TEVAR following prior abdominal aortic aneurysm surgery: Increased risk of neurological deficit

Article Outline

• Abstract
• Methods
  • Study design and data collection
  • Data analysis
• Results
  • Study population
  • Characteristics of TEVAR
  • Spinal cord ischemia (SCI)
  • Predictors of SCI after TEVAR following prior AAA repair
  • Other outcomes
• Discussion
• Author contributions
• References
• Copyright

Objective

Evidence regarding the impact of prior abdominal aortic aneurysm (AAA) repair on the risk of neurological deficit after thoracic endovascular aortic aneurysm repair (TEVAR) is lacking. The purpose of this study was to characterize the risk of TEVAR-related neurological deficit in patients who previously underwent infrarenal AAA surgery.

Methods

Prospective maintained databases of patients undergoing TEVAR in the participating institutions were searched for patients with a history of prior AAA surgery before TEVAR. Patient and procedural characteristics and postoperative mortality and morbidity were subsequently centrally collected and systematically entered in a database. Univariate and multivariate logistic regression were performed associating variables with postoperative spinal cord ischemia (SCI).

Results

Seventy-two patients were identified that underwent TEVAR after prior AAA repair. The risk of SCI was 12.5% (n = 9) and significantly higher than the 1.7% risk of SCI in patients without prior AAA repair (relative risk [RR] 7.2, 95% confidence interval [CI] 2.6 to 19.6, P < .0001). Symptoms of SCI completely resolved in 4 patients with prior AAA repair. Univariate analysis demonstrated that the following variables were significant predictors of SCI in patients with prior AAA repair: preoperative renal insufficiency (odds ratio [OR] 29.5; 95% CI 5.3-164, P < .001), increased length of aorta coverage by TEVAR (OR 1.1; 95% CI 1.0-1.2, P .039) and a lengthened time interval between prior AAA repair and TEVAR (OR 1.2; 95% CI 1.0-1.4, P .026). Preoperative renal insufficiency was also significantly associated with the risk of SCI in multivariate analysis (P .011).

Conclusion

Prior infrarenal AAA repair is associated with dramatic increased risk of SCI after TEVAR compared to patients without prior AAA surgery. Preoperative renal insufficiency appears to be an important predictor of SCI after TEVAR in patients with prior AAA repair. A thorough understanding of the risk profile in patients requiring TEVAR following prior AAA surgery is essential when determining appropriate surgical recommendations. If the diameter and rupture risk are large and TEVAR is indicated, the best available care should be offered for maximal protection of the spinal cord in these patients.

Spinal cord ischemia (SCI) is a frequent and poorly predicted complication after thoracic endovascular aortic aneurysm repair (TEVAR). Pooling of previously reported results of 1251 patients undergoing TEVAR revealed an average risk of postoperative SCI of 4.4% (range 0 to 12%).¹, ², ³, ⁴, ⁵, ⁶, ⁷, ⁸, ⁹, ¹⁰, ¹¹, ¹², ¹³ Vascular surgeons have long assumed that prior abdominal aortic aneurysm (AAA) repair is a risk factor for SCI following TEVAR. But is there any data that supports this widely believed association?

Some authors have indeed described a potentially increased risk of neurological deficit in patients undergoing TEVAR after prior AAA repair, although the relatively small numbers of patients with prior AAA repair in these studies limited their validity. Baril et al⁶ described 125 patients undergoing TEVAR of which 28 patients had previous or concomitant AAA repair. The risk of SCI was 14.3% in patients with previous or concomitant AAA repair (4 of 28 patients) vs 1.0% (1 of 97) in patients without previous or concomitant AAA repair. Cheung et al⁹ showed a risk of SCI after TEVAR of 11.8% in patients with prior AAA repair (2 of 17) and 5.2% in patients without prior AAA repair (3 of 58). Sandroussi et al¹⁴ showed that paraplegia was significantly associated with previous AAA repair in a group of patients that underwent TEVAR for aortic dissections, aneurysms, traumatic ruptures, penetrating ulcers, or other indications (relative risk [RR] 7.125, P .02). Chiesa et al⁸ described also a group of patients that underwent TEVAR for aneurysm, dissection, or ulcer and reported that patients with previous or concomitant AAA repair had an increased risk of neurological deficit (P .08). The European Collaborators on Stent/Graft Techniques for Aortic Aneurysm Repair (EUROSTAR) investigators performed a multivariate analysis of risk factors for SCI after TEVAR for aneurysm, dissection, traumatic rupture, or other indication.⁴ Concomitant open abdominal aorta surgery was one of the factors that correlated significantly and independently with increased risk of SCI in this study (odds ratio [OR] 5.5; P .037). Because no data about previous AAA repair was collected in the EUROSTAR registry, no conclusions with regard to the impact of prior AAA repair on the risk of SCI after TEVAR could be drawn.

With the currently largest available study consisting of only 28 patients undergoing TEVAR after prior or concomitant AAA repair, the evidence about the impact of prior AAA repair on morbidity and mortality of TEVAR is limited.⁶ This group should, however, not be neglected in literature, since approximately 1 out of 6 patients undergoing TEVAR have a history of prior AAA repair.¹⁵ The purpose of this study is to provide more insight into the risk of SCI after TEVAR of patients with prior AAA repair.

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Methods 

Study design and data collection 

Five institutions participated in this multicenter cohort study. All participating institutions maintained prospective databases of patients undergoing TEVAR. Each database was retrospectively reviewed by at least one vascular surgeon from the participating institution to identify patients who underwent TEVAR after prior AAA surgery. Traumatic ruptures and aortic dissections were not included. The data were subsequently centrally collected and systematically entered in a database.

Baseline data which were collected included gender, age, moment of prior AAA surgery, type of prior AAA surgery (open tube graft, open bifurcated graft or endovascular aneurysm repair [EVAR]), fitness for surgery as classified according to the American Society of Anesthesiology (ASA) classification, and preoperative renal insufficiency. Renal insufficiency was defined by a plasma creatinine >1.5 mg/dL. The following procedural characteristics were documented: date of TEVAR, time interval between prior AAA repair and subsequent TEVAR, intra-operative hypotension (systolic blood pressure <80 mm Hg), coverage of the left subclavian artery without revascularization, number of deployed stent grafts during TEVAR, total length of the aorta that was covered by TEVAR in cm, cerebrospinal fluid (CSF) drainage, timing of start of CSF drainage, and duration of CSF drainage in days.

Collected outcome data included hospital length of stay, postoperative mortality (<30 days), dialysis-dependent or non-dialysis-dependent renal insufficiency, stroke, postoperative symptoms of spinal cord ischemia, time of presentation of symptoms of SCI, and clinical course of these symptoms (temporary or permanent). Symptoms of SCI were defined as postoperative neurological deficits involving the lower extremities, regardless of whether the deficit was weakness (paraparesis) or paralysis without indication of a stroke. Stroke was defined as any new clinically-evident brain injury present after operation, including focal or global and transient or permanent deficits lasting >24 hours. Besides the above-mentioned data about patients with prior AAA repair, also the number of patients without prior AAA repair who underwent TEVAR and the number of these patients without prior AAA repair that developed postoperative symptoms of SCI in the participating institutions, were collected.

Data analysis 

Odds ratios and 95% confidence intervals (CIs) were calculated with univariate logistic regression to correlate patient and procedural characteristics with postoperative SCI. Age, gender, and variables with a P value < .2 in the univariate model were entered in a multivariate logistic regression model to calculate independent effects of patient and procedural characteristics on the risk of SCI.

Analysis of the data was performed with SPSS version 14.0 (SPSS, Chicago, Ill). The risk of SCI observed in the group of patients who underwent TEVAR after prior AAA repair was compared with the risk in patients without prior AAA repair from results from the same participating institutions. Relative risks and 95% CIs were calculated with Episheet.¹⁶ A P value less than .05 was considered significant.

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Results 

Study population 

Seventy-two patients were identified who underwent TEVAR after prior AAA repair. All patients underwent TEVAR for degenerative aortic aneurysm disease between 1998 and 2008. Mean age of these patients was 73 ± 6.8 year and 86% were male (n = 62). Table I provides detailed baseline characteristics of the included patients. The median time interval between prior AAA surgery and TEVAR was 3.0 years and ranged from 0.17 to 18 years (mean 3.8 ± 3.6). The distribution of the time interval between prior AAA repair and subsequent TEVAR is shown in the Fig.

Table I. Patient characteristics and specifications of TEVAR

	Total, n = 72
	N or mean	(%) or (± SD, range)
Males (%)	62	(86)
Age in years (± SD, range)	73	(±6.8,52-84)
ASA
I (%)	0	(0.0)
II (%)	2	(2.8)
III (%)	54	(75)
IV (%)	16	(22)
V (%)	0	(0)
Preoperative renal failure (%)	10	(14)
Prior AAA surgery	72	(100)
Open tube graft (%)	34	(47)
Open bifurcated graft (%)	20	(28)
EVAR (%)	16	(22)
Autologous VSM (%)	1	(1.4)
Unknown graft type (%)	1	(1.4)
Time interval in years (± SD, range)⁎	3.8	(±3.6,0.17-18)
Number of deployed stents
1	17	(24)
2	40	(56)
3	14	(19)
4	1	(1.4)
Aorta length covered by TEVAR in cm (± SD, range)	21	(±7.2,8.0-42)
<15.0 cm	10	(13.9)
15.0-19.9 cm	19	(26.4)
20.0-24.9 cm	17	(23.6)
25.0-29.9 cm	15	(20.8)
30.0-34.9 cm	8	(11.1)
≥35.0 cm	3	(4.2)
Intra-operative hypotension (%)	6	(8.3)
LSA covering without revascularization (%)	10	(14)
CSF drainage
Start preoperatively	47	(65)
No CSF drainage during procedure	25	(35)

ASA, American Society of Anesthesiologists classification of physical status; AAA, abdominal aortic aneurysm; EVAR, endovascular abdominal aortic aneurysm repair; VSM, vena saphena magna; TEVAR, thoracic endovascular aortic aneurysm repair; LSA, left subclavian artery; CSF, cerebrospinal fluid; SD, standard deviation.

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• Fig. 

  Time interval between prior AAA repair and subsequent TEVAR. AAA, Abdominal aortic aneurysm; TEVAR, thoracic endovascular aortic aneurysm repair.

Characteristics of TEVAR 

CSF drainage was started in 65% preoperatively (n = 47), and in 1.4% of all patients (n = 1) after the procedure and after the onset of symptoms of SCI. Mean duration of CSF drainage was 3.0 ± 0.6 days (range, 1 to 5 days).

The mean length of aorta coverage by TEVAR was 21 ± 7.2 cm and ranged from 8.0-42 cm. The left subclavian artery (LSA) was covered without revascularization in 14% of the patients. Intra-operative hypotension was documented in 8.3% of the patients (n = 6). Detailed information about the thoracic endovascular aortic procedures is shown in Table I.

Spinal cord ischemia (SCI) 

Symptoms of SCI occurred in 12.5% of all patients that underwent TEVAR after prior AAA repair (n = 9). Detailed information about the patients with SCI is shown in Table II. Symptoms of SCI completely recovered in 4 of these patients and were permanent in the other 5 patients. The risk of SCI in patients without prior AAA repair that were treated in the same participating institutions was 1.7% (6 of 345 patients). A univariate comparison of the 12.5% risk of SCI of patients with prior AAA repair with the 1.7% risk of patients without prior AAA repair resulted in a relative risk of 7.2 (95% CI 2.6-19.6, P < .0001).

Table II. Patients with spinal cord ischemia

Nr, Number; M, male; F, female; AAA, abdominal aortic aneurysm; TI, time interval between prior abdominal aortic aneurysm surgery and subsequent thoracic aortic aneurysm repair; RI, preoperative renal insufficiency; ASA, American Society of Anesthesiologists classification of physical status; LSA cover, left subclavian artery coverage without revascularization; LOS, hospital length of stay; CSF, cerebrospinal fluid drainage; OR, open repair; EVAR, endovascular abdominal aortic aneurysm repair.

Predictors of SCI after TEVAR following prior AAA repair 

Patient and procedural characteristics of patients undergoing TEVAR after prior AAA repair were subsequently associated with the risk of postoperative SCI. The results of the univariate regression analysis are shown in Table III. Preoperative renal insufficiency was significantly associated with higher risk of SCI (OR 29.5; 95% CI 5.3-164, P < .001). Increased risk of SCI was also found for increase in length of aorta coverage by TEVAR in cm (OR 1.1 per cm increase; 95% CI 1.0-1.2, P .039). The time interval between prior AAA repair and TEVAR in years was significantly associated with the risk of SCI as well (OR 1.2 per year increase; 95% CI 1.0-1.4, P .026).

Table III. Predictors of spinal cord ischemia after TEVAR in patients with a history of prior AAA repair, univariate analysis

Variable	Odds Ratio	(95% CI)	P value
Age in years	1.1	(0.9to1.2)	.287
Female gender	0.8	(0.1to6.7)	.797
Type of prior AAA surgery (EVAR, open tube or open bifurcated)	1.1	(0.5to2.6)	.841
Prior AAA surgery (open vs EVAR)	1.0	(1.0to1.0)	.729
Time interval between prior AAA repair and TEVAR in years	1.2	(1.0to1.4)	.026
Preoperative renal insufficiency	29.5	(5.3to164)	.000
ASA classification	2.0	(0.5to8.5)	.337
Number of stents deployed during TEVAR	0.6	(0.2to1.7)	.341
Aorta length coverage in cm	1.1	(1.0to1.2)	.039
LSA coverage without revascularization	4.0	(0.8to19.7)	.088
Intra-operative hypotension	4.7	(0.7to31.0)	.111
Preoperative start of CSF drainage	0.3	(0.1to1.3)	.118

CI, Confidence interval; AAA, abdominal aortic aneurysm; EVAR, endovascular abdominal aortic aneurysm repair; TEVAR, thoracic endovascular aortic aneurysm repair; ASA, American Society of Anesthesiologists classification of physical status; LSA coverage, left subclavian artery coverage without revascularization; CSF, cerebrospinal fluid drainage.

Several other factors tended to increase the risk of SCI, although no significant levels could be established, possibly due to relatively small numbers. These variables included LSA coverage without revascularization, intra-operative hypotension, and absence of CSF drainage. Other variables, including age, gender, type of prior AAA surgery (EVAR or open), number of deployed stents, and ASA classification were not significantly associated with the risk of SCI.

Age, gender, and all variables with a P value < .2 in the univariate analysis were subsequently entered in a multivariate logistic regression analysis. The results of the multivariate analysis of the risk of SCI in patients undergoing TEVAR after prior AAA repair are shown in Table IV. The only variable which significantly and independently associated with the risk of SCI was preoperative renal insufficiency (P .011). Increased length of coverage of the aorta in cm and increased time interval between prior AAA repair and TEVAR in years appeared to increase the risk of SCI too, although these variables did not reach significance (P .0762 and P .0505, respectively).

Table IV. Predictors of spinal cord ischemia after TEVAR in patients with a history of prior AAA repair: multivariate analysis

Variable	Odds Ratio	(95% CI)	P value
Age in years	1.1	(0.8-1.5)	.419
Female gender	1.4	(0.1-34)	.835
Time interval between prior AAA repair and TEVAR in years	1.8	(1.0-3.1)	.050
Preoperative renal insufficiency	70	(2.7to1.8×103)	.011
Aorta length coverage in cm	1.2	(1.0to1.6)	.076
LSA coverage	2.4	(0.2to30)	.499
Intra-operative hypotension	9.4	(0.1to9.3×102)	.339
Preoperative start of CSF drainage	91	(0.2to4.2×104)	.149

AAA, Abdominal aortic aneurysm; TEVAR, thoracic endovascular aortic aneurysm repair; LSA coverage, left subclavian artery coverage without revascularization; CSF, cerebrospinal fluid drainage; CI, confidence interval.

Other outcomes 

The median hospital length of stay was 5 days (mean 7.8 ± 9.0 days, range, 1 to 54 days). Hospital length of stay was ≤4 days in 25%, ≤5 days in 50%, ≤6 days in 75%, and ≤15 days in 90% of all patients. One fatal ischemic cerebrovascular accident was documented. No other strokes occurred in the study population. Renal insufficiency developed in 3.2% of the patients without preoperative renal insufficiency. Because 14% of the patients (n = 10) already had renal insufficiency before the procedure, 17% of all patients had renal insufficiency after the procedure (n = 12). One of these patients with renal insufficiency required dialysis and the other 11 did not require dialysis. Overall 30-day mortality was 4.2% (n = 3). None of the 9 patients with SCI had a stroke or fatal course during follow-up (<30 days).

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Discussion 

The risk of SCI after TEVAR appears to be dramatically increased in patients with prior AAA repair compared with patients without prior AAA repair: approximately seven-fold. SCI developed in 1 out of every 8 patients undergoing TEVAR after prior AAA repair. Significant predictors of SCI in the univariate analysis of patients undergoing TEVAR after prior AAA repair included preoperative renal insufficiency, increased length of aorta coverage by TEVAR, and increased time interval between prior AAA repair and TEVAR. Preoperative renal insufficiency was a significant and independent predictor of SCI in multivariate analysis too. Stroke occurred in 1.4%, postoperative renal insufficiency in 3.2%, and 30-day mortality in 4.2%.

To our knowledge, this study represents the largest cohort of patients undergoing TEVAR after prior AAA repair in the literature. This multicenter cohort study, therefore, provides unique and novel evidence. Because of the large number of patients, conclusions can be drawn with relatively high statistical validity, especially with regard to predictors of SCI and differences in prognosis between patients with and without prior AAA repair.

However, the study has several limitations. As a retrospective review of prospectively maintained data, our analysis was limited to the variables that were collected during clinical care. Another limitation is that we, unfortunately, lack information on differences in baseline characteristics between patients with and without prior AAA repair that could also have impacted their outcomes. A comparison of characteristics of patients with and without prior aortic surgery has been performed by Kawaharada et al¹⁷ and they found no differences between these groups except a slightly older age of patients who had no history of prior aortic surgery. Age is, however, never significantly correlated with the risk of SCI after TEVAR. EUROSTAR investigators showed that renal insufficiency and left subclavian artery occlusion are important risk factors for SCI after TEVAR.⁴ These risk factors for SCI were both less frequent in our cohort than in the EUROSTAR study population, and adjusting for baseline characteristics may therefore even increase the risk of SCI to a level that surpasses the presented risk. It is therefore very unlikely that confounding factors can explain the direction and extent of the presented effect of prior AAA repair on the risk of SCI after TEVAR. Based upon this information, a multivariate analysis may show that the independent effect of prior AAA repair on the risk of SCI is even higher than the presented univariate data. The drawn conclusion (patients with prior AAA repair are at higher risk of SCI after TEVAR than patients without prior AAA repair), therefore, has a good validity.

Because randomization of patients in groups “with prior AAA repair” and “without prior AAA repair” is not possible, cohort studies will continue to provide the best available evidence on this special group of patients.

The institutional databases primarily documented TEVAR characteristics and outcome after TEVAR, and information about the prior AAA procedure was limited to information about the medical history of the patients and type of prior AAA repair. Unfortunately, no valid information about coverage of the internal iliac arteries was available.

The decision concerning whether or not to perform CSF drainage was determined by the treating physician. Patients that underwent CSF drainage had a lower risk of postoperative SCI, although this was not significant (OR 0.3, 95% CI 0.1-1.3, P .118). Since patients at risk of SCI may have more likely undergone CSF drainage, our results may underestimate the beneficial effects of CSF drainage. Our results show a potential beneficial effect of CSF drainage and withholding of CSF drainage can, therefore, not be recommended on the basis of the currently presented data.

Renal insufficiency appeared to be an important risk factor of SCI in our study of patients with prior AAA repair who underwent TEVAR. The EUROSTAR registry showed similar results: renal insufficiency was independently associated with increased risk of SCI after TEVAR (OR 3.6, P .02).⁴ Several investigators have described that a reduced renal function is a significant risk factor for SCI after open thoracoabdominal aortic aneurysm repair too.¹⁸, ¹⁹, ²⁰ The underlying pathological mechanism is, however, not completely understood. Renal insufficiency may be a disease marker of more extensive peripheral atherosclerotic disease which may involve the collaterals of the blood supply of the spinal cord.⁴ Accumulation of one or more neurotoxic molecules may also play a role in the development of SCI in patients with more extensive renal disease.²¹ Patients with renal insufficiency are at increased risk of complications after surgery and may therefore be operated in a more advanced state of the aortic aneurismal disease, involving a greater segment of the aorta that is possibly involving the artery of Adamkiewicz and other critical regions that are important for sufficient blood supply to the spinal cord. A combination of mechanisms is therefore probably the cause of the increased risk of SCI in patients with renal failure and deserves attention in future research.

An increased time interval between prior AAA repair and TEVAR was associated with an increased risk of SCI in univariate and multivariate analysis. Time interval between prior AAA repair and TEVAR may be an indicator of the duration of symptomatic or clinically manifest atherosclerotic disease and may, therefore, be a disease marker that correlates with the state of atherosclerotic disease in the collaterals of the blood supply of the spinal cord.

Several other independent predictors of SCI have been described in literature. These included LSA coverage without revascularization (OR 3.9, P .027), concomitant open AAA surgery (OR 5.5, P .037) and deployment of three or more stent grafts (OR 3.5, P .043) in the EUROSTAR registry.⁴ An increase in length of aorta coverage and graft length are also associated with an increased risk of SCI after TEVAR.⁵, ¹², ²², ²³ Chiesa et al⁸ described that a perioperative lowest mean arterial pressure of <70 mm Hg was a significant risk factor for neurological deficit after TEVAR.

LSA coverage without revascularization, length of aorta coverage in cm, and intra-operative hypotension also increased the risk of SCI in our study as shown by the direction of the odds ratios in the univariate and multivariate analysis, although no significant associations could be established, possibly due to the relatively small size of the study cohort and relatively low total number of events of SCI.

TEVAR may result in spinal cord injury in patients with and without prior AAA repair because deployment of the graft results in a complete and sudden occlusion of several segmental vessels. Distal embolization to small end arteries in the spinal cord may also occur due to catheter or graft manipulation in the aorta. Griepp et al²⁴ have described another mechanism: blood may drain away from the spinal cord via retrograde flow via segmental vessels into visceral vessels that are connected with the excluded aneurysm sac. Such steal may further increase the vulnerability of the spinal cord in patients undergoing TEVAR.

What mechanisms may cause the increased risk of SCI in patients with prior AAA repair undergoing TEVAR? The anterior spinal artery supplies the anterior portion of the spinal cord and receives blood from an extensive collateral network over the vertebral column, including the vertebral arteries, the artery of Adamkiewicz²⁵ (arteria radicularis magna) and other anterior radiculomedullary arteries.²⁶ This collateral blood supply also supports the cauda equine and conus medullaris.²⁷ The importance of blood supply of the spinal cord in pigs from the median sacral artery and subclavian arteries via the collateral network has been described by Strauch et al.²⁸ Clamping of the median sacral artery made the spinal cord in these pigs dramatically more prone to injury. The level of the artery of Adamkiewicz ranges from T9 to L5 and occlusion does not, per se, lead to spinal cord injury because the artery is no strict-end artery due to blood supply from the collateral network. Khoynezhad et al¹ showed that a covered or occluded hypogastric artery is a significant risk factor for SCI. However, occlusion of lumbar arteries by prior AAA repair may reduce the total collateral blood supply and the spinal cord may therefore be more prone to injury in these patients.

Only one stroke occurred in our study (1.4%). Several large studies report a peri-operative risk of stroke between 3.6 and 3.8%.⁴, ⁵, ⁷ Several factors may explain this relatively low risk. The EUROSTAR study showed that female gender is an important risk factor for stroke after TEVAR (OR 3.3, P .023).⁴ Patients with prior AAA repair, such as the patients in our study, are less frequently female than average patients undergoing TEVAR. For example, the percentage of female patients was 14% in our study and 22% in the EUROSTAR registry. The relatively low number of women in our study may, therefore, partially explain the relatively low peri-operative stroke risk. Secondly, aortic pathology of patients undergoing TEVAR after prior AAA repair can be hypothesized to be localized closer to the abdomen and more distal to the aortic arch. Since patients with proximal thoracic aortic disease appear to be at increased risk for stroke, this may also lower the risk in our study population. However, because only one event (stroke) occurred in our study, no statistically valid conclusions can be drawn when our results are compared with other studies (eg, comparison with EUROSTAR: 1.4 vs 3.8%; RR 0.4; P .31).

A previously published meta-analysis from our institution showed that prior AAA repair is also a risk factor for SCI after open thoracic or thoracoabdominal aortic aneurysm repair.¹⁵ The overall risk of SCI after open thoracic or thoracoabdominal aortic aneurysm repair was 11% in patients with prior AAA repair (30 of 283 patients). The risk of SCI is therefore increased to a comparable level in patients with prior AAA repair that are undergoing open repair as in patients with prior AAA repair that are undergoing TEVAR.

In conclusion, prior infrarenal AAA repair appears to increase the risk of SCI after TEVAR. To make sure that we can provide the best care for these patients and can improve their prognosis, future research should be pointed towards long-term survival, treatments to protect the spinal cord of the patients, and should try to provide more insight into the effect of occlusion of collateral vessels and coverage of the internal iliac arteries on the risk of SCI after TEVAR. If the aneurysm diameter and rupture risk are large and TEVAR is indicated, best available care should be provided for maximal protection of the spinal cord in these patients.

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Author contributions 

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References 

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