groups were defined by mechanism: penetrating vs blunt. Subgroup analysis was performed of patients arriving with vital signs. Univariable/multivariable analyses compared injuries and outcomes. RESULTS:Seven hundred fifty-nine patients underwent REBOA: 152 (20%) penetrating and 607 (80%) blunt. Patients undergoing penetrating REBOA were less severely injured (injury severity score 25 vs 34; p < 0.001). The most common hemorrhage source was abdominal in penetrating REBOA (79%) and pelvic in blunt REBOA (31%; p = 0.002). Penetrating REBOA was more likely to occur in the operating room (36% vs 17%) and less likely in the emergency department (63% vs 81%; p < 0.001). Penetrating REBOA used more zone I balloon deployment (76% vs 64%) and less zone III (19% vs 34%; p = 0.001). Improved or stabilized hemodynamics were less frequent after penetrating REBOA (41% vs 62%, p < 0.001; 23% vs 41%, p < 0.001). On subgroup analysis of patients arriving alive, improvement or stabilization in hemodynamics was similar between groups (87% vs 86%, p = 0.388; 77% vs 72%, p = 0.273). Penetrating REBOA was not independently associated with mortality (odds ratio 1.253; p = 0.776). CONCLUSIONS:Despite lower injury severity, REBOA was significantly less likely to improve or stabilize hemodynamics after penetrating trauma. Among patients arriving alive, however, outcomes were comparable, suggesting that penetrating REBOA may be most beneficial among patients with vital signs. Because hemorrhage source, catheter insertion setting, and deployment zone varied significantly between groups, existing blunt REBOA data may not be appropriately extrapolated to penetrating trauma. Further study of REBOA as a means of aortic occlusion in penetrating trauma is needed.

OBJECTIVE:The optimal revascularization modality following complete resection of aortic graft infection (AGI) without enteric involvement remains unclear. The purpose of this investigation is to determine the revascularization approach associated with the lowest morbidity and mortality using real-world data in patients undergoing complete excision of AGI. METHODS:A retrospective, multi-institutional study of AGI from 2002 to 2014 was performed using a standardized database. Baseline demographics, comorbidities, and perioperative variables were recorded. The primary outcome was infection-free survival. Descriptive statistics, Kaplan-Meier survival analysis, and univariate and multivariable analyses were performed. RESULTS:A total of 241 patients at 34 institutions from seven countries presented with AGI during the study period (median age, 68 years; 75% male). The initial aortic procedures that resulted in AGI were 172 surgical grafts (71%), 66 endografts (27%), and three unknown (2%). Of the patients, 172 (71%) underwent complete excision of infected aortic graft material followed by in situ (in-line) bypass (ISB), including antibiotic-treated prosthetic graft (35%), autogenous femoral vein (neo-aortoiliac surgery) (24%), and cryopreserved allograft (41%). Sixty-nine patients (29%) underwent extra-anatomic bypass (EAB). Overall median Kaplan-Meier estimated survival was 5.8 years. Perioperative mortality was 16%. When stratified by ISB vs EAB, there was a significant difference in Kaplan-Meier estimated infection-free survival (2910 days; interquartile range, 391-3771 days vs 180 days; interquartile range, 27-3750 days; P < .001). There were otherwise no significant differences in presentation, comorbidities, or perioperative variables. Multivariable Cox regression showed lower infection-free survival among patients with EAB (hazard ratio [HR], 2.4; 95% confidence interval [CI], 1.6-3.6; P < .001), polymicrobial infection (HR, 2.2; 95% CI, 1.4-3.5; P = .001), methicillin-resistant Staphylococcus aureus infection (HR, 1.7; 95% CI, 1.1-2.7; P = .02), as well as the protective effect of omental/muscle flap coverage (HR, 0.59; 95% CI, 0.37-0.92; P = .02). CONCLUSIONS:After complete resection of AGI, perioperative mortality is 16% and median overall survival is 5.8 years. EAB is associated with nearly a two and one-half-fold higher reinfection/mortality compared with ISB. Omental and/or muscle flap coverage of the repair appear protective.

INTRODUCTION:Emergent endovascular repair of suprarenal (SRAAAs) and thoracoabdominal aortic aneurysms (TAAAs) poses a significant challenge due to the need for branch vessel incorporation, time constraints, and lack of dedicated devices. Techniques to incorporate branch vessels have included parallel grafting, physician-modified endografts, double-barrel/reversed iliac branch device, and in situ fenestration (ISF). This study describes a single-center experience and the associated outcomes when using these techniques for ruptured SRAAAs and TAAAs. METHODS:A retrospective review of patients who underwent endovascular repair of ruptured SRAAAs and TAAAs from July 2014 to March 2021 with branch vessel incorporation was performed. Clinical presentation, intraoperative details, and postoperative outcomes of those who underwent ISF were compared with those who underwent repair using non-ISF techniques. The primary outcome of interest was in-hospital mortality. Secondary outcomes were major adverse events including myocardial infarction, respiratory failure, renal dysfunction, new onset dialysis, bowel ischemia, stroke, and spinal cord ischemia. RESULTS:Forty-two patients underwent endovascular repair for ruptured SRAAAs and TAAAs, 18 of whom underwent ISF repair. Seventy-two percent of ISF patients were hypotensive before surgery, compared with 46% of the patients who underwent repair using non-ISF techniques (physician-modified endografts, parallel grafting, or double-barrel/reversed iliac branch device). The total procedural and fluoroscopy times were similar between the two groups despite a greater mean number of branch vessels incorporated with the ISF technique (3.1 vs 2.2 per patient, P = .015). In-hospital mortality was 19% for all ruptures and 25% for ruptures with hypotension. Compared with the non-ISF group, in-hospital mortality trended lower in the ISF group (11% vs 25%, P = .233), reaching statistical significance when comparing patients who presented with hypotension (8% vs 45%, P = .048). The rate of major adverse events was 57% across all techniques and did not significantly differ between the ISF and non-ISF groups, with postoperative renal dysfunction being the most frequent complication (48%). Overall, ISF became the most commonly used technique later in the study period. CONCLUSIONS:Although emergent endovascular repair of ruptured SRAAAs/TAAAs remains a challenge, a number of techniques are available for expeditious treatment. In this series, ISF was associated improve survival, including a fivefold reduction in mortality in patients presenting with hypotension, and has now become the dominant technique at our center. Despite these advantages, postoperative complications and reinterventions are common. Further experience and longer-term follow-up are needed to validate these initial results and assess durability.

During atherosclerosis, vascular smooth muscle cells (VSMCs) undergo a phenotypic transition from a healthy contractile state into pathological phenotypes including a proliferative and migratory, synthetic phenotype and osteochondrogenic-like phenotype that exacerbate plaques. Thus, inhibiting the transition of healthy, quiescent VSMCs to atherogenic cell types has the potential to mitigate atherosclerosis. To that end, previously, we reported that delivery of microRNA-145 (miR-145, a potent gatekeeper of the contractile VSMC phenotype) using nanoparticle micelles limited atherosclerotic plaque growth in murine models of atherosclerosis. Building on this preclinical data and toward clinical application, in this study, we tested the therapeutic viability of miR-145 micelles on patient-derived VSMCs and evaluated their effects based on disease severity. We collected vascular tissues from 11 patients with healthy, moderate, or severe stages of atherosclerosis that were discarded following vascular surgery or organ transplant, and isolated VSMCs from these tissues. We found that with increasing disease severity, patient-derived VSMCs had decreasing levels of contractile markers (miR-145, ACTA2, MYH11) and increasing levels of synthetic markers (KLF4, KLF5, and ELK1). Treatment with miR-145 micelles showed that an increase in disease severity correlated with a more robust response to therapy in VSMCs. Notably, miR-145 micelle therapy rescued contractile marker expression to baseline contractile levels in VSMCs derived from the most severely diseased tissues. As such, we demonstrate the use of miR-145 micelles across different stages of atherosclerosis disease and present further evidence of the translatability of miR-145 micelle treatment for atherosclerosis.

OBJECTIVES:Preservation of antegrade flow to the left vertebral artery (LVA) is often achieved by transposition or bypass to the left subclavian artery during zone 2 thoracic endovascular aortic repair. An anomalous LVA (aLVA) originating directly from the aortic arch is a common arch variant with a reported incidence of 4% to 6%. In addition, 6% to 10% of vertebral arteries terminate in a posterior inferior cerebellar artery, increasing the risk of stroke if not revascularized. Few series of aLVA to carotid transposition have been reported. The aim of this study was to evaluate the outcomes of patients who underwent aLVA to carotid transposition for the management of aortic disease. METHODS:A retrospective review of all aLVA-carotid transpositions performed for the management of thoracic aortic dissection or aneurysm at a single center from 2018 to 2021 was performed. The primary outcomes were postoperative stroke and patency of the transposed aLVA. Secondary outcomes were spinal cord ischemia, postoperative cranial nerve injury, and Horner's syndrome. RESULTS:Seventeen patients underwent aLVA to carotid transposition as an adjunct to management of aortic disease during the study period. Most were men (n = 14) and the mean age was 54 ± 16 years. The primary indication for aortic repair was dissection in 10, aneurysm in 6, and Kommerell diverticulum in 1. Nine patients underwent zone 2 thoracic endovascular aortic repair, seven received open total arch repair, and there was one attempted total endovascular arch repair that was aborted owing to unfavorable anatomy. Twelve transpositions were performed before or concomitant with planned aortic repair owing to high-risk cerebrovascular anatomy (three posterior inferior cerebellar artery termination, six dominant aLVA, four intracranial LVA stenosis), and two were performed postoperatively for treatment of type II endoleak. LVA diameter ranged from 2 to 6 mm (mean, 3.3 mm). The mean operative time for transposition was 178 ± 38 minutes, inclusive of left subclavian artery revascularization, and the mean estimated blood loss was 169 ± 188 mL. No patients experienced 30-day postoperative spinal cord ischemia, stroke, or mortality. There were two cases of postoperative hoarseness, presumably owing to recurrent laryngeal nerve palsy, both of which resolved within 4 months. There were no cases of Horner's syndrome. At follow-up (mean, 306 days; range, 6-714 days), all transpositions were patent. CONCLUSIONS:Vertebral-carotid transposition is a safe and effective adjunct in the management of aortic disease with anomalous origin of the LVA.

Thoracic endovascular aortic repair (TEVAR) is a commonly performed operation for patients with type B aortic dissection (TBAD). The goal of TEVAR is to cover the proximal entry tear between the true lumen (TL) and the false lumen (FL) with an endograft to induce FL thrombosis, allow for aortic healing, and decrease the risk of aortic aneurysm and rupture. While TEVAR has shown promising outcomes, it can also result in devastating complications including stroke, spinal cord ischemia resulting in paralysis, as well as long-term heart failure, so treatment remains controversial. Similarly, the biomechanical impact of aortic endograft implantation and the hemodynamic impact of endograft design parameters such as length are not well-understood. In this study, a fluid-structure interaction (FSI) computational fluid dynamics (CFD) approach was used based on the immersed boundary and Lattice-Boltzmann method to investigate the association between the endograft length and hemodynamic variables inside the TL and FL. The physiological accuracy of the model was evaluated by comparing simulation results with the true pressure waveform measurements taken during a live TEVAR operation for TBAD. The results demonstrate a non-linear trend towards increased FL flow reversal as the endograft length increases but also increased left ventricular pulsatile workload. These findings suggest a medium-length endograft may be optimal by achieving FL flow reversal and thus FL thrombosis, while minimizing the extra load on the left ventricle. These results also verify that a reduction in heart rate with medical therapy contributes favorably to FL flow reversal.

We have described a patient with a history of type A-11 dissection repair, who subsequently underwent thoracic endovascular aortic repair with distal bare metal dissection stents (provisional extension to induce complete attachment) and renal artery stenting for malperfusion. During the next 3 years, the thoracoabdominal aorta had continued to enlarge to 6.9 cm, despite false lumen embolization and thoracic endovascular aortic repair extension. Given the continued aortic enlargement, physician-modified fenestrated endovascular aortic repair was performed within the prior aortic and renal stents with successful aneurysm sealing. The results from the present case have illustrated that continued aneurysmal degeneration can occur after provisional extension to induce complete attachment and that subsequent physician-modified fenestrated endovascular aortic repair is feasible.