Management of chronic type B aortic dissection

INTRODUCTION — Chronic type B aortic dissection is defined as an intimal tear originating anywhere in the aorta distal to the innominate artery (zone 1 or greater (figure 1)) and which has been present for more than 90 days. Chronic type B aortic dissection is particularly challenging to manage, and the approach to treatment continues to evolve with advancements in endovascular techniques.

The approach to managing chronic type B aortic dissection is predominantly based upon clinical features. Patients with uncomplicated chronic type B aortic dissection are generally managed medically with periodic clinical and imaging surveillance [1]. Patients who develop complications (eg, aneurysmal degeneration, malperfusion) or have certain high-risk features require intervention. Some uncomplicated patients with clinical features that are predictive of the development of complications may benefit from earlier, rather than later, intervention.

Thoracic endovascular aortic repair is the first-line treatment when anatomically feasible in patients without connective tissue disorders. For patients who are not candidates for endovascular repair, open surgical repair provides a durable option but is associated with increased perioperative morbidity and mortality.

The management of chronic type B aortic dissection is reviewed. The clinical features and diagnosis of aortic dissection and the management of acute aortic dissection are discussed separately. (See "Clinical features and diagnosis of acute aortic dissection" and "Management of acute type B aortic dissection" and "Surgical and endovascular management of acute type A aortic dissection" and "Surgical and endovascular management of acute type B aortic dissection".)

TYPE B AORTIC DISSECTION — Aortic dissection is defined as a tear in the innermost layer of the aortic wall (intima) that results in high-pressure flow of blood between the layers of the aorta, creating a true and false lumen. Aortic dissection is classified based upon the anatomic location of the entry tear (type A, type B), the clinical severity of the dissection (uncomplicated, complicated, high-risk features), and the duration of symptoms (hyperacute, acute, subacute, chronic), all of which impact the type and timing of treatment. Chronic type B aortic dissection involves an intimal tear that originates anywhere in the aorta distal to the innominate artery (zone 1 or greater (figure 1)) and has been present for more than 90 days [2-4].

The etiology of aortic dissection can be sporadic (eg, hypertension, infection/inflammatory), genetically mediated (eg, Marfan, Ehlers-Danlos, Loeys-Dietz, bicuspid aortic valve, Turners), or traumatic (eg, blunt aortic injury, iatrogenic). (See "Epidemiology, risk factors, pathogenesis, and natural history of thoracic aortic aneurysm and dissection", section on 'Etiology and risk factors'.)

Classification

●Anatomic – The DeBakey and the Stanford aortic dissection classification systems (figure 2), which are commonly used, have limitations [5,6]. Both are relatively nonspecific regarding the precise extent of the dissection and are ambiguous regarding the involvement of the aortic arch. A task force commissioned by the Society for Vascular Surgery (SVS) and Society for Thoracic Surgery (STS) has addressed these issues with a classification system that distinguishes type A from B by entry point (figure 1) [2]. Type A aortic dissection is classified as an entry tear in zone 0, and the distal extent can range from zone 1 to 12. Type B aortic dissection has an entry tear in zone ≥1, and the proximal and distal extent are noted. Approximately two-thirds of acute aortic dissections present as type A, and one-third are type B [7]. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Classification'.)

For chronic type B aortic dissections that have become aneurysmal, the Safi modification of Crawford classification (figure 3) helps describe the extent of disease and extent of thoracoabdominal replacement.

●Clinical severity – The clinical severity of aortic dissection is described as complicated, uncomplicated, or dissection with high-risk features. Complicated type B aortic dissections have evidence of rupture and/or clinical malperfusion (figure 4 and figure 5). High-risk features include refractory or recurrent pain (>12 hours), refractory hypertension (>3 classes of antihypertensive medications at maximum doses), and radiographic features such as entry tear on lesser curvature, aortic diameter >4 cm, false lumen >2.2 cm, bloody pleural effusion, and radiographic-only malperfusion. Patients without rupture, clinical malperfusion, or high-risk features are considered uncomplicated [1,2]. (See 'Predictors of adverse aortic events' below and 'Intervention for complicated disease' below.)

●Duration – Type B aortic dissection was previously classified simply as acute (<14 days) or chronic (>14 days) based on the timing of death in the era of open surgery [3,4]. The SVS/STS reporting guidelines have established a classification based on the timing from the onset of symptoms as follows [2]:

•Hyperacute – <24 hours

•Acute – 1 to 14 days

•Subacute – 15 to 90 days

•Chronic – >90 days

For the purposes of this discussion on chronic type B aortic dissection, we will use the term "acute" type B aortic dissection to broadly refer to the period ≤90 days encompassing the hyperacute, acute, and subacute periods.

Natural history — From the time of its occurrence, aortic dissection transitions from an acute to chronic state as the aorta remodels [8]. This transition is complex and is described in terms of the dissection flap architecture, false lumen patency or thrombosis, and degree and rate of aortic expansion. The natural history aortic remodeling has implications on the optimal timing for treatment and clinical outcomes of thoracic endovascular aortic repair [9].

In an analysis from the VIRTUE Registry, differences in aortic remodeling were observed when comparing acute and chronic type B aortic dissections. Aortic morphology and plasticity were similar for various time points during the acute period [4]. The intimal flap/septum and aorta are thin and fragile in the acute period, and the risk for retrograde type A dissection is increased during endovascular repair; however, because the intimal flap/septum is more soft/flexible, thoracic endovascular aortic repair more fully expands the true lumen compared with chronic type B aortic dissection. (See 'Endovascular versus open repair' below and 'Technical issues' below.)

Predictors of adverse aortic events — Several studies have sought to identify risk factors associated with the need for intervention or adverse outcomes in patients with type B aortic dissection. In one review of 294 patients with an average follow-up of 3.7 years, predictors of intervention and mortality included age >60 years, aortic diameter >4.4 cm on presentation, and false lumen diameter in the proximal descending aorta >2.2 cm [10]. In a smaller review of 104 patients with a mean follow-up of 87.6 months, 46 had one or more dissection-related events [11]. The actuarial event-free rate for any dissection-related event was 95, 75, 53, and 13 at 1, 5, 10, and 20 years, respectively. Initial aortic diameter ≥4 cm and blood flow in the false lumen were significant risk factors for dissection-related events in univariate and multivariate analysis.

A systematic review identified several predictors of aortic expansion in patients with uncomplicated type B aortic dissection. Predictors were separated into patient characteristics and radiographic signs [12].

●Younger age at presentation was a clinical predictor of aortic expansion. Patient age <60 years was significantly associated with increasing aortic diameter, which was thought to be due to a less rigid aortic wall, making the aorta more prone to dilation in younger patients. Other patient characteristics associated with increased aortic expansion rates were being a White person, Marfan syndrome, and heart rate >60 beats/minute.

●Radiologic predictors of aortic expansion included a maximal aortic diameter ≥4 cm in the acute phase, a patent false lumen, a partially thrombosed false lumen, false lumen diameter ≥2.2 cm on initial imaging, a large entry tear ≥1 cm in the proximal part of the dissection, and an intimal tear located on the inner aortic curvature.

MANAGEMENT — Type B aortic dissection is primarily managed based upon the clinical severity of disease. Repair of chronic type B aortic dissection is generally reserved for those who progress from uncomplicated to complicated disease. For most patients with uncomplicated chronic type B aortic dissection, we suggest watchful waiting and ongoing medical treatment, rather than intervention. However, patients with uncomplicated type B aortic dissection and high-risk features for aortic expansion or other dissection-related events may benefit from early endovascular repair rather than awaiting the development of complications.

Uncomplicated dissection — Patients with uncomplicated chronic type B aortic dissection are generally managed medically (anti-impulse therapy) with periodic clinical and imaging surveillance [1].

Anti-impulse therapy — For patients with acute uncomplicated type B aortic dissection, the mainstay of treatment focuses on strict control of heart rate (HR) and blood pressure (also referred to as "anti-impulse therapy") [1,13,14]. (See "Management of acute type B aortic dissection", section on 'Anti-impulse therapy'.)

The goals of anti-impulse therapy, which are to maintain reduced shear stress on the aortic wall to prevent progression of the dissection, malperfusion, aneurysmal degeneration, or rupture, are the same as for acute type B aortic dissection [15]. Guidelines recommend a target HR 60 to 80, and systolic blood pressure (SBP) of <120 mmHg [1]. Adequate management of any recurrent pain is also important to limit tachycardia and hypertension. Patients with optimal control of HR and SBP have better outcomes, with reduced rates of aortic expansion and rupture [12]. For patients who have survived the acute period, chronic type B aortic dissection is managed similarly, with best medical therapy focused on chronic long-term management of blood pressure and heart rate. Beta-blockers (table 1) reduce the contractility and HR to effectively reduce the blood pressure and aortic wall stress. In addition to beta-blockers, observational studies suggest that aortic expansion is reduced and survival is improved for patients with chronic type B aortic dissection who receive calcium channel blockers for maintenance therapy [16-18].

Unfortunately, many patients with chronic type B aortic dissection do not adhere to their prescribed anti-impulse medications. In a small review of 47 patients, adherence was reported as "high" in 43 percent, "moderate" in 21 percent, and "low" in 10 percent [19]. Factors associated with higher adherence were previous aortic surgery, a greater number of medications, perceived benefit from treatment, good memory, and low fears of side effects.

Serial imaging — An estimated 20 to 50 percent of medically managed patients with type B aortic dissection will eventually require intervention [12,20]. Given the high failure rate of best medical therapy and potential for serious complications or death, close surveillance and recognition of when to intervene are critical.

For patients diagnosed with uncomplicated type B aortic dissection, we generally obtain follow-up computed tomographic (CT) angiography at 1, 6, and 12 months after the onset of the dissection, and annually thereafter, provided the patient remains a candidate for an intervention [1,21,22]. (See "Management of acute type A aortic dissection", section on 'Serial imaging' and "Management of acute type B aortic dissection", section on 'Surveillance imaging'.)

The following abnormalities can be detected on serial vascular imaging:

●Extension or recurrence of the dissection

●Aneurysmal degeneration

●Malperfusion

Noncontrast magnetic resonance (MR) is an alternative for patients with impaired renal function. Alternating CT and MR angiography is reasonable for patients with good renal function.

Transthoracic echocardiography is not considered a monitoring alternative, but it may be necessary to monitor ongoing valvular dysfunction.

Intervention for high-risk features — Patients with chronic type B aortic dissection with uncomplicated disease who have high-risk clinical features appear benefit from earlier rather than later thoracic endovascular aortic repair, but a universally accepted set of criteria has not been determined [10,12-14,23-25].

Best medical therapy is associated with a significant rate of failure (about 60 percent within six years [26]), and mortality associated with chronic type B aortic dissection (20 to 50 percent at five years) has been attributed to a lack of aortic remodeling [14,24,25,27,28]. In the Investigation of Stent grafts in Aortic Dissections (INSTEAD) trial, patients with uncomplicated subacute or chronic type B aortic dissection (between 2 and 52 weeks after onset) were randomly assigned to best medical therapy alone or best medical therapy and thoracic endovascular aortic repair [29,30]. While thoracic endovascular aortic repair failed to improve overall survival or adverse event rates at two-year follow-up despite favorable aortic remodeling, at five years, aorta-specific survival was improved for the endovascular group [29]. With these encouraging results, attempts have been made to predict which cohort of patients may benefit from earlier rather than later thoracic endovascular aortic repair [10,12]. High-risk features included maximal aortic diameter >4 cm, false lumen diameter >2.2 cm, an intimal tear located on the inner aortic curvature, bloody pleural effusion, refractory pain or hypertension, radiographic-only malperfusion, and readmission related to aortic dissection [31]. (See 'Natural history' above and 'Predictors of adverse aortic events' above.)

A study from the Society for Vascular Surgery Vascular Quality Initiative (VQI) database reviewed 606 patients with uncomplicated acute type B aortic dissection and found patients treated in the hyperacute period (<24 hours) were higher risk and had higher postoperative complications. This is consistent with existing data regarding early treatment of type B dissection. Notably, there was a trend toward lower mortality in the patients treated in the acute period (1 to 14 days) when compared with the subacute (15 to 90 days), with no difference in reinterventions or postoperative complications between the two groups [31].

Intervention for complicated disease — Patients with complicated chronic type B aortic dissection require emergency intervention (endovascular or open surgical) for clinical malperfusion or rupture [14]. Patients who progress to high-risk features, such as aneurysmal degeneration of the aorta >4 cm, false lumen expansion to >2.2 cm, recurrent pain, radiographic malperfusion, and persistent uncontrolled hypertension should be considered for intervention. Some studies suggest that certain patients who are at high risk for later complications may benefit from earlier, rather than later, intervention.

The frequency of complications that indicate the need for intervention differs somewhat for chronic compared with acute type B aortic dissection, with aneurysmal degeneration being most common indication for intervention [32-34].

●Aneurysmal degeneration – Approximately 20 to 55 percent of medically managed patients with type B aortic dissection will develop aneurysmal degeneration at five years [12,24]. In agreement with guidelines for the management of thoracic aortic disease, intervention should be performed once the thoracic aortic diameter reaches 5.5 to 6 cm [1]. Patients with connective tissue disorder should be considered for repair at smaller diameters.

●Rupture or impending rupture – As with degenerative (true) aortic aneurysms, the risk of rupture increases with increasing aortic diameter. In a review of 571 patients with type B aortic dissection, the incidence of rupture was 0, 3.3, 15.3, 18.8, and 28.6 percent for aortic diameters of 4 to 4.4, 4.5 to 4.9, 5 to 5.4, 5.5 to 5.9, and 6 to 6.4 cm, respectively [35]. Fewer than 10 percent of interventions on patients with chronic type B aortic dissection are due to frank rupture [33]. However, the mortality associated with rupture is high, and therefore it is important to recognize signs of impending rupture and act quickly to treat these patients. Increases in periaortic hematoma and hemorrhagic pleural effusions in two subsequent CT exams during medical expectant management are findings suggestive of impending rupture [14]. According to data from the International Registry of Acute Aortic Dissection, recurrent pain and uncontrolled hypertension are important prognostic factors and should be taken seriously, as these clinical markers may herald impending rupture in the subacute or chronic stage [24].

●Aortic expansion rate >0.5 cm/year – Aortic expansion >0.5 cm/year is considered a sign of instability in the chronic phase and is an indication for repair.

●Recurrent pain – Recurrent pain is the second most common indication for repair in chronic type B aortic dissection, as pain attributed to the dissection can be an ominous sign of potential rupture [33].

●Malperfusion – Malperfusion syndrome is another indication for repair. Approximately 4 percent of chronic type B aortic dissections are repaired due to development of malperfusion syndrome [24,33]. Lower extremity malperfusion is much less likely to develop in the chronic setting compared with the acute setting, with <5 percent of lower limb complications occurring in the chronic setting [36].

●Uncontrolled hypertension – Patients who require ≥3 classes of antihypertensive medications at maximal recommended or maximal tolerated doses should be considered for intervention; however, the decision to intervene should be at the clinical discretion of the surgeon and largely depends on the presence or absence of the features discussed above.

ENDOVASCULAR VERSUS OPEN REPAIR — Repair of the thoracic aorta can be accomplished using traditional open surgical techniques, or with thoracic aortic endovascular repair. For those with appropriate indications for repair (no connective tissue disorder), thoracic endovascular aortic repair is the first-line treatment, when anatomically feasible [1,13,14,23,24,37,38]. For patients who are not candidates for endovascular repair, open surgery provides a durable repair, but is associated with increased perioperative morbidity and mortality. (See 'Dissection repair techniques' below.)  

In the past, open surgical repair was the "gold standard" for repair of chronic type B aortic dissection. Thoracic endovascular aortic repair was subsequently adapted to the treatment of aortic dissection and other acute aortic syndromes following the initial approval of stent-grafts in 2005 for the treatment for thoracic aortic aneurysms. Observational studies confirmed the feasibility, safety, and improved perioperative outcomes for endovascular repair of type B aortic dissection compared with open repair, similar to those for repair of abdominal or thoracic aortic aneurysm [34,39]. While long-term survival rates are similar, long-term durability remains inferior for endovascular repair [14,24,27,33,40]. Although there are no randomized trials comparing open surgical repair with thoracic endovascular aortic repair for chronic type B aortic dissection, a randomized trial comparing outcomes for early endovascular versus best medical therapy for treatment of uncomplicated type B aortic dissection provides some indirect support for an endovascular approach for chronic type B dissection [29,30]. In agreement with guidelines for thoracic aortic disease and an interdisciplinary expert consensus on the management of type B aortic dissection, we suggest endovascular repair in anatomically suitable patients who do not have a connective tissue disorder [1,14]. This recommendation places higher value on reducing early morbidity and mortality and less on the need for long-term surveillance and potential need for reintervention with endovascular repair. Open surgical repair remains the preferred approach for patients with connective tissue disorders, such as Marfan, Ehlers-Danlos, or Loeys-Dietz syndrome, given the poor results of endovascular repair in this setting [41,42].

Endovascular repair is especially advantageous to patients with disease limited to the descending thoracic aorta because it avoids the morbidity of a thoracotomy incision and aortic cross-clamping required with open surgical repair. The endovascular approach also provides an opportunity to treat patients who would otherwise not be candidates for repair, such as older or frail patients. (See "Endovascular repair of the thoracic aorta".)

Perioperative morbidity and mortality — Endovascular repair has a high technical success rate for treatment of chronic type B aortic dissection [33,39,43,44], with lower perioperative morbidity and mortality and shorter hospital length of stay compared with open surgical repair [24,40].

●In a systematic review that included 63 observational studies, the pooled early mortality rate for thoracic endovascular aortic repair in patients with chronic type B aortic dissection was 6.6 percent (95% CI 5.0-8.7) [14]. Among four comparative studies, pooled perioperative mortality for open repair was significantly increased relative to endovascular repair (odds ratio [OR] 4.13, 95% CI 1.10-15.4). Five-year survival rates ranged from 77.7 to 84.4 percent. Freedom from reintervention was 83 percent at one year and 72 percent at three years. In later studies, lower rates of all-cause and in-hospital mortality were reported for thoracic endovascular aortic repair.

●The Investigation of Stent grafts in Aortic Dissections (INSTEAD-XL) trial reported a mortality rate of 2.8 percent [29,30], and a systematic review limited to chronic type B aortic dissection reported a perioperative mortality rate of 2 percent [45]. By contrast, open surgical repair has a higher perioperative morbidity and mortality, with perioperative mortality ranging from 7.5 to 9.3 percent [14,45-47].

●In a retrospective review of 427 patients who underwent open surgical repair for chronic distal aortic dissection and whose anatomy was amenable to thoracic endovascular aortic repair, perioperative mortality was 8.5 percent [48]. Independent risk factors for increased perioperative mortality on multivariate analysis included low estimated glomerular filtration rate (<60 mL/min/1.73 m²), prior descending thoracic aortic repair, and chronic obstructive pulmonary disease. Patients without all three risk factors had a perioperative mortality rate of 2.6 percent.

●A later systematic review included 48 studies with a total of 2641 patients who underwent thoracic endovascular aortic repair for chronic type B aortic dissection [49]. Early (<30 days) all-cause and aortic-related mortality was 1.6 and 0.5 percent, respectively. Late aortic-related mortality was 2.4 percent, and reintervention rates were 10.1 percent for endovascular treatment and 6.7 percent for open surgical treatment.

Thoracic endovascular aortic repair also offers significant early benefits with respect to systemic (eg, respiratory, dialysis) and ischemic complications (eg, stroke, paraplegia) compared with open surgical repair [14,40,45]. For open surgical repair, stroke rates range from 3 to 11.3 percent, and spinal cord injury rates range from 2.4 to 16.4 percent [14,45,47,48]. For thoracic endovascular aortic repair, stroke rates range from 0 to 7.5 percent, and spinal cord injury rates range from 0 to 6.2 percent [14,33,39,49,50].

●In a review from the Vascular Quality Initiative (VQI), the overall rate of spinal cord ischemia in patients who underwent thoracic endovascular aortic repair (any indication) was 3.7 percent; 2.1 percent of those had a permanent functional deficit [50]. In this same study, it was noted that patients who developed any spinal cord ischemia, transient or permanent, had significantly lower one-year survival compared with those without spinal cord ischemia, and those with permanent spinal cord ischemia have worse survival compared with transient.

●In a systematic review of retrospective studies from 2002 through 2021 of chronic type B aortic dissection, the rates of stroke and spinal cord ischemia following thoracic endovascular repair for chronic type B dissection were 1.1 and 0.9 percent, respectively [49].

●In a review that included four comparative studies of patients undergoing repair of chronic type B aortic dissection, complication rates that were significantly lower for thoracic endovascular aortic repair compared with open surgical repair included stroke (OR 4.33, 95% CI 1.02-18.35) and respiratory issues (OR 6.88, 95% CI 1.52-31.02) [45]. Patients who underwent endovascular repair were older than those receiving open surgical repair. Dissection was more likely to be associated with a connective tissue disorder in those who underwent open surgical repair. Outcomes of open surgical repair among those with Marfan syndrome, who tend to be younger and have few comorbidities, were generally excellent [51].

Durability and reintervention — In general, open surgical repair provides a durable repair with lower rates of reintervention compared with thoracic endovascular aortic repair [14,34,40,52-54]. Freedom from reintervention for thoracic endovascular aortic repair was reported to be 83 percent at one year and 72 percent at three years, compared with 99 percent rate at one year for open surgical repair [14,34]. Reintervention following endovascular repair is typically due to stent-graft complications, with nearly half related to endoleak, stent graft collapse, or stent-graft-induced new entry tear, and the remainder due to metachronous pathology or progressive aneurysmal disease related to persistent distal fenestrations. In a systematic review, reintervention rates for open surgery were as high as 12 percent [45]. The causes for reintervention in the open surgical repair group were mostly due to development of disease distal to the treated segment and was similar for thoracic endovascular aortic repair patients as well.

Late rupture and mortality — Long-term survival rates are similar for endovascular versus open surgical repair [14,40]. Five-year survival ranges from 77.7 to 84.4 percent [14]. In a retrospective review, among patients who underwent open surgical repair for chronic type B aortic dissection and whose anatomy was suitable to thoracic endovascular aortic repair, mid- to long-term survival rates were similar compared with those who underwent thoracic endovascular aortic repair [48]. In a review of 169 patients, reported survival rates for open repair were 76, 69, and 55 percent at one, two, and five years, respectively [46]. In the large systematic review, one- and three-year survival rates for open repair were 84 and 80 percent, respectively [45]. Midterm and long-term survival rates were similar with one- and three-year survival rates of 91 percent. Late secondary aortic rupture was rare, occurring in 1.2 percent of open surgical and 3 percent of endovascular repair patients over a mean follow-up of 65 and 30 months, respectively.

PREOPERATIVE EVALUATION AND PREPARATION — A thorough preoperative evaluation should be conducted on all patients with planned intervention for chronic type B aortic dissection. This includes a comprehensive history and physical exam, with a focus on the patient's functional status, cardiopulmonary and renal function, and smoking history. Preoperative risk stratification should be performed. (See "Evaluation of cardiac risk prior to noncardiac surgery" and "Evaluation of perioperative pulmonary risk".)

As with any major operation, appropriate patient selection and thorough preoperative planning are important. The patient should be counseled regarding the general periprocedural risks and the specific risks pertaining to the planned operation. Complications associated with treatment of chronic type B aortic dissection can range from minor to catastrophic.

Anatomic suitability for endovascular approach — Evaluation of the patient's vascular anatomy should preferably be performed using computed tomographic angiography with three-dimensional reconstruction to determine suitability for endovascular repair or alternatively magnetic resonance angiography (eg, patients with iodinated contrast allergy, renal insufficiency). Images are obtained to identify the location of the entry and reentry tears and to aid with graft selection and sizing, as well as operative planning.

To identify the full extent of aortic disease, the study should encompass the chest, abdomen, pelvis, and proximal lower extremities, including the aortic arch and its branch vessels, the descending thoracic and abdominal aorta, and the iliofemoral vessels down to the common femoral artery bifurcation.

●Aortic arch – The anatomy of the aortic arch, including its branches, angulation, diameter, and location of the primary entry tear, are all assessed. Planned coverage of aortic branches may require an arch-debranching procedure prior to endovascular repair. Branched and fenestrated endografts are increasingly being used to treat arch pathologies. Aberrant anatomy (figure 6) such as a right-sided arch or aberrant right or left subclavian arteries may also change the approach.

●Access vessels – The common femoral and iliac arteries should be evaluated. The diameter of the artery must be adequate to support the typically large sheath sizes of the delivery system. Brachial access may be necessary in some cases.

Patients who are not suitable for endovascular repair due to anatomic considerations, such as inadequate proximal or distal landing zones, severe tortuosity or calcifications, inadequate vascular access, or extremes of aortic diameter should be considered for open surgical repair, if possible.

Preventing spinal cord ischemia — Spinal cord ischemia is a serious complication common of both thoracic endovascular aortic repair and open surgical repair. The blood supply to the spinal cord arises from intercostal and lumbar artery branches directly from the aorta, as well as branches of the subclavian and internal iliac arteries. Patients are at increased risk if extensive coverage or replacement of the aorta is planned, especially the T8 to L1 region. The artery of Adamkiewicz originates from this area in 75 percent of individuals (figure 7) [55].

●Prior to thoracic endovascular aortic repair, patients at high risk for spinal cord ischemia should have a lumbar drain placed [56,57]. The extent of thoracic aortic coverage was identified as the most important determinant of spinal cord injury for patients undergoing endovascular repair of thoracoabdominal aortic aneurysms (atherosclerotic, post-dissection) [58]. Other factors to consider include previous aortic surgery, pre-existing internal iliac occlusions, and/or planned coverage of the left subclavian artery without revascularization. (See "Endovascular repair of the thoracic aorta", section on 'Minimizing spinal ischemia'.)

●All patients undergoing open surgical repair for chronic type B aortic dissection should have a lumbar drain placed, since the risk of spinal cord injury with open surgical repair is significantly higher compared with thoracic endovascular aortic repair. The risk of spinal cord injury is highest for Crawford extent I/II thoracoabdominal replacement (figure 8A-B) [59-62]. In a review 2286 patients undergoing open surgical repair of thoracoabdominal aortic aneurysm (24 percent for chronic dissection), the overall incidence of paraparesis/paraplegia was 3.8 percent, with the highest rate among those with extent II (6.3 percent) and extent I (3.3 percent) replacement (figure 8D) [61]. In a randomized trial of 145 patients, cerebrospinal fluid drainage significantly reduced the rate of paraplegia in open surgical repair, with a relative risk reduction of 80 percent [60]. In another review, the use of cerebrospinal fluid drainage plus distal aortic perfusion and moderate hypothermia lowered the incidence of spinal cord injury from 10 to 1 percent in open thoracic repair of thoracoabdominal aortic aneurysms [62]. (See "Overview of open surgical repair of the thoracic aorta", section on 'Anesthesia, monitoring, and organ protection'.)

Adjunctive measures include intraoperative neuromonitoring and the use of somatosensory evoked potentials and/or motor evoked potentials to identify spinal cord injury and institute prompt therapeutic measures. Increasing the mean arterial pressure and/or increasing the cerebrospinal fluid drainage from the lumbar drain are methods to improve spinal cord perfusion [44]. Somatosensory evoked potentials and/or motor evoked potentials should be considered in high-risk patients undergoing endovascular repair and all patients undergoing open surgical repair [63]. (See "Anesthesia for open descending thoracic aortic surgery", section on 'Neuromonitoring for spinal cord ischemia'.)

Lumbar drainage should be continued for at least 48 hours postoperatively for a target cerebrospinal fluid pressure of 10 mmHg or less. Target mean arterial pressure is >80 mmHg, and a target hemoglobin level >10 g/dL is recommended in patients who sustain spinal cord injury to increase spinal cord perfusion and oxygen delivery [63]. In patients who are neurologically intact postoperatively, drainage of up to 15 mL/hour of cerebrospinal fluid for a target pressure <10 mmHg is recommended. In patients with a delayed neurologic deficit, adherence to the cerebrospinal fluid drain status/oxygen delivery/patient status (ie, "Modified COPS") protocol is recommended. In this scenario, the patient is kept flat, the cerebrospinal fluid target pressure is <5 mmHg, with no maximum rate or quantity of drainage, while maintaining adequate oxygen delivery (oxygen saturation and hemoglobin >10 g/dL, cardiac index >2.5 L/min/BSA) and spinal cord perfusion pressure by targeting a systolic blood pressure >140 mmHg [64,65]. (See "Anesthesia for open descending thoracic aortic surgery", section on 'Strategies to prevent renal and visceral ischemia'.)

DISSECTION REPAIR TECHNIQUES

Endovascular repair — Endovascular repair for treatment of chronic type B aortic dissection significantly reduces perioperative morbidity (eg, stroke, respiratory complications) and mortality compared with open surgical repair [14,40,45]. (See 'Endovascular versus open repair' above.)

Although thoracic endovascular aortic repair can be performed with procedural sedation, we prefer general anesthesia [66]. Precise deployment of the endograft requires brief moments of apnea for optimal imaging, and adjunctive measures, such as rapid ventricular pacing, permissive hypotension, or adenosine-induced cardiac arrest can be used with some devices during deployment. (See "Endovascular repair of the thoracic aorta" and "Anesthesia for endovascular aortic repair".)

Goals of endovascular repair — The main objective of endovascular repair for chronic type B aortic dissection is to seal the primary entry tear to exclude flow into the false lumen, which restores the true lumen pressure and re-expands the true lumen (figure 9). This leads to false lumen thrombosis and subsequent aortic remodeling, both of which improve outcomes [27].

Thrombosis of the false lumen following endovascular repair is more likely to be achieved in the acute versus chronic setting [4,43,67]. Critics of endovascular repair in the chronic setting argue that a thickened aortic septum and persistent false lumen pressurization from uncovered distal fenestrations impact the durability and success of thoracic endovascular aortic repair. However, several studies have reported successful false lumen thrombosis, depressurization, aortic remodeling, and sac shrinkage in the majority of patients [68-72]. In a systematic review of 17 observational studies (567 patients), immediate technical success was achieved in 90 percent of patients; complete false lumen thrombosis occurred in nearly 86 percent [39].

Thrombosis of the false lumen is a negative predictor of aortic expansion [73] and is significantly associated with increased survival [12]. In a review of 58 patients with a mean aortic diameter of 6.4 cm who underwent repair of chronic aortic dissection, midterm survival was significantly higher in patients who demonstrated aortic remodeling (reduction in aortic diameter) compared with those who did not (89 versus 54 percent) [27]. Although complete false lumen thrombosis is associated with improved survival, partial false lumen thrombosis appears to have a negative impact on survival [74].

Technical issues — Endovascular devices and techniques for repair of the thoracic aorta are discussed in detail separately. Issues of specific interest for treating chronic type B aortic dissection are reviewed briefly below. (See "Endovascular devices for thoracic aortic repair" and "Endovascular repair of the thoracic aorta".)

●Vascular access – A significant calcium burden and/or tortuosity of the iliac arteries can prevent passage of the device or delivery sheath from the common femoral artery. In these cases, a conduit should be created by suturing a 10 mm Dacron or polytetrafluoroethylene graft to the common iliac artery via a transperitoneal or retroperitoneal incision. If the common iliac arteries are not suitable, a conduit to the infrarenal aorta is another option. Following completion of the repair, the conduit can be ligated near the origin of the anastomosis, leaving a small stump, or the conduit can be used as an iliofemoral bypass to improve the inflow in cases of severe external iliac stenosis.

An "endoconduit" for delivery of the device can also be created using endovascular methods such as the "pave and crack" technique, which involves angioplasty and controlled rupture of the iliac vessels followed by relining with covered stents. A novel technique for pretreatment of calcified vascular access vessels is using intravascular lithotripsy; however, further studies are needed to evaluate the short- and long-term results of this approach. (See "Endovascular repair of the thoracic aorta", section on 'Vascular access'.)

●Intravascular ultrasound – Intravascular ultrasound (IVUS) is recommended during endovascular repair of chronic type B aortic dissection. IVUS can confirm wire access within the true lumen and can help identify the location of the primary entry tear and fenestrations throughout the aorta, while also monitoring for dynamic occlusions of branch vessels in real time. IVUS can also be used to accurately measure the length of the proximal landing zone (zone 1 to 3 (figure 1)) and the diameter of the aorta at the proximal and distal landing zones, aiding in graft size selection.

●Proximal and distal extent and landing zones – Graft-wall apposition, particularly in the proximal landing zone, is critical to prevent type 1 endoleak or device migration. A minimum of 2 cm is required at the proximal and distal landing zone to achieve an adequate seal. Because the proximal entry tear in type B aortic dissection is often just distal to the origin of the left subclavian artery, coverage of the left subclavian is often necessary to provide an adequate length landing zone to achieve an adequate seal. (See 'Arch debranching' below.)

Although the primary objective of endovascular repair is to cover the proximal entry tear, the extent of distal coverage is important as well. Patients with chronic type B aortic dissection can have multiple fenestrations or reentry tears that can continue to pressurize the false lumen even after the proximal entry tear is covered [75]. In general, all major distal fenestrations should also be covered, and to achieve this goal, extension of the graft to the level of the celiac artery may be necessary. Firm apposition of the graft to the aorta is rarely achieved distally in chronic type B aortic dissection.

It is also important to note that the risk of spinal cord injury is significantly increased with more extensive coverage of the descending thoracic aorta [58]. Adjunctive measures should be used to help prevent spinal cord ischemia. (See 'Preventing spinal cord ischemia' above.)

●Device and diameter – The graft diameter is selected based on the diameter of the healthy aorta immediately proximal to the primary entry tear. Measurements can be obtained using preoperative CT scan and should be confirmed intraoperatively with IVUS. In contrast to graft sizing for degenerative (true) aneurysmal disease, which over-sizes the graft 10 to 20 percent, for repair of thoracic aortic dissection, care should be taken to limit graft oversizing to no more than 10 percent to avoid potential retrograde type A aortic dissection.

The use of devices with proximal metal stents or metallic barbs should be avoided, and post-deployment balloon dilation is contraindicated in the setting of aortic dissection to reduce the risk of precipitating retrograde type A dissection, although the risk is less for chronic compared with acute type B aortic dissection [24,76].

Endovascular-specific complications — Complications of thoracic endovascular aortic repair include access-related issues, iatrogenic vessel injury (dissection, perforation, thrombosis), endoleak, stent graft migration or collapse, unintentional coverage of branch vessels, stroke, spinal cord ischemia/paraplegia, retrograde type A dissection, and vessel rupture. (See "Endovascular repair of the thoracic aorta", section on 'Perioperative mortality and complications'.)

●Access-related complications – Access-related complications include hematoma, pseudoaneurysm, arteriovenous fistula, infection, and acute thrombosis causing limb ischemia. Access-related complications occur most often during removal of the sheath or use of closure devices but can also occur during initial vascular access. The use of ultrasound guidance and proper technique can decrease the incidence of access-related complications. A significant change in blood pressure following sheath removal, although potentially related to extremity reperfusion, should be attributed to bleeding until proven otherwise, and prior to sheath removal, anesthesia personnel should be alerted to closely monitor hemodynamics.

●Retrograde type A dissection – Retrograde type A dissection is a serious complication of thoracic endovascular aortic repair. The incidence of retrograde type A dissection during chronic type B endovascular repair ranges from 1.6 to 5 percent [33,39,40]. The risk is much higher in the acute compared with chronic phase of type B aortic dissection, likely due to the more fragile septum and plasticity of the aorta earlier in the course of the disease [4]. To minimize the risk, devices with proximal metal stents or metallic barbs are not used, excessive graft oversizing is avoided (no more than 10 percent), and post-deployment balloon dilatation is not used [24,76].

●Endograft complications – Endograft reintervention is due to the development of endoleak and other complications, such as stent-graft fracture, compression, collapse, or migration. Endoleak is the most common early complication observed, with rates ranging from 4.8 to 11.1 percent [33,39]. A large systematic review of endovascular repair for chronic type B aortic dissection reported an overall rate of endoleak of 8.1 percent at midterm follow-up at 24 months, and type I endoleak was the most prominent [39]. (See "Endoleak following endovascular aortic repair".)

Following endovascular repair, periodic surveillance is required to identify endograft complications. (See "Endovascular repair of the thoracic aorta", section on 'Postoperative endograft surveillance'.)

●Post-implantation syndrome – Post-implantation syndrome is a systemic inflammatory response syndrome that occurs within 72 hours of stent-graft implantation with an incidence of about 15 percent. Clinical features include fever (>38°C), leukocytosis, and elevated C-reactive protein. Blood cultures are negative, and clinical infection is absent. Interleukin 6 level is an important biomarker and is increased within 24 hours after thoracic endovascular aortic repair among those who will develop post-implantation syndrome [77]. Post-implantation syndrome is self-limiting, and management is largely supportive. (See "Endovascular repair of the thoracic aorta", section on 'Postimplantation syndrome'.)

Open surgical repair — Open surgical repair of chronic type B aortic dissection is technically demanding and, depending on the extent of the dissected aorta (figure 8A-E), involves replacement of the descending thoracic aorta or the entire thoracoabdominal aorta with reimplantation of the visceral, renal, and, where appropriate, intercostal vessels [24,46,59]. Open surgical repair requires either a thoracotomy or thoracoabdominal incision, resulting in significant perioperative pain and an increased risk for respiratory and wound complications. Depending on the extent of disease, open surgical repair may require circulatory arrest, left heart bypass, and/or deep hypothermia. Compared with thoracic endovascular aortic repair, open surgical repair has a significantly increased risk for stroke, spinal cord ischemia, and systemic complications, with longer intensive care unit and hospital lengths of stay [14,20,40]. (See 'Endovascular versus open repair' above and "Overview of open surgical repair of the thoracic aorta".)

An experienced cardiovascular anesthesiologist should be involved. Transesophageal echocardiography is routinely used along with hemodynamic monitoring with arterial line placement, and central venous access for large volume resuscitation, if necessary. A lumbar drain is placed to reduce the risk of spinal cord ischemia, especially for extent I/II thoracoabdominal replacement. (See 'Preventing spinal cord ischemia' above.)

Safi approach — There are several approaches to open surgical repair of chronic type B aortic dissection. Our preferred approach is that described by Safi [59]. Additional information regarding open surgical repair of the thoracic aorta, including alternative approaches, is presented separately. (See "Overview of open surgical repair of the thoracic aorta", section on 'Descending aorta'.)

●Positioning – The patient is positioned in the semi-lateral right decubitus position, with the hips tilted (45 degrees) toward the left to facilitate thoracoabdominal exposure and to access to the femoral vessels for left heart cardiopulmonary bypass and distal aortic perfusion.

●Incision and surgical exposure – The location of the incision depends on the extent of the anticipated aortic repair. A formal thoracoabdominal incision is used for disease that extends into the abdomen with the incision extending from the pubic symphysis to the umbilicus curving left toward the costal cartilage to join a posterolateral thoracotomy incision. The sixth rib can be excised for improved exposure. For disease that is limited to the thoracic aorta or extends just to the visceral segment, a modified thoracoabdominal incision is used.

●Cannulation – Following the incision and placement of a self-retaining retractor, cannulation for distal aortic perfusion is performed. The outflow cannula is typically placed in the left atrium or pulmonary vein, and the inflow cannula is placed in the left common femoral artery.

●Proximal anastomosis – The descending thoracic aorta distal to the left subclavian artery is exposed (zone 3 (figure 1); extent I/II thoracoabdominal replacement (figure 3)) with care to identify and preserve the vagus and recurrent laryngeal nerves. Careful dissection separating the descending thoracic aorta from the esophagus is critical to prevent aorto-esophageal fistula. An aortic clamp is placed proximally, and a second mid-descending aortic clamp is placed at the sixth or eighth intercostal space. The aorta is opened, and an appropriately sized woven Dacron graft is sewn into place proximally with running 3-0 polypropylene suture. The anastomosis is inspected for hemostasis, and any bleeding is reinforced with pledgeted sutures. After the proximal anastomosis is completed, the mid-descending aortic clamp is moved distally to the infrarenal aorta. The remainder of the aorta is opened, back bleeding is controlled, and the visceral and renal vessels are perfused. The distal thoracic intercostal arteries are reimplanted, and the graft is passed through the aortic hiatus into the abdomen.

●Visceral anastomosis – For disease that involves the visceral segment (zone 6 to 8 (figure 1)), the visceral vessel anastomoses are performed next. If the visceral and renal arteries are close together, a single patch can be used. Often the left renal artery cannot be included and is anastomosed separately to the graft as a Carrell patch or using a bypass graft. Once the visceral anastomoses are completed, the patient is placed in Trendelenburg position, the graft is flushed proximally, and the clamp is released and moved distal to the next visceral anastomoses. In patients with connective tissue disorders who are prone to patch aneurysm degradation, individual anastomoses to each of the visceral vessels and renal arteries are performed using a multibranched graft.

●Distal anastomosis – The level of the distal anastomosis depends on the extent of disease.

•For disease the extends to, but not beyond the visceral segment (zone 6 to 8 (figure 1); extent I (figure 8A)), the distal anastomosis can be created in a beveled fashion to include the visceral and renal vessels (figure 8A).

•For disease that extends to the aortic bifurcation (zone 9 (figure 1); extent II (figure 8A)), the distal graft anastomosis is created just proximal to the bifurcation (figure 8B).

Prior to completion, the graft is flushed proximally and the aorta distally, and the distal aortic clamp is released. The anastomoses are inspected for hemostasis, and necessary repairs are performed.

Complications — Complications of open thoracic aortic surgery are reviewed separately. (See "Overview of open surgical repair of the thoracic aorta", section on 'Morbidity and mortality'.)

Hybrid repair — The hybrid approach combines open surgical and endovascular techniques to reduce the extent of repair with the positive effects of lowering the morbidity of the procedure and improving overall outcomes [78]. It typically involves open surgical debranching the aortic arch vessels to obtain an adequate landing zone for thoracic endovascular aortic repair, or open surgical debranching the visceral and/or renal vessels. The hybrid approach is especially useful for high-risk patients. Another advantage of the hybrid approach is the ability to stage the repair, which decreases overall morbidity, including spinal cord injury, as well as reducing perioperative mortality [79]. In one review, perioperative mortality was 12.5 percent, and the incidence of spinal cord injury was 8.3 percent in patients who underwent hybrid endovascular repair of thoracoabdominal aneurysm. There was no mortality difference in patients who required a larger number of visceral vessel bypasses; however, patients requiring only one or two vessel bypasses had a shorter length of stay.

Arch debranching — Hybrid arch procedures are performed for patients with inadequate proximal landing zones for thoracic endovascular aortic repair. All commercially available thoracic endovascular devices require a minimum of 2 cm of proximal seal zone. If coverage of an arch branch is necessary, then an open surgical debranching procedure is necessary.

●The most common hybrid approach involves coverage of zone 2 (ie, just distal to the left common carotid artery (figure 1)) and involving the origin of the left subclavian artery. If the proximal extent of the endovascular repair requires coverage of the left subclavian artery, the Society for Vascular Surgery suggests preoperative extremity revascularization [80]. Debranching the left subclavian artery is accomplished by a left common carotid artery to left subclavian artery bypass or a left subclavian artery to common carotid artery transposition. A prosthetic graft is the preferred conduit when performing a carotid-subclavian bypass. Patency rates are significantly higher for grafts compared with autologous vein (94 versus 58 percent at five years in one review [81]). Similar results were reported in a later review [82]. When planning a transposition, it is important to screen the patient for previous coronary artery bypass graft; a prior left internal mammary artery (LIMA) to left anterior descending bypass is an absolute contraindication to a transposition. In this scenario, a carotid-subclavian artery bypass is performed, ensuring that the subclavian clamp is placed distal to the LIMA during the creation of the distal anastomosis to allow continued coronary perfusion.

●A hybrid approach that involves landing in zone 1 (ie, just distal to the innominate artery (figure 1)) involves coverage of both the left common carotid artery and left subclavian artery, and a debranching procedure involves a right common carotid artery to left common carotid artery bypass, typically tunneled retropharyngeal, combined with a left common carotid artery to left subclavian artery bypass or transposition. The origins of the left common carotid artery and left subclavian artery should be ligated surgically or plugged using an endovascular device (eg, Amplatzer) to prevent type 2 endoleak after placement of the stent-graft.

●Arch branch and fenestrated devices are increasingly being used in zone 0 to 2 coverage (figure 1); however, future studies are required to determine the outcomes of these devices. The US Food and Drug Administration (FDA) recently approved a thoracic branch endoprosthesis for treatment of lesions requiring zone 2 coverage in patients who are at high risk for left subclavian artery debranching procedures and have appropriate anatomy.

Visceral debranching — For patients with chronic type B aortic dissection and disease involving the visceral segment (zone 6-8 (figure 1)), debranching can create an adequate distal landing zone for subsequent placement of an endograft. A midline laparotomy incision is the preferred approach for visceral debranching, as it allows access to the four visceral vessels. An alternative is a left retroperitoneal approach, especially in the case of the "hostile abdomen"; however, it may be difficult to access the right renal artery.

The availability of an adequate inflow vessel, commonly the distal infrarenal aorta or common iliac artery, should be confirmed prior to visceral debranching. The external iliac artery is avoided, as this artery is typically diseased or small.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Aortic dissection and other acute aortic syndromes".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Aortic dissection (The Basics)" and "Patient education: Thoracic aortic aneurysm (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Type B aortic dissection – Chronic type B aortic dissection involves only the descending aorta (figure 1) and by definition has been present for more than 90 days. (See 'Type B aortic dissection' above.)

●Approach to management – The approach to management of chronic type B aortic dissection depends on the clinical severity of the dissection (uncomplicated, complicated, high-risk features). (See 'Management' above.)

•Uncomplicated dissection – Patients with uncomplicated chronic type B aortic dissection are generally managed medically with periodic clinical and imaging surveillance, and monitoring for signs of progression to high-risk features. Medical management includes ongoing control of heart rate and blood pressure (ie, anti-impulse therapy) with a goal heart rate <60 beats per minute and systolic blood pressure <120 mmHg. Beta-blockers are continued as maintenance therapy in the chronic setting. The addition of calcium channel blockers in the chronic setting helps reduce aortic expansion and has been associated with a survival benefit. (See 'Uncomplicated dissection' above.)

Our approach to intervention for uncomplicated disease is as follows:

-Patients without high-risk features – For patients without high-risk features, we suggest ongoing medical management, rather than intervention (Grade 2C). However, the patient and clinician may reasonably choose endovascular intervention in addition to ongoing medical therapy to prevent malperfusion or other aortic complications, placing more value on potentially improved aortic outcomes in the long term over potential perioperative complications (eg, stroke, spinal cord ischemia). Factors that may influence decision-making include the age of the patient, life expectancy, medical risk, and the presence of certain anatomic factors that may increase the risk for future aortic events.

-Patient with high-risk features – For patients presenting with or progressing to high-risk features, we suggest intervention (Grade 2C). High-risk features include intractable or refractory pain >12 hours, refractory hypertension (>3 classes of antihypertensive medications at maximum doses), and radiographic features such as entry tear on lesser curvature, aortic diameter >4 cm, false lumen >2.2 cm, bloody pleural effusion, and radiographic-only malperfusion.

•Complicated dissection – For patients with complicated chronic type B aortic dissection, which includes progression to clinically relevant malperfusion and/or rupture, repair is required. Nearly two-thirds of patients with chronic type B aortic dissection will develop complications. The frequency of these complications differs compared with acute type B aortic dissection, with aneurysmal degeneration being most common. (See 'Intervention for complicated disease' above.)

•Type of repair – For patients with chronic type B aortic dissection (no connective tissue disorder) with indications for intervention and suitable anatomy, we suggest endovascular repair, rather than open surgical repair (Grade 2C). Thoracic endovascular aortic repair is associated with reduced perioperative mortality with lower rates of major perioperative complications (eg, stroke, spinal cord ischemia, systemic complications) compared with open repair; however, reintervention rates are higher for endovascular compared with open surgical repair. For good-risk surgical patients (normal renal and pulmonary function) treated at a high-volume center, open surgery provides a more durable repair. (See 'Endovascular versus open repair' above.)

•Prevention of spinal cord ischemia – For patients who undergo repair, measures should be taken to decrease the risk of spinal cord ischemia associated with thoracic aortic repair. A lumbar drain is used in all patients undergoing open surgical repair and for high-risk patients undergoing thoracic endovascular repair, which includes those with planned extensive endograft coverage of the distal thoracic aorta (T8 to L1), previous aortic surgery, pre-existing internal iliac occlusions, and/or planned coverage of the left subclavian artery without revascularization. (See 'Preventing spinal cord ischemia' above.)