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Ann Thorac Surg 2007;84:1201-1205
© 2007 The Society of Thoracic Surgeons
a Department of Thoracic and Cardiovascular Surgery, University of Virginia, Charlottesville, Virginia
b Department of Interventional Radiology, University of Virginia, Charlottesville, Virginia
Accepted for publication May 7, 2007.
* Address correspondence to Dr Reece, 4049 S. Wisteria Way, Denver, CO 80237 (Email: brett.reece{at}uchsc.edu).
Presented at the Forty-third Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 29–31, 2007.
| Abstract |
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Methods: The charts of all patients undergoing TEVAR performed at a single tertiary care center from 1999 to 2006 were reviewed. The review included the preoperative radiographic evaluations, the assessment of comorbidities, the anatomic position of the proximal and distal landing zones, outcomes, complications, and the need for preoperative or postoperative subclavian artery revascularization.
Results: Sixty-four patients underwent TEVAR and 27 (42%) of these patients required exclusion of the LSA from the thoracic aorta. Seven of these 27 patients (25.9%) required preoperative LSA revascularization. Four patients developed late symptoms, necessitating LSA revascularization. No patients died or developed paraplegia, but three adverse neurological events occurred unrelated to the posterior fossa circulation. No patient developed any left arm disability.
Conclusions: The TEVAR coverage of the LSA with selective revascularization was safe for patients, but greater than 11 of 27 (40.7%) required either preoperative or postoperative LSA revascularization. Although this study represents our early experience with TEVAR, these data suggest that selective revascularization after TEVAR exclusion of the origin of the LSA may be required more frequently than previously reported.
| Introduction |
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The TEVAR literature divides the thoracic aorta into five zones describing various proximal device landing zones (Fig 1) [4]. Two different strategies for dealing with the left subclavian artery during TEVAR extension in to zone 2, coverage of the LSA origin, prevail in the literature. The first scheme involves preoperative revascularization of the LSA with either transposition or bypass from the carotid artery in all patients in order to eliminate the potential for ischemic complications. The second approach involves selective revascularization of the LSA based on the estimation of the risk of ischemic consequences of LSA exclusion. Despite the apparent adequacy of extensive preoperative evaluation with angiography and cross-sectional imaging, some patients who have not undergone preendograft revascularization of the LSA will develop symptoms of subclavian steal or left arm claudication. These symptomatic patients will require late LSA revascularization to alleviate symptoms and maintain optimal function. Overall, the literature suggests that using the selective LSA revascularization approach is reasonable and that late revascularization is rarely needed [5–9].
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| Patients and Methods |
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Patient demographics were recorded. Comorbidities were recorded including history of coronary artery disease, cerebrovascular disease, hypertension, peripheral vascular disease, chronic obstructive pulmonary disease, chronic renal insufficiency, neoplasm, and aortic trauma. Preoperative radiographic evaluation of the thoracic aortic pathology and the cerebral vasculature, the anatomic location of the proximal and distal landing zones for the device were also reviewed. Periprocedural and postoperative complications were assessed as well as hospital and intensive care unit (ICU) lengths of stay. We reviewed the need for preoperative or postoperative LSA revascularization. We also noted the incidence of endoleaks with particular emphasis on endoleaks from the excluded subclavian stump. The post-TEVAR follow-up was recorded with attention to more delayed complications, the need for late intervention, and 30-day and overall mortality rates.
| Results |
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The mean age among these patients was 60.4 years, ranging from 29 to 82 years. The gender distribution in the series was 16 males and 11 females. The indications for thoracic aortic intervention included 15 aneurysms, 7 acute aortic traumas, 2 chronic dissections, 1 subacute dissection, and 2 psuedoaneurysms from previous aortic interventions. The incidence of patient comorbidities included 9 with coronary disease, 4 with cerebrovascular disease, 17 with hypertension, 12 with peripheral vascular disease, 2 with chronic obstructive pulmonary disease, 4 with chronic renal insufficiency, and 1 with remote aortic trauma. These comorbidities were present almost exclusively in the 20 patients without acute trauma. Seven patients presented with acute aortic trauma.
Seven of these 27 patients needed preemptive revascularization of the LSA based on their specific vascular anatomy and the estimated risk of ischemic complications due to LSA exclusion (Table 1). One patient underwent revascularization during the same anesthetic as the stent graft placement. The other six patients requiring preendograft LSA revascularization were intervened on 1 to 14 days prior to endografting. Access for endograft deployment was as follows: 2 through conduits to the aorta, 6 through conduits to the iliac arteries, and 19 by access to the femoral arteries. In the current series 1 patient received an AneuRx device (Medtronic, Inc, Minneapolis, MN), 7 received Talent devices (Medtronic, Inc), and 19 received Gore TAG (W. L. Gore and Associates, Flagstaff, AZ) devices.
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Follow-up ranged from 10 to 50 months, with a mean follow-up of 19 months. During this period, two patients developed a retrograde dissection requiring replacement of the ascending aorta. One of these two patients also developed subclavian steal syndrome that led to a carotid-to-subclavian bypass at the time of the ascending aortic repair. Three other patients developed symptoms leading to LSA revascularization with all undergoing carotid-to-subclavian bypass, summarized in Table 2. One patient had growth in the aneurysm despite endograft exclusion, obliging open repair within a month of the original endograft procedure.
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| Comment |
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Two approaches have been undertaken to deal with this LSA exclusion with TEVAR. The first option is a more conservative approach to revascularization. All patients undergo either carotid-to-subclavian bypass or subclavian transposition preemptively. This approach avoids the uncertainty regarding the adequacy of flow to the LSA and its branches. However, because all patients may not require revascularization of the covered vessel, some patients, maybe even the majority of patients, will undergo an unnecessary procedure that can have a mortality as high as 5% [12–14]. The other approach, which we have preferred, involves selective revascularization of the excluded subclavian artery with two separate indications; one prior to stenting, based on preoperative imaging, and the second after TEVAR based on the development of symptoms. The selective approach reserves revascularization prior to endograft deployment for cases in which compromised LSA blood flow could cause predictable ischemic consequences. Although vertebrobasilar isolation gets the most consideration, other indications include aberrant vasculature and patent internal mammary conduits to the coronaries. A complete list of indications and considerations for preoperative LSA revascularization is presented in Table 3. Patients not undergoing preoperative LSA revascularization are educated for the signs and symptoms of left upper extremity ischemia including extremity claudication and subclavian steal. Development of significant symptoms requires reevaluation for LSA revascularization.
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While we effectively avoided immediate posterior circulation strokes through detailed preoperative imaging, we were unable to predict the development of late symptoms. The incidence of left upper extremity claudication and (or) subclavian steal is not clear in the literature [15]. Furthermore, the significance of these symptoms is unknown. Four (4 of 20, or 20%) patients in this series developed claudication or subclavian steal symptoms after TEVAR exclusion of the LSA. No symptoms were apparent at the time of discharge from the TEVAR procedure. These four patients developed symptoms between three and 26 months after their procedure. Some centers have chosen to observe patients with arm claudication [6, 7, 9]. These centers note that LSA revascularization carries its own risks. In the vascular literature, the mortality alone in these patients undergoing LSA revascularization can be significant [12–14]. Moreover, troublesome recurrent laryngeal nerve and phrenic nerve injuries have been reported [16]. We do not approach LSA revascularization lightly, but our experience thus far with revascularization has been very good without any significant complications. Since the inception of our thoracic endovascular program, we have embraced LSA revascularization in all patients who develop significant and persistent left arm symptoms post stenting. Their symptoms were severe enough that it was limiting their function. All underwent carotid subclavian bypass without any residual symptoms after LSA revascularization.
Some authors suggest that claudication may not require revascularization. Rehders and colleagues [6] reviewed the early reports of LSA coverage with TEVAR. They found a total of 16% to have some symptoms in their left upper extremity. The authors of these combined studies chose to observe these patients with claudication rather than vascularize them as we did. Both reports suggest that LSA exclusion will lead to late symptoms in close to 20% of the patients who do not require preoperative LSA revascularization. Although Rehders and colleagues reported no complications following these patients with claudication, our low threshold for LSA revascularization is validated given complete resolution of any ischemic symptoms while avoiding any long-term posterior circulation or left upper extremity disability. The need for late LSA revascularization is probably more common than implied by the literature, with selective management of the excluded LSA with TEVAR, which speaks to the need to educate these patients about their need for strict follow-up and for an understanding of potential late complications.
We acknowledge that the increased need for subclavian revascularization may be a function of a relatively limited number of patients. The incidence of significant arterial anomalies in this series was higher than expected for all comers, which may suggest the possibility of a type 2 error asserting the need for revascularization. However, the presence of the anomalies may bias physicians toward endovascular intervention and revascularization rather than open repair. Only further experience will demonstrate the true need for subclavian revascularization. The need for subclavian revascularization may be influenced by our limited cohort, yet the approach to revascularization appears to be validated by our initial results.
As demonstrated in the current series, a selective approach to LSA revascularization in patients undergoing TEVAR exclusion of aortic pathology is safe. However, the need for LSA revascularization may be more common than previously proposed. These current data suggest that the need for LSA revascularization may be 40% or higher; however, we still advocate selective LSA revascularization to avoid unnecessary procedures in the majority of patients. Our experience with selective approach to LSA revascularization with TEVAR and coverage of the LSA is justified given no significant posterior circulation strokes or permanent left arm deficits, but the need for revascularization is higher than reported by most other groups performing these procedures.
| Discussion |
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DR REECE: Thank you for your comments. I think we would agree that is something we would definitely discuss in a multidisciplinary way of who needed it. If we were going to cover the aorta more distally down towards the renals past the T8, especially, we would consider revascularizing the subclavian artery for that very reason. However, I dont think we have any data on that yet. And are we trading off the possibility of paraplegia on one hand for the complications of the transposition or bypass on the other hand? I dont think that has played out yet, but it is definitely something that we need to consider.
DR JOSEPH E. BAVARIA (Philadelphia, PA): First of all, this is a very nice paper and I thought it was very well presented. Thank you very much for presenting here at the STS. I have a couple of comments and a question. What about type II endoleaks originating from the subclavian artery, did you have any of those? The carotid-subclavian bypass, in my opinion, is a lot less complicated than the subclavian artery transposition, and we at PENN have now gone completely to subclavian bypasses. It takes away all the problems associated with deep neck dissection, especially in distorted anatomy with proximal descending aneurysms and distal arch aneurysms. One of the things that we have been doing, and I agree with the concepts of Dr Griepp, is that for all AAA cases with complete descending aortic coverage we would always perform a subclavian bypass to try and reduce possible paraplegia. But additionally, at the present time, for all high arch applications of stent grafts, we have gone to routine elective subclavian bypass. The most important reason for subclavian bypass, besides all the other reasons that you stated, is a technical consideration. We really like getting wire through the bypass, into the carotid artery, and then down into the arch so we can nail our proximal landing zone right at the carotid orifice and not into the carotid or too distal. So this technique gives one a really nice road map, so to speak, to reliably "hit" your proximal landing zone when you have small clearances in the high arch. This is just some amplification of a little technical nuance that I would like your comments on. We would then end up coming out of the carotid-subclavian bypass with a coil embolization of the intrathoracic left subclavian artery in all cases requiring supra-subclavian landing zones. Thank you very much for a very nice presentation.
DR REECE: In terms of type II endoleaks, one patient developed a leak that was thought to be secondary to back flow from the left subclavian artery. As you mentioned, we intervened with a cuff over the subclavian takeoff and a retrograde coil from the brachial to stop the endoleak. Nearly all the cases done since the end of this study have undergone preemptive retrograde coiling of the proximal subclavian following deployment of the device.
As far as paraplegia, we have not reviewed our more proximal deployments as of yet. However, we will certainly explore this question as we do more arch and proximal aortic stent grafts.
You bring up a good point about utilizing the bypass to identify the carotid orifice. As you state, this landmark can help identify the proximal landing zone without blindly passing instrumentation further than needed. This may help reduce the chance of embolization as well as reducing the amount of contrast needed to define the anatomy.
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