Percutaneous Transluminal Stent Placement to Treat Subclavian Steal Syndrome1 Ben L. Sueoka, M D Index terms: Arteries, subclavian, 942.767 Arteries, transluminal angioplasty, 942.1286 Stents and prostheses, 942,1286 Subclavian steal syndrome, 942.767
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Abbreviations: PTA = percutaneous transluminal angioplasty, SSS = subcla. vian steal syndrome
JVIR, 1996; 7:351-356
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From the Vascular and Interventional Section, Department of Radiology, William Backus Hospital, Norwich, CT 06360. Received October 5, 1995; revision requested November 9; revision received December 15; accepted December 18. Address correspondence to the author.
o SCVIR, 1996
PURPOSE: To describe nonsurgical stent placement to treat subclavian steal syndrome after failure of traditional balloon angioplasty. PATIENTS AND METHODS: Seven patients with subclavian steal syndrome underwent diagnostic angiography, which showed four stenoses and three occlusions of the proximal left subclavian artery. Most patients presented with vertigo, left arm claudication, or syncope. Initial balloon angioplasty failed; there was elastic recoil with more than 30%residual stenosis or subintimal dissection. The three occlusions were treated with urokinase pulse-spray thrombolysis. All seven patients then underwent stent placement. RESULTS: Initial technical success was achieved in all seven cases (loo%),with an average right versus left arm blood pressure gradient of 0 mm Hg (-11 to 12 mm Hg) at mean follow-up of 12 months (4-24 months) (positive gradient = systolic pressure of right arm > that of left arm; negative gradient = systolic pressure of left arm > that of right arm). Symptoms of arm claudication and syncope resolved, and vertigo improved or resolved after the procedure. There were no deaths, strokes, or emboli in the perioperative or follow-up period. CONCLUSION: Percutaneous transluminal stent placement may be an effective treatment of subclavian steal syndrome in patients with lesions that are refractory to traditional angioplasty. THE subclavian steal syndrome (SSS) was first described in 1961. This syndrome is caused by a stenosis of the proximal subclavian artery that causes reduced blood flow to the upper extremity and reversal of flow in the vertebral artery. The symptoms of this syndrome include vertigo, syncope, ataxia, cephalgia, paresthesia, motor or visual defects, and intermittent arm claudication. The traditional therapy has been surgical bypass (2-51, which has had a complication rate of up to 23% (3) and a mortality rate of 4.8%-8% (4,6). Balloon angioplasty has been Su~~eSSfully used to treat subclavian artery stenosis and SSS (7-10); a technical success rate of 86% and a complication rate of 6% have been reported (11). Atherectomy has also been used successfully to treat sub-
clavian stenosis, although this method is frequently complicated by restenosis (12). Although percutaneous transluminal angioplasty (PTA) appears to be associated with fewer complications than other modalities, its long-term durability has been questioned because of the possibility of restenosis (13). There have been few reports of the use of intraarterial stents to repair subclavian stenoses (14-16). In this study, we review our experience with nonsurgical stent repair of SSS after failed traditional balloon angioplasty.
PATIENTS AND METHODS Between September 1992 and October 1995, 18 patients presented for diagnostic angiography and PTA re-
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Summary of Patient Symptoms and Blood Pressure Gradients
Blood Pressure Gradient (mm Hg)*
Symptoms
Patient Age (Y
Subclavian Lesion
Preoperative
Postoperative
Preoperative
Postoperative
71
Occlusion
80
0
63
Stenosis
68
0
64
Stenosis
50
-7
62 83
Stenosis Stenosis
67 30
0 0
77
Occlusion
30
0
52
Occlusion
47
1
V CD CVA, associated left carotid stenosis V CD V V CD V CD V CD S
V improved CD resolved No CVA extension V improved CD resolved V resolved V resolved CD resolved V improved CD resolved V improved CD resolved S resolved
Follow-up (mo)/ Gradient (mm Hg) 2410 1910' 411 61-11 16/12; 912 61-2
Note.-CD = claudication, CVA = cerebrovascular accident, S = syncope, and V = vertigo. *Gradient = right arm systolic blood pressure versus left arm systolic blood pressure. + Systolic blood pressure of the left arm versus systolic blood pressure of the left thigh (patient's right arm pulse became nonpalpable during follow-up period). i Blood pressure measured peripheral to brachial saphenous venous bypass. A gradient may be partially due to stenosis a t venous bypass anastomosis.
Figure 1. (a) Preoperative thoracic arch aortogram via right common femoral approach is shown. Eccentric stenosis of the proximal left subclavian artery can be seen. The left vertebral artery is not visible (because of reversal of flow in this vessel). (b) Preoperative selective left subclavian angiogram shows an eccentric plaque and secondary high-grade stenosis of the proximal aspect. ( c ) Angiogram obtained after failed angioplasty of the proximal left subclavian artery and placement of a Palmaz stent. Postprocedural selective angiogram of left subclavian artery shows that the left vertebral artery is now patent, with antegrade flow. .
pair after having undergone a noninvasive vascular ultrasound (US) examination that documented the presence of SSS. Eleven of 18 patients underwent successful diagnostic angiography and PTA repair of SSS. In seven of these 18 patients, PTA failed; PTA failure was defined as greater than 30% elastic recoil
(diameter) or flow-limiting subintima1 dissection of the lesion (systolic intraarterial pressure gradient across the lesion of >5 mm Hg). These seven patients had a mean systolic blood pressure gradient (right arm vs left arm) of 53 mm Hg (range, 30-80 mm Hg) (Table). The seven patients in whom initial PTA
failed had three eccentric lesions (Fig I), three occlusions (Figs 2, 31, and one ostial critical stenosis. PTA treatment of all occlusions and the ostial stenosis failed because of elastic recoil, and treatment of two of three eccentric stenoses failed because of subintimal dissection. These seven patients, aged 52-83
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b. c. Figure 2. (a)Preoperative cervicocerebral angiogram shows complete occlusion of the left subclavian artery; SSS was seen on a later phase image. (b) Selective left subclavian angiogram obtained from a left low brachial approach confirms the complete
a.
proximal left subclavian artery occlusion and reveals a patent left vertebral artery. ( c ) Postprocedural left subclavian angiogram via the left brachial approach was obtained after failed angioplasty of the proximal left subclavian artery, Wallstent (10 x 42 mm) placement, and balloon dilation (after stent placement) to 8 mm in diameter.
a. b. c. Figure 3. (a)Preoperative cervicocerebral angiogram shows a complete left subclavian artery occlusion. This lesion was initially identified during diagnostic work-up of the carotid arteries from the right groin. Imaging of a later phase of this same injection showed delayed filling of the left subclavian artery from retrograde flow in the left vertebral artery. (b) Selective angiogram of the proximal left subclavian artery after angioplasty with a 6 mm x 4-cm balloon from a left brachial artery approach shows persistent proximal stenosis due to elastic recoil. ( c ) After failed left subclavian PTA, a Palmaz stent was successfully placed across the former proximal left subclavian occlusion. Selective angiogram obtained after stent placement in the left subclavian artery shows no residual stenosis.
years, presented with vertigo ( n = 6), left arm claudication ( n = 4), and syncope ( n = 1).
Diagnostic examinations of all seven patients were performed via the right common femoral artery
with digital thoracic aortography and selective left subclavian angiography. In patients with carotid dis-
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ease identified by means of Doppler US examination, the carotid arteries were also studied during the same procedure. The first five consecutive patients, who had nonpalpable pulses, underwent puncture of a left brachial percutaneous artery (singlewall technique) with a n 18-gauge Smart Needle (PSG, Temecula, Calif). In all five of these patients, 5-F vascular sheaths (Terumo, Tokyo, Japan) were initially inserted, and a diagnostic examination was performed with injection of the left subclavian artery. All lesions were traversed with a 0.035-inch Wholey wire (PSG), and a 210-cm exchange wire was deflected down the descending aorta with a 5-F Tennis Racquet catheter (Medi-tech/Boston Scientific, Watertown, Mass). The subclavian artery (distal to the left vertebral artery origin) was then vasodilated with 100 pg of intraarterial nitroglycerin. All occlusions were treated with pulse-spray thrombolysis via a Mewissen catheter (Medi-techBoston Scientific); 250,000 U of urokinase was mixed with 3,000-5,000 U of heparin, for a total volume of 50 mL. The thrombolytic infusions were completed in 30 minutes. The two remaining patients with high-grade stenosis of the proximal left subclavian artery underwent diagnostic examination (aortic arch, left subclavian) via the right common femoral artery with a 5-F sheath (Terumo), followed by selective left subclavian catheterization. The lesions were then crossed with a 0.035-inch Wholey wire from the right groin. The subclavian lesions of all seven patients were then dilated by means of balloon angioplasty (Ultrathin [Medi-tech/Boston Scientific] or Classique [Meadox-Surgimed, Oakland, NJI), from either the left brachial or right femoral routes, respectively, to a diameter of 1mm less than the diameter of the subclavian artery distal to the stenosis or occlusion. If angioplasty failed because of elastic recoil, the angioplasty balloon was replaced with a balloon that was 1mm larger in diameter. The diameter limit of PTA was
sometimes reached with smaller angioplasty balloons i n patients with onset of excessive pain during angioplasty. Diagnostic angiography was then performed to examine the left subclavian artery. The lesions of all seven of these patients showed either elastic recoil with residual stenosis of more than 30% or subintimal dissection with systolic gradients across the lesion of more than 5 mm Hg (measured with the intraarterial technique). Stents were then placed in the lesions via a 7-F Check-flo vascular sheath (Cook, Bloomington, Ind) (70-cm sheaths for Palmaz stents [Johnson & Johnson Interventional Systems, Warren, NJ], 30-cm sheaths for Wallstents [Schneider, Minneapolis, Minn]). The 70-cm vascular sheaths were successfully placed across the left subclavian lesions in all patients in whom they were used. Palmaz stents (20 or 29 mm, medium series) were deployed over 7 mm x 4-cm Opta 5 balloon angioplasty catheters (Cordis, Miami, Fla) and were then overdilated (when patients did not experience significant pain) with a n 8 mm x 4-cm Opta 5 balloon catheter. The 10 x 42-mm Wallstent was also seated into the target area with a n 8 mm x 4-cm Opta 5 balloon angioplasty catheter after deployment. Digital angiography was performed a t the completion of stent placement. After stent placement, blood pressure was measured in both arms (with a blood pressure cuff), and gradients were compared with the gradients obtained in the noninvasive vascular laboratory baseline examination (a positive gradient was defined a s systolic pressure in the right arm greater than that in the left arm; a negative gradient was defined as systolic pressure in the left arm greater than that in the right arm). This technique was used because it was noninvasive and could be compared with a n examination performed in a similar manner a t patient follow-up. After the procedure, all patients were treated with 5,000 U of heparin administered by means of subcutaneous injection (single dose) and were given aspirin antiplatelet therapy for 3 months.
All seven patients were seen a t follow-up and were asked whether their initial symptoms had improved, resolved, or recurred. All patients then underwent a follow-up blood pressure measurement of both upper extremities (with a blood pressure cuff), with the right arm used a s a control.
I RESULTS The immediate postprocedural results showed that the six patients with vertigo experienced diminished severity of symptoms after subclavian stent placement, and two of six patients were cured. All four patients with left arm claudication were cured of symptoms after stent placement. The one patient with syncope experienced cessation of symptoms. Immediately after stent placement, the mean right to left arm systolic blood pressure gradient was -0.86 mm Hg (range, -7 to 1mm Hg) (Figs lc, 2c, 3c). The mean preoperative gradient was 53 mm Hg (range, 30-80 mm Hg) (Table). Systolic arm blood pressure (right vs left) was measured a t follow-up a mean of 12 months later (range, 4-24 months). The average arm blood pressure gradient a t follow-up was 0 mm Hg (range, -11 to 12 mm Hg) (Table). Four of seven patients experienced advancement of atherosclerotic disease in the contralateral arm, with negative gradients (right vs left) obtained a t follow-up. In three of these four patients the right arm was asymptomatic. The one patient with a nonpalpable right arm pulse a t follow-up had symptoms of right arm claudication. The pressure in this patient's left thigh was compared with that in her left arm. This parameter was selected because of identical preoperative noninvasive examination pressures in her right arm and left thigh. Twenty-two months after subclavian stent placement this patient underwent followup cervicocerebral angiography and bilateral carotid and left subclavian artery angiography because she was experiencing new left carotid transient ischemic attacks. This study
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showed a new stenosis in the right axillary artery and a stenosis in the left internal carotid artery. During the 22-month follow-up interval, 1 mm of intrastent intimal hyperplasia was found in the segment of the left subclavian artery with the stent; no substantial stenosis recurred. At follow-up, all seven patients were questioned about their presenting symptoms. No patient had experienced a recurrence or increase in symptoms during the period between subclavian stent placement and follow-up. Three of the five patients with 7F brachial percutaneous vascular sheaths developed moderate hematomas a t the entry sites. One of these patients had a high brachial artery entry (because of concern that a 7-F vascular sheath could not span the target area) and developed immediate postprocedural transient hypertension to 220 mm Hg (systolic pressure). He developed a 4-cm pseudoaneurysm of the brachial artery; surgical exclusion bypass of the pseudoaneurysm was performed with a saphenous vein graft (when compression US failed). The followup blood pressure measurement was obtained below the lower-graft anastomosis and may have been artificially low due to a n asymptomatic stenosis a t the graft anastomosis.
DISCUSSION PTA repair was successful in 11 of the 18 patients presenting with SSS, and it failed in all patients presenting with occluded subclavian arteries and secondary SSS. PTA also failed in patients with highly eccentric lesions or ostial critical stenosis. The options for percutaneous transluminal repair after PTA failure are limited. If no further treatment is rendered, restenosis, thrombosis, or embolization is likely. Overdilation with a balloon is one option, but with the possibility of dissection or rupture into the thorax it would seem hazardous. Atherectomy has been used successfully in the proximal subclavian artery but is associated with a high rate of restenosis and runs the risk of uncontrolled perforation or embolization.
Percutaneous transluminal stent placement should be considered as a n option in cases of failed PTA for SSS. In our small series ( n = 7) the technical success rate was 100%. The possibility of embolization occurring as a complication of intraarterial stent placement immediately after failed balloon angioplasty is reduced. This reduction is due partly to the delayed reversal of flow phenomenon reported to occur in the left vertebral artery after repair (7,10,17), as well as the left upper extremity vasodilation, which results in increased flow to the arm. Arm vasodilation theoretically can direct possible emboli away from the left vertebral artery. Intraarterial stent placement in this region must be precise to avoid overhanging of the stent into the aortic lumen or overlying of the left vertebral orifice. Use of the Palmaz stent allows precise placement, and there is only a small amount of metal surface area that is exposed to blood flow after deployment. The opacity of the stent is excellent in the thorax because of the low density of the surrounding lung. The natural opacity of the aortic wall a t its interface with aerated lung also aids in optimal stent deployment in the left anterior oblique projection. The origin of the left vertebral artery can easily be noted with digital road mapping and a n overlying towel clamp. None of the lesions treated with stents were bridging the orifice of the vertebral artery. Lesions that span the origin of the vertebral artery may occlude the vertebral artery during stent placement in the subclavian lesion. The use of stents to repair perforations without covering graft material is contraindicated. Lesions extending up to the margin of the vertebral artery or to the aortic wall can be successfully treated with this technique. Because of the problem of brachial hematomas a t sheath entry sites, the last two patients of the series were treated via the right groin without complications. This site would seem to be the preferred orientation for percutaneous stent placement in the subclavian artery.
If a n occlusion were encountered, it could be opened by the brachial route via a 5-F sheath, and a stent could ultimately be placed by using the right femoral approach. Guiding catheters (8 F) could also be used in this procedure. When a n introducer sheath is used as a guiding catheter, the hole in the artery does not need to be any larger than the diameter of a 7.07.5-F sheath. The 70-cm Check-flo sheaths can be obtained by special order, and their tips can be formed bv hand to conform to the curve of the subclavian artery from the aortic arch: thus modified. these sheaths can function a s guiding catheters. The efficacy of thrombolysis during percutaneous transluminal stent placement to treat SSS in patients with occlusions is unknown. Thrombolysis was performed a s a precursor to PTA, not as a specific stand-alone therapy. Thrombolysis was used to treat these occlusions because of the author's anecdotal experience with embolization to the lower extremities during PTA of occlusive arterial disease in patients who were not pretreated with urokinase. The Wallstent was used in one patient because of the lack of availability of the extra-long 7-F sheaths a t that time, a low brachial entry, and a tortuous approach route. The use of percutaneous transluminal stent placement to repair SSS refractory to traditional angioplasty is still under investigation, but it appears to be a promising method. We have had excellent clinical results, with resolution of arm claudication and syncope and improvement or resolution of vertigo. No substantial stenoses (determined bv means of measurement of systolic pressure gradient or repeat angiography) had recurred a t follow-up of 2 years. Percutaneous transluminal stent placement can benefit patients undergoing percutaneous repair of SSS in whom angioplasty has failed and who are a poor operative risk, patients with substantial ipsilateral carotid disease, or patients who are not willing to undergo surgical bypass.
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Acknowledgments: We thank Wendy Aarnio, RN, Lisa Nason, RT, Linda Wiseman, RTCV, Leila Cahalan, RT, and Sandra Whitehead, RT. Their hard work and dedication made this article possible. References 1. A new vascular syndrome: "the subclavian steal." N Engl J Med 1961; 265:912-913. 2. Ziomek S, Quinones-Baldrich WJ, Busuttil RW, et al. The superiority of synthetic arterial grafts over autologous veins in carotid-subclavian bypass. J Vasc Surg 1986; 3:140145. 3. Beebe HE, Stark R, Johnson ML, et al. Choices of operation for subclavian-vertebral arterial disease. Am J Surg 1980; 139:616-623. 4. Diethrich EB, Garrett HE, Amersio J, Crawford ES, El-Bayar M, DeBakey ME. Occlusive disease of the common carotid and subclavian arteries treated by carotid-subclavian bypass. Am J Surg 1967; 114:800-808. 5. Herring M. The subclavian steal syndrome: a review. Am Surg 1977; 43:220-228.
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