Stroke Following Open and Endovascular Thoracic Aortic Repair

VASCULAR DISEASE MANAGEMENT 2013:10(2):E45-E51

Abstract

Endovascular repair of descending thoracic aortic pathology has led to a substantial reduction in mortality, complications, and length of stay. However, the incidence of postoperative stroke remains similar to open surgery and presents a major challenge. Stroke carries a poor prognosis for timely discharge, and if the stroke is not fatal, affected patients often require prolonged neurorehabilitation. The presence of underlying aortic, cardiac, and/or cerebrovascular disease, in combination with procedural factors, is likely to dictate the risk of stroke. The cause of stroke following endovascular aortic interventions has been inadequately studied. Stroke is more common following deployment in a more proximal landing zone. The evidence for left subclavian artery revascularization remains equivocal. We discuss the absolute and relative indications for left subclavian revascularization prior to deliberate coverage in endovascular repair. Further research is required to determine the rates of emboli associated with different devices and to clarify techniques for avoiding embolic events. When cerebrospinal fluid drainage is undertaken, drainage should be monitored and controlled to reduce the risk of hemorrhagic stroke.

Endovascular repair for thoracic aortic pathology over the past 2 decades has yielded important benefits in terms of overall mortality, morbidity, and reduced hospital stay but not stroke.^1-4 Although the overall incidence and mortality from stroke in the developed world is falling, it remains a significant problem following thoracic aortic surgery, due to a combination of patient and procedural factors.⁵ Stroke carries a poor prognosis for discharge and approximately 30% to 50% of affected patients die in the hospital.^6,7 Following repair of ruptured thoracic aneurysms, stroke is a significant independent risk factor for 30-day (OR 8.11, P=.004) and 1-year (P=0.006) mortality.⁷ Prolonged neurorehabilitation is required for survivors.⁸ A comprehensive understanding of the classification, etiology, and risk factors for surgery-associated stroke is essential to address this important problem, particularly when procedures performed to prevent stroke can themselves directly cause stroke.

The diagnosis of stroke is based on clinical findings, but this is often difficult in the perioperative period due to other causes of neurologic impairment, including delirium and sedation.⁵ Although the distinction between neurologic events lasting more or less than 24 hours is entirely arbitrary (and permanent tissue damage may be seen following transient ischemic attack [TIA]), little data are available on the incidence of TIA following surgery.⁵

Clinical vs Imaging Diagnosis

Stroke may be ischemic or hemorrhagic; because the management of each is different the ability to make the distinction between them quickly is important and relies on computed tomography (CT) or magnetic resonance imaging (MRI).^9-11 MRI is now a readily available and increasingly utilized imaging modality.⁵ MRI (including diffusion-weighted imaging) is more sensitive than CT, particularly in the early stages post infarction. Modern thoracic endovascular aortic repair (TEVAR) devices are classified as MRI conditional and signal voids are localized to the region around the device; complications resulting from MRI of patients who have received endovascular devices have not been reported.^12,13 CT remains an essential tool for ruling out hemorrhage. It is important to be aware that clinically detectable neurologic deficits correlate poorly with imaging findings, particularly during the early period following an ischemic stroke.

Attempts to ascertain the most likely causes of peri-TEVAR stroke have been challenging because stroke aetiology in this relatively new procedure has not been thoroughly investigated. In addition, patients often have multiple underlying risk factors including cardiac arrhythmia and a high burden of atheroma, which predisposes patients to embolic stroke. Even in primary ischemic stroke, the etiology remains cryptogenic in approximately a third of cases.¹⁴

Postoperative ischemic strokes are most commonly focal and occur as a result of small emboli from extracranial sources, including carotid and arch atheroma or cardiac arrhythmias. Large watershed infarcts may also occur following large emboli or exclusion of the origins of the aortic arch branches. The functional patency of the Circle of Willis is an important collateral pathway (Figure 1).

Hemorrhagic Stroke 

Hemorrhagic stroke is less frequent than ischemic stroke following surgery. Primary hemorrhagic stroke usually occurs as a result of rupture of small lipohyalinotic aneurysms secondary to hypertensive small vessel disease.⁵ Drainage of cerebrospinal fluid (CSF) using a catheter inserted into the subarachnoid space may be required following thoracic aortic surgery to improve perfusion pressure of the spinal cord and reduce the risk of (or treat) postoperative paraplegia.¹⁵ Excessive uncontrolled drainage of CSF can cause subdural and intracerebral hemorrhage and a strict protocol should be followed to limit hourly drainage volumes (Box 1).^6,16

Stroke After Open Surgery 

Stroke is reported in 1.8% to 5.9% of all series.^17-20 The etiology of stroke in these patients is likely to be embolization of atherosclerotic debris or thrombus from the aorta. Diffuse injury is usually due to air embolism, cellular debris, insufficient cooling, or uneven cooling during cardiopulmonary bypass. If the circulatory arrest exceeds 40 minutes then the rate of stroke rises sharply.²¹ Patients at risk of stroke are those >65 years of age, those with severe peripheral arteriopathy, those with severe occlusive carotid disease, and those with specific neurologic histories. These patients need special evaluation and preoperative work-up.

Antegrade cerebral protection strategies after the construction of the distal anastomosis and the use of retrograde cerebral perfusion might lower the risk of stroke in patients that need circulatory arrest (Figure 2).^22-25 Careful preoperative evaluation of patients with multidetector CT and aortic echocardiography allows operative planning and can guide aortic clamping and cannulation strategies. The benefits of retrograde cerebral circulation are primarily two-fold. First, there is homogeneous cooling of the brain. Second, it flushes embolic debris from the cerebral vasculature.²⁶ Effective nutrient delivery is best achieved with antegrade cerebral protection.²⁶ Most surgeons resume antegrade cerebral and systemic circulation after the construction of the distal aortic anastomosis. This is usually performed by placing the aortic cannula in a side arm of the aortic interposition graft. This is in preference to retrograde systemic circulation (via femoral vessels) after a period of circulatory arrest and avoids embolization of distal aortic debris. 

A meta-analysis of nonrandomized comparative studies including 5,888 patients found no difference in stroke rate between TEVAR and open surgery for descending thoracic aortic (DTA) pathology, but TEVAR had significant benefits with regard to overall mortality, paraplegia, renal failure, myocardial infarction, pneumonia, and length of stay.⁴ For thoracic aortic rupture, a meta-analysis also failed to show significantly reduced stroke rates when comparing an open versus endovascular approach.³ In a recent series of 100 patients with acute DTA pathology, the incidence of stroke was also similar in those treated by open surgery (9%) or endovascular stent grafting (8%).²⁷

Stroke After Endovascular Surgery

Does left subclavian artery revascularization before coverage reduce the risk of stroke?

Left subclavian artery (LSA) coverage is required in 10% to 50% of patients to achieve an adequate proximal landing zone during TEVAR.^28-29 Early reports of TEVAR suggested that the LSA may be covered with impunity, but subsequent studies of cerebrovascular complications have resulted in the current Society for Vascular Surgery’s Practice Guidelines suggesting revascularization prior to intended coverage.^30-34 The results of the EUROSTAR registry are proposed to be pivotal, despite the fact that multivariate analysis did not suggest that LSA revascularization protects from stroke.^30,34 The evidence to date is generated from nonrandomized studies and the debate is ongoing; a recent review concluded that elective patients undergoing TEVAR should have prophylactic revascularization when preoperative imaging reveals abnormal aortic anatomy or pathology.^28,34,35 

The total number of microembolic signals (MES) in the middle cerebral arteries (MCA) detected by transcranial Doppler during TEVAR correlates with the rate of TIA, stroke, and death.³⁶ During TEVAR, the “embolic load,” which is similar in the left and right MCAs, seems to be highest during deployment of the endoluminal device and insertion/manipulation of the pigtail catheter.³⁶ This is unsurprising, because aortic arch atheroma is associated with stroke (and death) even prior to intervention.^37,38 MES are in general more frequent when the landing zone is more proximal; landing the stent graft in Zones 0-2 has been associated with greater risk of stroke compared with deployment in Zones 3-4.² Approximately 90% of postoperative strokes occur within 24 hours of TEVAR, which is consistent with embolic etiology.⁶ The need to cover the origin of the LSA may serve as a surrogate marker for a more proximal landing zone, which is itself associated with a larger embolic burden and stroke rate. Confounding factors, together with the difficulty in assigning a specific cause of stroke in individual patients, may preclude interpretation of the existing nonrandomized literature.

Useful information may be gained from femoral transcatheter aortic valve implantation (TAVI) studies since the procedure involves wire manipulation over a guidewire in the aortic arch and ascending aorta. Imaging in 180 patients in four studies demonstrated multiple diffuse areas of deficit on diffusion-weighted MRI in 68% to 91% of cases.^39-43 The incidence of clinical stroke in these patients was only 0% to 10%; the vast majority of emboli were silent and over 75% of patients experienced multiple lesions. Given the size, number and distribution of infarcts, emboli are the likely etiology; deficits occurred equally in both hemispheres and in the anterior and posterior circulation. Age, the severity of arch atheroma, and catheterization time predicted the number of infarcts.^43-44 

Chung et al reported results of  793 procedures where LSA coverage (required in nearly 40% of cases) was associated with a higher risk of stroke (OR 2.17, 1.14-4.14, P<.001). Urgent procedures were also associated with a significantly higher risk of stroke compared with elective cases.⁴⁵ In a recent series (albeit in a smaller cohort of patients), coverage of the LSA was significantly associated with a higher risk of spinal cord ischemia, but not stroke.⁴⁶ The authors concluded that the presence of significant aortic plaque on preoperative CT angiography increased the risk of stroke. Conversely, Melissano et al. recently concluded that the extent of arch involvement is an important factor, reporting stroke rates for Zone 0, Zone 1, and Zone 2 cases of 9.4%, 0%,  and 1.3% respectively.⁴⁷ In their study, stroke rate was not significantly lower following LSA revascularization (2.6% vs 2.9% in patients not revascularized).  All of these strokes were ischemic in nature and mainly involved the cerebellar territory (indicating likely posterior cerebral embolism from the subclavian and vertebral arteries). Interestingly, the authors reported no strokes occurred if the LSA was occluded prior to deployment of the stent graft, vs 4.5% in patients where the LSA was patent at the time of deployment. These data suggest that LSA occlusion may be a useful strategy to prevent embolic stroke.⁴⁷ The severity of atheromatous disease of the aortic arch may have the greatest influence in determining the risk of stroke and, therefore, preoperative routine LSA revascularization may not protect the brain. 

Although it has been reported that the incidence of stroke is lower following LSA revascularization (4.7% vs 7.2%, P<.001), overall mortality has been reported to be greater (10.5% vs 3.4%, P=.03) and revascularization does not seem to reduce the risk of spinal cord ischemia.^29,48 Furthermore, there is a higher incidence of stroke in patients undergoing LSA coverage, regardless of preoperative LSA revascularization (pooled OR, 3.18; 95% CI, 1.17-8.65) or LSA coverage alone (pooled OR, 2.28; 95% CI, 1.28-4.09).⁴⁹ In a meta-analysis of 278 patients undergoing left common carotid to LSCA bypass or LSCA transposition, complications were nerve injury (8.6%), lymph leak (2.5%), thrombosis (1.1%), graft infection (0%), hemorrhage (1.1%), wound dehiscence (0.4%), and stroke (0.7%), but no deaths.²⁹

In our current practice, in addition to suggested absolute indications for LSA revascularization we have adopted a low threshold policy for LSA revascularization prior to TEVAR (Figure 3). We often revascularize prior to intended coverage unless the right vertebral is dominant or the left is atretic. Intraluminal wires should be manipulated with care, and exchanges and ballooning should be minimized where possible. Whilst this article is concerned with stroke, spinal cord and arm ischemia are important additional considerations.²⁸

Is there a difference in outcomes between dissection and aneurysm cases?

There are few available data sets comparing cerebrovascular outcomes following treatment of thoracic aortic aneurysms with dissections. Paraplegia and stroke rates following TEVAR of chronic type B aortic dissection are very low (reported as 0.45% and 1.5% respectively).⁵⁰ Kang et al. reported no occurrence of paraplegia in their study of 76 patients undergoing TEVAR for chronic distal aortic dissection.⁵¹ Conversely, for acute complicated type B dissection, stroke and paraplegia rates are higher (6.3% and 4.9% respectively).⁵² In the STABLE trial (where a composite thoracic construct consisting of a proximal stent graft and distal bare metal stent was used for the treatment of complicated type B dissection), the rates of stroke, TIA, and paraplegia were 7.5%, 2.5% and 2.5% respectively.⁵³ White et al, who reported equal stroke and paralysis rates of 9.4% following treatment of complicated type B dissections, concluded that endovascular repair significantly reduced the risk of paralysis and paraplegia (OR 0.256, P=0.001) but not stroke compared with open repair.⁵⁴

Conclusion

Although endovascular repair of descending thoracic aortic pathology has resulted in significant reduction of mortality and postoperative complications, stroke rates remain comparable to open repair and present a major challenge. Proximal landing zones, procedure length, female sex, coverage of the LSA, emergency procedures, arch atheroma, prior stroke, and placement of a proximal cuff have been associated with higher stroke rates after TEVAR. Good evidence that revascularization of the LSA reduces stroke rate is lacking. The evidence that stroke is due to emboli rather than hypoperfusion is increasing. Further research is needed to determine the cause of stroke after TEVAR, and the rates of emboli associated with the range of endovascular devices currently available. We currently revascularize the LSA prior to deliberate coverage, unless the left vertebral is small or absent, or the right vertebral is clearly dominant.

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