European Journal of Vascular & Endovascular Surgery
Volume 33, Issue 6 , Pages 664-667, June 2007

Deliberate Subclavian Artery Occlusion during Aortic Endovascular Repair: Is it Really that Safe?

SITE - Serviço Integrado de Técnicas Endovasculares, Brazil

Accepted 13 December 2006. published online 14 February 2007.

Article Outline

Purpose

To report a series of cases in which deliberate occlusion of the left Subclavian Artery (SA) caused the Subclavian Steal Syndrome (SSS).

Methods

Between January 2001 and August 2006, we performed 81 endovascular repairs of the Thoracic Aorta. 21 patients required left SA occlusion for an adequate proximal landing zone. 17 of these patients were treated by deliberate SA occlusion. Four patients (23.5%) developed a SSS, of which three were treated by a secondary Subclavian-to-carotid transposition, with complete remission of the SSS.

Results

The subclavian-to-carotid transposition was successful in the treatment of the 3 patients selected. One patient refused to be operated, and had only partial remission of the SSS symptoms. Mean follow-up was 28 months (range 2–48).

Conclusion

In this series deliberate occlusion of the SA led to SSS in a significant number of patients. Consideration should be given to primary subclavian transposition in some patients requiring subclavian occlusion.

Keywords: Subclavian artery, Thoracic aorta, Endovascular repair

 

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Introduction 

The term subclavian steal syndrome (SSS) has been used to describe the occurrence of retrograde blood flow in the vertebral artery (VA) associated with proximal occlusion of the ipsilateral subclavian artery (SA) causing neurological symptoms.1

Despite its low incidence,2, 3 this syndrome is receiving increased attention due to the large number of patients undergoing endovascular procedures for the treatment of diseases involving the aortic arch requiring occlusion of the left SA occlusion to provide an adequate proximal landing zone (PLZ).

The diagnosis of SSS can be established through a careful clinical evaluation of the occurrence of posterior cerebrovascular symptoms, usually related to situations where higher blood flow is required in the arm. The Doppler examinations of these patients shows flow reversal in the VA and a degree of obstruction of the proximal SA.

There is diverging literature about the necessity for SA revascularization prior to endovascular occlusion of the SA and during the last years we initially adopted the practice of non-revascularization. However contrary to our initial expectations, a review of our data showed that the number of patients with neurological findings compatible with SSS was significant. This resulted in a change of practice in the way we now manage our patients with a short PLZ requiring SA coverage.

In a recent review of the SA revascularization related to endovascular repair of thoracic pathology, Morasch et al.4 noted a significant complication rate in patients who underwent deliberate covering of the SA when compared to those in whom VA flow was preserved. On the other hand, there are few publications affirming that the SA coverage is a safe procedure.5, 6, 7 In this study we report our experience of SA occlusion.

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Methods 

From 2001 to 2006, 81 patients underwent endovascular repair of the thoracic aorta. Twenty one patients had lesions close to or involving the aortic arch, ranging from aneurysms to Stanford type B dissections and penetrating ulcers, and required coverage of the left SA by the endograft. Of these patients, two underwent a primary left subclavian-carotid transposition in order to provide a proximal landing zone of at least 15mm for the endograft. These patients were selected for subclavian revascularization due to concerns regarding cerebral perfusion in one patient and arm perfusion in the other. In two other patients, we performed a primary carotid-carotid retropharyngeal bypass to gain an adequate PLZ. The remaining 17 patients were submitted to the implant of an aortic endograft with deliberate left SA occlusion. During follow-up, 4 of these 17 patients (23.5%) showed symptoms of SSS, varying from left superior limb paresis (n=1), dizziness and syncope (n=2) and a major cerebrovascular accident (CVA) (n=1). Three of the patients underwent a secondary subclavian-to-carotid transposition for the restoration of cerebral blood flow (Fig. 1). In the patients not submitted to subclavian occlusion there was no occurrence of vertebrobasilar symptoms.

  • View full-size image.
  • Fig. 1 

    Subclavian artery secondary transposition: A and B- Intra-operative angiography, with arrows depicting the SA transposition; C and D- Angio CT control, arrows depicting the transposition.

Subclavian-to-carotid transposition technique 

The subclavian artery can be revascularized in many ways, but most commonly either with a direct arterial transposition or by a bypass using an artificial or endogenous graft to the adjacent common carotid artery. In our experience, all cases could be accomplished with a transposition, which we consider to be a superior technique, due to its higher patency rates and lower morbidity when compared to results with synthetic grafts.8, 9, 10 The flow to the VA and the internal mammary is preserved in both methods of SA revascularization. This is noteworthy since a mammary steal could take place in patients with previous coronary revascularization in the case where revascularization was not performed.11

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Results 

Three of our patients underwent secondary SA transposition. A fourth patient refused to have an operation for personal reasons. The main diagnostic test used, besides specific clinical evaluation by a neurologist, was Doppler examination of the carotid and vertebral arteries. In all four cases Doppler demonstrated flow reversal in the VA and no significant carotid artery disease.

Case reports 

In June 2002, a 65-year-old male patient had two episodes of syncope. He had recently been treated with a second endograft (Talent-Medtronic) that occluded the SA. This graft was required to treat a Type I endoleak of a previous endoprosthesis (Gore Tag-Gore), which failed to obliterate a Stanford Type B Aortic Dissection.

Clinical evaluation by a neurologist suggested posterior cerebrovascular related symptoms and Doppler examination showed flow reversal in the ipsilateral VA. After the SA transposition a complete remission of symptoms was accomplished and antegrade flow was re-established in the VA. No other adverse events occurred during 48 months follow-up.

In December 2002, a 56-year-old male patient underwent an endovascular repair (Zenith TX2 – COOK) of a Penetrating Aortic Ulcer, with deliberate left SA occlusion. After 40 days, he developed symptoms of left limb ischemia, with markedly effort related pain. Doppler demonstrated reverse blood flow in the ipsilateral VA. After the SA transposition, complete remission of symptoms was accomplished, with re-established antegrade flow in the VA. No other adverse events occurred during 42 months follow-up.

In April 2006, a 70-year-old male patient was admitted with acute thoracic pain, attributed to a Penetrating Aortic Ulcer with an intra-mural haematoma next to the SA. A complete MRI scan of the carotid and vertebral arteries was done, with no signs of significant hemodynamic impairment. However, three days after the endovascular repair (Zenith TX2 – COOK), the patient had episodes of syncope and dizziness, which were initially not attributed to the SA occlusion.

The patient was referred to a neurology service and clinical examination suggested a posterior cerebrovascular cause. Doppler demonstrated flow reversal in the VA. After the SA transposition a complete remission of symptoms was accomplished, with re-established antegrade flow in the VA. No other adverse events occurred during 2 months follow-up.

In September 2004, a 72-year-old male patient, was submitted to a Stanford Type B Aortic Dissection endovascular repair (Zenith TX2 – COOK), including SA occlusion by the endograft. During the immediate post-operative period, he developed motor, hearing and visual impairment. This was diagnosed clinically and confirmed by CT scan as vertebrobasilar ischemia. For personal reasons, the patient refused to have transposition surgery. During 21 months follow-up there was partial remission of his symptoms but currently the patient still has residual motor symptoms.

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Discussion 

There is considerable anatomical variation in the vertebro-basilar blood supply.10, 11, 12, 13, 14, 15 Thus it would be expected that subclavian artery occlusion would be not tolerated by all patients. In our series, in contrast to other reports,5, 6, 7 deliberate occlusion of the SA led to neurological consequences in a significant number of patients. Usually, SSS is not specifically described as a complication of endovascular repair of the thoracic aorta16, 17 and in our experience only occurs if the SA is covered.

We found that 23.5% (4 out of 17) of patients in which the SA was covered developed neurological symptoms. All 3 patients that underwent secondary VA revascularization had complete recovery of symptoms. In addition, neither of the 2 patients with primary SA revascularization experienced neurological symptoms. The SA transposition was performed without major adverse events confirming that this is a relatively safe procedure.13, 14

Morasch and colleagues4 reported a combined 23% complication rate when the left subclavian artery orifice was covered, compared to a 3% complication rate when flow into the left subclavian artery was preserved. In our opinion, SA revascularization might be considered in all patients requiring SA occlusion by an endograft.

In addition to maintaining adequate perfusion of the left arm and the VA, SA revascularization can also improve collateral flow to the spinal cord. Retrograde flow in the SA is also eliminated thereby minimizing the risk of type II endoleak. We strongly believe that the SSS as a complication from the thoracic endovascular repair should have more attention paid to it. We believe that in the following situations, left SA revascularization should be performed:

1.When the left VA is dominant.15

2.When there is an incomplete fusion of the VAs at C1 level.12, 15

3.When there is a previous myocardial revascularization using the internal mammary artery.15

In addition, SA revascularization might also be considered in the following situation:

4.When the SA is included in the aneurysm. In this instance, one option is to embolize the proximal SA after a bypass.

5.When there is an associated significative obstruction of the carotids, brachiocephalic trunk or vertebral arteries.

6.In young patients or in those who make intense use of the upper limbs.

In elective procedures, we consider that a Doppler US and cerebral MRA should be performed to evaluate the cerebral circulation before choosing between either deliberate occlusion or a revascularization of the SA. Further knowledge of this issue may bring additional evidence related to the event of SSS after endovascular repair of thoracic pathologies.

It is evident though that as the number of endovascular procedures performed in the aortic arch increases,16, 17 the management will have to evolve. Currently the ability to provide our patients an adequate treatment for lesions in this territory may involve primary subclavian-to-carotid transposition, however with advancements in stent graft technology, the management of SSS and other complex arch pathology may be undertaken solely using endovascular techniques.

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References 

  1. Fischer CM. A new vascular syndrome: “The subclavian steal. N Engl J Med. 1961;265:912–913
  2. Fields WS, Lemak NA. Joint Study of extracranial arterial occlusion. VII. Subclavian steal – a review of 168 cases. JAMA. 1972;222(9):1139–1143
  3. Bournstein NM, Norris JW. Subclavian steal: a harmless haemodynamic phenomenon?. Lancet. 1986;2(8502):303–305
  4. Morasch MD, Peterson B. Subclavian artery transposition and bypass techniques for use with endoluminal repair of acute or chronic thoracic aortic pathology. J Vasc Surg. 2006 Feb;(Suppl):73A–77A
  5. Landwehr P, Schulte O, Voshage G. Ultrasound examination of carotid and vertebral arteries. Eur Radiol. 2001;11:1521–1534
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  16. Leurs LJ, Bell R, Degrieck Y, Thomas S, Hobo R, Lundbom J, et al. Endovascular treatment of thoracic aortic diseases: combined experience from the EUROSTAR and United Kingdom Thoracic Endograft registries. J Vasc Surg. 2004 Oct;40(4):670–679[discussion 679–680]
  17. Iyer VS, Mackenzie KS, Tse LW, Abraham CZ, Corriveau MM, Obrand DI, et al. Early outcomes after elective and emergent endovascular repair of the thoracic aorta. J Vasc Surg. 2006 Apr;43(4):677–683

PII: S1078-5884(07)00006-8

doi:10.1016/j.ejvs.2006.12.013

European Journal of Vascular & Endovascular Surgery
Volume 33, Issue 6 , Pages 664-667, June 2007