Injury to the aorta and great vessels of the thorax may occur secondary to penetrating or blunt trauma. The management strategy involves control of immediate hemorrhage with prevention of distal malperfusion or pseudoaneurysm development and rupture. Blunt thoracic aortic injury (BTAI) is the most common thoracic vascular injury and is the second leading cause of death in the United States from nonpenetrating trauma. Its incidence is estimated at 7500 to 8000 cases per year.¹ In 75 to 90% of cases, death occurs at the accident scene, typically in those with four or more serious injuries in addition to their aortic transection.² Current data suggest that approximately 4% of patients die during transport from the scene, and an additional 19% die during the initial trauma evaluation.³ A meta-analysis in 2011 reported that in-hospital mortality of patients managed nonoperatively was as high as 46%, whereas mortality was 9% in patients treated by endovascular repair and 19% for open repair.⁴ After aortic transection at the isthmus, aortic disruption at the base of the innominate artery is the most common site of injury, followed by the base of the left subclavian artery, and the base of the left carotid. Central venous structures are rarely injured with blunt trauma, but this can occur with penetrating trauma.⁵ Traditionally, open surgical repair of these injuries has proved effective. Since the first endovascular thoracic aortic device became commercially available in the United States in 2005, the treatment of BTAI has rapidly evolved as high-volume trauma centers applied the principles of endovascular aneurysm repair to BTAI in an off-label manner. With the growing shift from open repair to thoracic endovascular aortic repair (TEVAR) as the primary treatment in patients with BTAI, outcomes have improved with significantly reduced mortality and morbidity, including procedure-related paraplegia.⁶ This chapter describes the traumatic injuries to the thoracic aorta and its brachiocephalic branch vessels. The mechanism, clinical presentation, and treatment strategies are presented. The emphasis is directed to endovascular strategies which have emerged as the most commonly utilized intervention in blunt aortic and brachiocephalic branch vessel trauma. The chapter is divided into the ascending, arch, and descending zones and both open surgical and endovascular approaches are described with regard to the specific zones.

Zonal Divisions of the Thoracic Aorta

In order to facilitate international correspondence and a clinically more useful system with regard to anatomical identification of the thoracic aorta, an “anatomical endograft landing zone map” was advocated at the First International Summit on Thoracic Aortic Endografting held in Tokyo in 2001.⁷ We suggest using this landing zone map to classify not only the proximal deployment site of an endograft but also extent of open surgical repairs. In 2002, this landing zone map was expanded to include the position of the distal end of the endograft. Since then, the map (Fig. 51-1) has achieved consensus as the standardized anatomical definition to evaluate outcomes.⁸ On a more personal notation, we refer to the aortic root as the “double-0” site.

Clinical Presentation

Patients presenting to the emergency department with injury to a great vessel should be evaluated according to standard advanced trauma life support (ATLS) protocols. Those suffering blunt trauma are often hemodynamically stable; therefore, a high index of suspicion for intrathoracic vascular disruption must be based on the mechanism and constellation of related injuries. In addition to high-speed collisions involving automobiles or motorcycles, crush injuries and falls often have sufficient force to rupture a thoracic vessel.^9-12 There are often clues evident in the initial evaluation of a trauma patient that can suggest aortic disruption. In contrast to blunt injury to the arch vessels, patients sustaining descending thoracic aortic rupture are often hemodynamically stable on presentation at the emergency department. Although patients may complain of dyspnea or back pain and display differential blood pressures in the upper versus lower extremities, specific signs or symptoms of aortic rupture have been identified in less than 50% of cases. Complete de-gloving injury may result in intussusception of the aortic media into the descending thoracic aorta, with resultant “pseudocoarctation” and subsequently variable degrees of distal malperfusion (Fig. 51-2). Commonly associated complaints include neck and chest pain, and physical examination may reveal ecchymosis across the chest and neck from the seatbelt shoulder harness.^13,14 Physical examination findings concerning for rupture of a great vessel include supraclavicular swelling or bruit, diminished pulse in the ipsilateral upper extremity, neck hematoma with or without tracheal deviation, acute Horner’s syndrome, and an acute superior vena cava-like syndrome.^11,14-16 In a stable patient with evidence of a stab or gunshot wound located between the mid clavicular lines or in zone I of the neck, great vessel penetration should be suspected.¹⁷ A precordial bruit suggesting arteriovenous fistula (AVF) formation may be noted in up to 30% of patients.¹⁸ Penetrating distal subclavian injuries may demonstrate pulsatile bleeding during initial evaluation.¹⁹ More commonly, patients suffering penetrating injury to the chest or neck will be hemodynamically unstable on arrival to the emergency department, possibly with evidence of cardiac tamponade, and those in extremis should undergo emergent thoracotomy. Hypotensive patients may proceed directly to the operating room without diagnostic imaging; the mortality of patients presenting with hypotension is nearly three times greater than that of stable patients.^18,19 Therefore, an organized, efficient, and effective evaluation of these patients is necessary to prevent unnecessary loss of life.

Classification System for Traumatic Aortic Injury

The classification scheme for grading the severity of BTAI has been widely accepted and is shown in Fig. 51-3.²⁰ Grade I demonstrates an intimal tear or flap. Grade II demonstrates an intramural hematoma without significant change in the external contour of the aorta. Grade III demonstrates a contained pseudoaneurysm with extension beyond the normal contours of the aorta. Grade IV involves full-thickness aortic injury with extravasation. The Society of Vascular Surgery guidelines recommend TEVAR for grade II through IV BTAIs, given that grade I injuries typically heal spontaneously.

Initial Evaluation

A multitrauma patient should be evaluated according to standard ATLS protocols regardless of whether aortic disruption is suspected. The primary and secondary survey, routine radiographs, and hemodynamic stabilization must be completed before the team can begin investigating specific injuries. The first step in diagnosing a blunt traumatic aortic injury is identifying the at-risk patient. Motor vehicle collisions, falls from height, explosions, and crush injuries have the impact and deceleration forces required to cause aortic transection; therefore these patients should undergo imaging directed at ruling out this potentially fatal injury.^21-24 Operative management of intracranial space-occupying lesions and intra-abdominal hemorrhage takes priority over nonbleeding aortic injuries. Hemodynamically unstable patients with signs of exsanguinating hemorrhage should go directly to the operating room for control of hemorrhage, and transesophageal ultrasound may be used to evaluate for aortic injury. Ninety-five percent of patients with aortic disruption have associated injuries. Data accrued from a trial which included approximately 50 trauma centers across the United States and Canada, the American Association for the Surgery of Trauma (AAST) trial,²⁵ demonstrated that current advancements in emergency medical resuscitation in the field have provided more patients the opportunity to reach the hospital and receive aggressive definitive care. There are often clues evident in the initial evaluation in these patients that can suggest aortic disruption (Table 51-1).

CHEST X-RAY

In the majority of trauma patients, a supine chest radiograph is obtained as part of the initial evaluation, and the constellation of grossly widened mediastinum, hemothorax, and transient hemodynamic instability on arrival appear to be predictive of early in-hospital death from BTAI.²⁶ During the evaluation of a blunt trauma patient, an anteroposterior chest radiograph is routinely obtained and ought to be examined for one of the 15 signs that have been associated with aortic rupture (Table 51-2).²⁷ Widening of the mediastinum to a width exceeding 25% of the total chest width, obliteration of the aortic knob, apical pleural capping, and fractures of the sternum, scapula, clavicle, or first rib are some of the most common findings (Fig. 51-4). None of these signs have demonstrated sufficient sensitivity or specificity to effectively rule out aortic injury, however, and up to 40% of patients with aortic rupture have had chest x-ray findings interpreted as normal.^22,23,28-32 When abnormalities are identified, however, they can aid the practitioner in determining which patients require aggressive imaging to definitively rule out an aortic injury.

COMPUTED TOMOGRAPHY

In the typical hemodynamically stable blunt trauma patient, head and abdominopelvic computed tomography (CT) should be conducted to identify closed-head or intra-abdominal injury. Those with an abnormal chest x-ray or a traumatic mechanism consistent with aortic injury should undergo helical CT scan of the chest with intravenous contrast at this time. Since its introduction in the early 1990s, CT has become the screening tool of choice at most medical institutions to detect traumatic aortic rupture due to its availability, speed, and ease of interpretation. Additionally, sensitivities and negative predictive values nearing 100% have been reported for volumetric helical or spiral CT.^22,23,32-35 Normal aorta portrays homogeneous enhancement, while filling defects, contrast extravasation, intimal flaps, periaortic hematoma, pseudoaneurysm, and mural thrombi may suggest the presence of an aortic injury (Fig. 51-5).³⁴ Moreover, the enhanced resolution of CT imaging has allowed identification of minimal aortic injuries, such as small intimal flaps with minimal or no mediastinal changes, that may be safely managed with anti-impulse therapy.^23,34,36

TRANSESOPHAGEAL ECHOCARDIOGRAPHY

Transesophageal echocardiography (TEE) has become a valuable tool in cardiothoracic surgery due to its ability to image the entire descending thoracic aorta along with portions of the ascending aorta arch and its portability. In unstable blunt trauma patients requiring laparotomy, TEE can be utilized to evaluate the descending aorta for evidence of rupture, such as a mural flap or a thickened vessel wall concerning for mural thrombus. Multiplanar TEE probes permit acquisition of cross-sectional images at different angles along a single rotational axis. The typical 5- or 7-MHz transducer permits adequate resolution of structures as small as 1 to 2 mm. Doppler mapping of turbulent blood flow near a vessel wall abnormality may be suggestive of blunt aortic disruption, and time-resolved imaging allows evaluation of the movement of anatomic structures, thereby enhancing the ability to define the physiologic consequences of such abnormalities. Chronic atheromatous disease of the aorta can complicate obtaining and interpreting TEE images; therefore observation of multiple-related signs of injury, such as mural flap with a surrounding mediastinal hematoma, is more reliable. A disadvantage of TEE, and potential inhibitor to its widespread use as a screening tool for aortic injury, is its operator-dependent nature with sensitivities as low as 63% documented for this modality.³⁷ A prospective comparison of imaging techniques for diagnosis of blunt aortic trauma reported, however, sensitivity and specificity of 93 and 100% for TEE compared to 73 and 100% for helical CT.³⁵ Thoracoscopy has also been used to evaluate traumatic hemothoraces, however with experienced practitioners intraoperative TEE has superb sensitivity and specificity for aortic transection.^38,39 TEE is more invasive than helical CT, but overall the associated risk is low. Contraindications include concomitant injury to the cervical spine, oropharynx, esophagus, or maxillofacial structures.³⁵

MAGNETIC RESONANCE ANGIOGRAPHY

Vascular structures are well imaged by magnetic resonance angiography (MRA), particularly the thoracic aorta, and its utility in the diagnosis and follow-up of complex aortic disease including aortic dissections and aneurysms is firmly established.^40-42 The time required to capture images inhibits the utility of MRA in the acute evaluation of a trauma patient, however it may be effective in posttherapeutic surveillance of traumatic thoracic injuries.

AORTOGRAPHY

Aortography may be useful when helical CT or TEE fail to definitively identify or adequately characterize an aortic injury. The role of aortography in evaluating blunt thoracic injuries was firmly established prior to the advent of noninvasive, sophisticated imaging techniques, and it may still be considered the gold standard. In experienced hands its sensitivity and specificity both approach 100%.⁴³ Intra-arterial digital subtraction is most often used because it allows rapid generation of images (Fig. 51-6). In the past, intravenous digital subtraction was used as well. After injecting intravenous contrast, time-delayed images of the arch and descending aorta were obtained, and although this technique greatly decreased the duration of the procedure, it was abandoned because the diagnostic accuracy for aortic disruption was less than 70%.⁴⁰ With the availability and speed of helical CT, aortography is now rarely used for diagnosis, but routinely utilized for endovascular stent graft placement. This intervention requires a highly trained team of endovascular specialists and can be time-consuming; therefore trauma patients with additional life or limb threatening injuries should be otherwise stabilized before entering the endovascular suite. Rates of exsanguination and death of up to 10% have previously been reported during diagnostic aortography, but this incidence has decreased significantly as endovascular proficiency has improved.^40,44,45 In fact, complication rates attributed directly to aortography are low, but patients may suffer contrast reactions, contrast nephropathy, groin hematomas, or femoral artery pseudoaneurysms. False-positive studies are usually attributed to atheromata or ductal diverticula.

Decision to Repair Versus Expectant Management

Uniformly, hemodynamically unstable blunt trauma patients should bypass diagnostic imaging and be taken to the operating room immediately. During a damage control exploratory laparotomy or thoracotomy, TEE may be conducted to diagnose contained aortic rupture.³⁵ Operative repair of the aorta should not be attempted at this time, however, as this group of patients benefit from immediate transfer to the intensive care unit for further resuscitation. Once hemodynamic stability is achieved, anti-impulse therapy with beta-blockade should be initiated to minimize aortic wall stress. Hemodynamically stable patients diagnosed with blunt aortic injury, and lacking severe associated injuries requiring interventions, warrant immediate repair. Treatment of all nonlife-threatening injuries should be delayed until after definitive aortic repair. As such, delayed management has demonstrated to be safe and effective in carefully selected patients with severe associated injuries or comorbidities.^46-57 Patients with thoracic, intraperitoneal or retroperitoneal hemorrhage, or intracranial bleeding that cause mass effect should be managed with aggressive anti-impulse therapy to minimize the risk of aortic rupture while these injuries are addressed.⁵⁵ The goal of anti-impulse therapy should be to maintain a systolic blood pressure less than 120 mm Hg and/or a mean arterial pressure less than 80 mm Hg.²³ The aortic insult should also be monitored by TEE during surgical repair of concomitant injuries, and routinely imaged with CT during the delayed management period. The mortality rate of patients awaiting aortic repair has ranged from 30 to 50%, but the majority of deaths have not been related to the aortic injury.^49,50,55 In the AAST trial, those presenting in extremis or with evidence of free aortic rupture were excluded, and the mortality rate of patients with associated injuries that precluded initial aortic repair was 55%.²⁵ Therefore, evidence supports operative delay or even nonoperative management in select patients with blunt aortic injury who may be considered poor operative candidates. Even in carefully selected patient with BTAIs deliberate nonoperative management has been shown to be a reasonable alternative in the polytrauma patient.⁵⁸ Anti-impulse therapy with beta-blockers should be initiated in patients proceeding directly to the operating room for aortic repair, as well as in those selected for delayed repair, to reduce blood pressure and thereby reduce aortic wall stress.^23,24,59 In-hospital aortic rupture rates have been reduced through aggressive beta-blockade without adversely affecting the outcome of associated injuries.²³

Mechanism of Injury

Descending thoracic aortic transection is the most common vascular injury resulting from blunt thoracic force. The ascending aorta and arch vessels, however, may also be disrupted, commonly leading to dissection or pseudoaneurysm formation.^11,14 Mechanistically, the transmission of force through the thoracic cavity from blunt injury is believed to cause torsion of the ascending aorta, leading to disruption of the wall with an associated shearing effect on the heart.⁶⁰ Additionally, a waterhammer effect is described in which an aortic occlusion at the diaphragm occurs with impact and a high pressure wave is reflected back to the ascending aorta and aortic arch.⁶¹

Operative Repair

Pseudoaneurysm of the ascending aorta should be repaired using cardiopulmonary bypass. Femorofemoral or axillo-femoral cannulation and commencement of cardiopulmonary bypass before sternotomy may decompress the ascending aorta and decrease the risk of pseudoaneurysm rupture on opening the chest.¹⁶ After entering the pericardium, the pseudoaneurysm should be carefully mobilized, if possible, to gain proximal and distal control. Depending on the nature and extent of the injury, repair may be conducted by primary repair, patch angioplasty, or prosthetic replacement of aortic segment. If aortic valve insufficiency is encountered, prosthetic valve replacement may be warranted.⁶² Occasionally, deep hypothermic circulatory arrest is required, especially if proximal and distal control cannot be comfortably obtained or the pseudoaneurysm extends into the proximal aortic arch. This will allow for excision of the pseudoaneurysm and closure of the aortic defect with a prosthetic patch.⁶⁰ As with descending thoracic aortic injuries, a delay in operative management may be considered in hemodynamically stable patients with associated injuries at high risk for bleeding, especially intracranial lesions.⁶⁰ The application of this delayed approach depends on the nature of the ascending aortic injury. For instance, it must be a discrete lesion without evidence of circumferential involvement or compromised adjacent structures. Safe observation entails maintaining a mean arterial pressure less than 80 mm Hg and cerebral perfusion pressure greater than 50 mm Hg, typically through short-acting intravenous beta-blockade.⁶³ Conservative management must be accompanied by regular assessment of the aortic lesion through serial CT scans of the thorax and a low threshold for operative intervention if enlargement of the pseudoaneurysm is identified.⁶³

Endovascular Interventions

Several studies have reported safety and effectiveness of TEVAR of the descending aorta, but the role of TEVAR for treating ascending aortic pathology is less well known. Especially the role of ascending TEVAR (or A-TEVAR) in the setting of trauma has not been evaluated and reported to date. Only a small number of studies have described outcomes with this approach.^64-66 The reported experience demonstrates that endovascular repair of the ascending aorta is technically feasible in settings of chronic aneurysms or acute aortic dissections and can be accomplished with promising early results. Currently there are no commercially available endovascular devices specifically designed to treat the ascending aorta. Compared with TEVAR of the descending thoracic aorta, endovascular therapy for the ascending aorta is challenged by more complex pathology, hemodynamic characteristics, and anatomy. As such, the proximity of the aortic valve and coronary arteries to the ascending aorta makes it particularly challenging to obtain seal and fixation within the proximal landing zone. Thus far the only intervention is the open surgical approach via median sternotomy and cardiopulmonary bypass as described in the previous section.

Mechanism of Injury

The pathogenesis of blunt innominate artery rupture has been postulated to be the result of anteroposterior compression of the mediastinum between the sternum and vertebrae, displacing the heart posteriorly and to the left, thereby increasing the curvature of the aortic arch and increasing tension on all of its outflow vessels.⁶⁷ Hyperextension of the cervical spine with head rotation provides additional tension on the right carotid artery, which is transmitted to the innominate artery, and can lead to rupture.⁶⁷ The left carotid artery undergoes stretching injury with rapid deceleration, producing an intimal tear and subsequent dissection.¹¹ Additional mechanisms of carotid artery injury include hyperflexion of the neck to cause compression between the mandible and cervical spine, basilar skull fracture transecting the artery, and strangulation injury.¹¹ Blunt subclavian artery injuries are more common in the middle and distal third of the artery and are theorized to be caused by downward forces fracturing the first rib with the anterior scalene acting as a fulcrum so that the subclavian artery is pinched between the first rib and clavicle.⁹ The abrupt deceleration of the shoulder, owing to the seatbelt shoulder harness, is also believed to cause subclavian artery shearing injuries.⁹

Operative Repair

INNOMINATE ARTERY

The innominate artery is the second most common site of thoracic vascular injury following blunt trauma. In a review of 117 reported cases of blunt innominate artery rupture, 83% were in the proximal vessel, 3% were in the middle, 9% were distal, and the remaining injuries involved multiple sections.¹⁰ The most common finding was disruption of the intima and media with pseudoaneurysm formation (Fig. 51-7).¹⁰ Although primary repair may be possible in some cases, surgical repair of an innominate artery rupture has traditionally been performed by a prosthetic aorto-innominate bypass graft from the aortic arch to healthy distal vessels through a full or upper median sternotomy with extension of the incision along the anterior border of the right sternocleidomastoid as necessary.^17,68 Operative repair of a penetrating innominate artery injury is approached in the same manner.¹⁷ The entire length of the innominate artery should be mobilized to achieve distal control and the pericardium opened to gain proximal control at the level of the aortic arch.⁶⁹ After systemic administration of heparin, a partial occlusion clamp is applied to the aortic arch and the proximal anastomosis of the prosthetic graft performed end-to-side with polypropylene suture.⁶⁹ Depending on the location and extent of the injury, the distal end-to-end anastomosis may involve only the innominate artery or a Y-graft may be required to reconstruct the proximal portions of the right carotid and right subclavian arteries individually.¹⁰ The origin of the innominate artery should then be fully exposed and oversewn with pledgeted nonabsorbable sutures.⁶⁹ Healthy patients typically tolerate temporary innominate artery occlusion caused by adequate collateral flow through the contralateral carotid and vertebral arteries.⁶⁹ Cerebral protection, cardiopulmonary bypass, electroencephalogram monitoring, hypothermia with circulatory arrest, or carotid shunting (for stump pressure < 50 mm Hg) should be employed in patients with neurologic abnormalities or suspicion of a contralateral carotid artery injury.^68,69 Long-term patency of prosthetic aorto-innominate artery bypass grafts has been reported to be greater than 96% at 10 years.⁷⁰

CAROTID ARTERY

Therapeutic management of blunt carotid artery injury must be directed at preventing cerebral ischemia and surgical intervention should be weighed against observation and anticoagulation.⁷¹ Small intimal flaps may resolve, whereas larger flaps can lead to thrombosis and therefore require anticoagulation to prevent thromboembolism.⁷² Arterial dissection may progress to luminal narrowing, placing the patient at risk for thrombosis, and anticoagulation therapy is especially important in patients with bilateral carotid artery dissection owing to the morbidity and mortality associated with bilateral thrombosis.⁷³ When operative intervention is indicated because of pseudoaneurysm formation (Fig. 51-8), the surgeon may bypass the lesion, but reconstruction or ligation of the artery can also be employed.¹¹ Open repair of an intrathoracic carotid artery injury should occur through a median sternotomy with extension along the anterior border of the ipsilateral sternocleidomastoid muscle as necessary to gain adequate exposure.¹⁸ After gaining proximal and distal control, arterial repair may be accomplished by primary repair or interposition grafting with saphenous vein or prosthetic material.¹⁸

SUBCLAVIAN ARTERY

Injury to the subclavian artery, from blunt or penetrating trauma, carries a mortality rate of 5 to 30% resulting from the inability to obtain adequate hemorrhagic control through direct pressure.^74,75 Additionally, because of the close proximity of the trachea, esophagus, subclavian vein, and brachial plexus, subclavian artery injuries are associated with 40% morbidity.⁷⁴ Operative exposure may be achieved by median sternotomy, limited sternotomy, supraclavicular incision, infraclavicular incision, thoracotomy, or a combination of these depending on the location of the injury.⁷⁶ Left-sided lesions are often managed through an anterolateral thoracotomy with either an infraclavicular or supraclavicular counter incision; however, some surgeons perform a median sternotomy for a proximal injury.^9,76 Right-sided injuries, on the other hand, require median sternotomy with supraclavicular extension.⁹ In cases in which the defect involves a long segment of the subclavian artery, a portion of the clavicle may be resected to optimize exposure, although this procedure carries considerable postoperative morbidity.^19,76 Once establishing proximal and distal control of the subclavian artery, the damaged arterial segment may be excised and arterial reconstruction accomplished with an interposition graft using a saphenous vein or prosthetic material.⁹ In cases in which minimal arterial debridement is required, primary repair is often attained.⁷⁷ Ligation of the subclavian artery may be performed on critically ill patients unable to tolerate an extensive operative repair, and minimal short-term morbidity in the affected limb has been reported.^19,76,77 When planning operative repair of the subclavian artery, concomitant injuries to nearby structures such as the subclavian vein and brachial plexus should be considered.

Endovascular Interventions

Arteriography is considered the gold standard for diagnosis and characterization of an intrathoracic vascular injury, and as endovascular stent technology and surgeon proficiency continue to advance, arteriography may become the preferred method of treatment in hemodynamically stable patients. The literature is currently populated with small case series and case reports documenting the feasibility of this approach and minimal short-term morbidity and mortality, but very little long-term data exist. Similar to other minimally invasive techniques, endovascular management of a traumatic injury to an intrathoracic vessel can provide an opportunity for patients to avoid sternotomy or thoracotomy and the associated pain, prolonged recovery time, and infection risk.^78,79 An analysis of endovascular versus open procedures in the National Trauma Database revealed a survival advantage for endovascular repair when controlling for injury severity score, associated injuries, and age.⁸⁰ Widespread application of endovascular techniques to manage great vessel trauma in hemodynamically stable patients is constrained by lesion anatomy. With regard to accessing the injury, the relationship of the vascular defect to the aortic arch is rarely an issue because brachial and carotid artery approaches, with or without a concomitant femoral approach, are increasingly employed.⁷⁹ However, the likelihood that the adjacent healthy vessel segments will provide adequate landing zones and the preservation of branch vessels are important considerations.⁸¹ Therefore, critical assessment of each individual lesion is required to assure appropriate use of this technology. Common endovascular modalities such as bare-metal or covered stents (stent grafts) and coil embolization have been employed in vascular trauma. Stent grafts were not commercially available before 2000; therefore, case reports published in that timeframe described use of home-made devices in which the surgeon affixed autologous tissue, expanded polytetrafluoroethylene (ePTFE), or polyester to a bare-metal stent and then repackaged the device for endovascular deployment across an AVF or pseudoaneurysm.⁸² There are currently a number of self-expandable and balloon-expandable stent grafts approved for coronary or peripheral vascular interventions that have been successfully used in the aortic arch vessels, specifically the wallstent endoprosthesis (Boston Scientific, Natick, MA), the Gore Viabahn endoprosthesis (W.L. Gore & Associates, Flagstaff, AZ), and the Jostent stent-graft coronary or peripheral (Abbott Vascular, Redwood City, CA).⁸³