You are in: eMedicine Specialties > Radiology > VASCULAR/INTERVENTIONAL Subclavian Steal SyndromeArticle Last Updated: Feb 15, 2007AUTHOR AND EDITOR INFORMATIONAuthor: David P Brophy, MD, Consultant Vascular and Interventional Radiologist, Department of Radiology, University College Dublin; Consulting Staff, St. Vincent's University Hospital David P Brophy is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Massachusetts Medical Society, and Radiological Society of North America Editors: Robert A Koenigsberg, DO, MSc, FAOCR, Director of Neuroradiology, Professor, Department of Radiology, Drexel University College of Medicine; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Douglas M Coldwell, MD, PhD, Professor of Interventional Radiology, Department of Radiology, University of Texas Southwestern Medical Center; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Kyung J Cho, MD, FACR, William Martel Professor of Radiology, Fellowship Program Director, Department of Radiology, Division of Interventional Radiology, University of Michigan Medical School Author and Editor Disclosure Synonyms and related keywords: subclavian steal phenomenon, subclavian steal steno-occlusive disease, SSP, SSS INTRODUCTIONBackgroundSubclavian steal phenomenon (SSP) refers to subclavian artery steno-occlusive disease proximal to the origin of the vertebral artery and is associated with flow reversal in the vertebral artery. While Contorni first described retrograde flow in the vertebral artery in 1960, Reivich in 1961 first recognized the association between this phenomenon and neurologic symptoms. Fisher dubbed this combination of retrograde vertebral flow and neurologic symptoms subclavian steal syndrome (SSS), suggesting that blood is stolen by the ipsilateral vertebral artery from the contralateral vertebral artery. It was later suggested that such "steal" may cause brainstem ischemia and stroke, either continuously or secondary to arm exercise. The term SSS should be reserved for retrograde vertebral artery flow associated with transient neurologic symptoms related to cerebral ischemia. SSP refers to retrograde flow in the vertebral artery only. First diagnosed angiographically in the early 1960s, SSS is now most commonly diagnosed during Doppler ultrasound (US) examination of the neck arteries. PathophysiologyThe primary lesion causing vertebral artery flow reversal is proximal subclavian artery stenosis or occlusion, resulting in decreased blood pressure in the arm distal to the steno-occlusive disease. This pressure reduction initially causes ipsilateral vertebral artery blood flow alteration provided the subclavian disease is proximal to the origin of the vertebral artery. Ultimately, a flow reversal occurs in the ipsilateral vertebral artery as compensatory collateral to the compromised vascular territory beyond the subclavian steno-occlusive lesion. Other potential collateral pathways are those between the external carotid artery (ECA) and the subclavian artery, from the occipital branch of the ECA to the deep cervical branch of the costocervical trunk, and from the superior thyroid artery of the ECA to the inferior thyroid artery branch of the thyrocervical trunk. Classification of subclavian steal can be defined by territory from which blood is stolen, as described by Vollmar et al. Vollmar recognized 4 types of subclavian steal: vertebro-vertebral, carotid-basilar, external carotid-vertebral, and carotid-subclavian (can only occur with occlusion of brachiocephalic artery). Another classification is based on vertebral artery hemodynamics as described by Branchereau and colleagues. Hemodynamic abnormalities ranged from reduced antegrade vertebral flow (stage I), reversal of flow during reactive hyperemia testing of the arm (stage II), and permanent retrograde vertebral flow (stage III). The 3 stages correlate with disease severity with stage III, usually indicating subclavian artery occlusion. Arm symptoms may be provoked by an increased blood flow requirement to the compromised upper extremity (eg, during arm exercise or after producing peripheral reactive hyperemia by arm cuff inflation), or, alternatively, by limiting vertebral compensatory flow to the subclavian artery (eg, during neck movements). Subclavian steno-occlusive disease produces neurologic symptoms when compensatory flow to the subclavian artery from the vertebral artery diverts too much flow toward the arm and away from intracranial structures. The quality of collateral blood supply and the capacity to increase collateral flow to the intracranial circulation (brainstem in particular) may be the principle determinant as to which patient develops neurologic symptomatology. In times of reversed flow in the vertebral arteries, the most important collateral circulation to the posterior fossa is through the circle of Willis, principally through the posterior communicating artery. In situations where this communication is absent or inadequate, possibly from concurrent extracranial carotid stenoses, increased demand in the ipsilateral upper extremity may cause neurologic symptoms. This is the foundation for the belief that hemodynamically important disease in the cerebral arterial circulation (or vessels supplying that circulation) is a prerequisite of SSS. Spontaneous resolution of vertebrobasilar symptoms may be related to the establishment of extracranial collaterals to the subclavian circulation. FrequencyUnited StatesThe Joint Study of Extracranial Arterial Occlusion reported a 17% rate of subclavian or innominate artery stenosis but angiographic steal occurred in only 168 (2.5%) of 6534 cases; of those with angiographic steal, 80% had associated extracranial obstructions and 9 (5.3%) of 168 had neurologic symptoms. A 6.4% rate of SSP was observed in 500 asymptomatic patients with neck bruits undergoing Doppler US and subclavian steal test (to provoke vertebral artery flow reversal). In 680 symptomatic patients examined with angiography, 23% had severe proximal subclavian disease or occlusion, with 6% showing reversed vertebral artery flow. InternationalThe rate of SSP is 1.3% (324 cases in 25,000 persons) in European patients referred for carotid and vertebral artery Doppler US; of these patients, 5% have nonhemispheric neurologic symptoms. In the Far East, up to 36% (9 in 25) of patients undergoing surgical management of SSS have an etiology of Takayasu, with atherosclerosis accounting for the remaining patients. Nonatherosclerotic etiologies are rare in whites. Mortality/MorbidityIn SSS patients, risk of stroke is poorly documented but seems low. Bornstein and Norris prospectively followed 500 patients for 2-4 years, having documented SSP in 45 (9%) of 500 persons. None of their SSP patients had a stroke during the follow-up period while symptoms developed in 5 patients: 3 had dizzy spells and 2 had numbness of the affected arm at rest. Field et al noted that of 168 patients with vertebral flow reversal, only 9 (5.35%) of 168 had vertebrobasilar symptoms and all of these 9 patients had other lesions that might explain their symptoms. Despite apparent low stroke risk, patients with SSS may be severely debilitated by episodes of arm and related intracranial ischemia symptoms. Given the differences in survival between medically and surgically treated patients, surgical "prophylaxis" of stroke should be reserved for patients with disabling vertebrobasilar symptoms.
RaceSSS is most frequently described in Caucasians because of increased incidence of atherosclerosis in this population. In the Far East, as many as 36% (9 in 25) of patients undergoing surgical management of subclavian steal syndrome have Takayasu arteritis as the etiology, with atherosclerosis accounting for the remaining patients. Nonatherosclerotic etiologies are rare in whites. SexIncidence is greater in males than in females (1.5-2:1). However, when Takayasu arteritis is causative rather than atherosclerosis, there is a female predilection. AgeSSS usually affects people older than 50 years when the disease is secondary to atherosclerosis while SSS presents far earlier ( <30 y in 90%) when Takayasu arteritis is implicated. AnatomyThe ratio of left-sided to right-sided SSP is 3-4:1; most likely, this relates to turbulence-related atherosclerosis in the proximally more acutely angled left subclavian artery. In 2% of the population, the left vertebral artery arises directly from the aortic arch; in these patients, severe stenosis or occlusion of the proximal left subclavian artery would not reverse flow in the left vertebral artery (ie, it lacks communication with the subclavian artery). Classify SSS by the territory from which blood is stolen as follows:
Coronary-subclavian steal syndrome refers to decreased or reversed internal mammary artery flow, which causes angina related to severe subclavian steno-occlusive disease in patients with in situ internal mammary-to-coronary artery graft. Clinical DetailsHistory Commonly asymptomatic, subclavian artery steno-occlusive disease associated with flow reversal in the ipsilateral vertebral artery is diagnosed as an incidental finding during Doppler US examination of the carotid and vertebral arteries. Symptoms that occur (eg, dizziness, unsteadiness, vertigo, visual changes) most typically are related to vertebrobasilar and posterior cerebral circulation ischemia. Arm ischemia occurs, causing arm claudication and rest pain. SSS can be associated with hemispheric or global cerebral symptoms such as focal sensory or motor loss, dysphasia, and unilateral visual disturbances. Concomitant carotid or cerebral artery disease is a factor. Vertebrobasilar symptoms provoked by ipsilateral arm exercise are considered a characteristic, though rare, feature. Neck movement may provoke symptoms. In most patients, there is a clear provoking or reproducible event. Hand ischemia is uncommon in SSS; therefore, consider a different etiology (eg, atheroembolic disease). The physician often elicits a history of smoking, hypertension, hyperlipidemia, diabetes, and coronary and/or peripheral vascular disease. Physical Weak or absent radial and ulnar pulse in the presence of ipsilateral reduced blood pressure (change is >20 mm Hg) when compared to the contralateral arm suggests SSS. A bruit may be localized to the proximal subclavian artery. Reactive hyperemia testing (temporary arm cuff inflation above systolic pressure on the side of subclavian disease) can provoke vertebrobasilar symptoms by causing peripheral vasodilation and decreasing peripheral resistance with a resulting sump effect favoring increased flow from the vertebral circulation to the involved upper extremity. Preferred ExaminationColor Doppler US is the preferred examination. Limitations of TechniquesColor Doppler US is operator-dependent; direct examination of the proximal subclavian is compromised by overlying clavicle, ribs, and sternum. DIFFERENTIALSAorta, Dissection Arteritis, Giant Cell Arteritis, Takayasu Embolization, Vascular Lesions
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| Media file 1: Arch aortogram initially shows apparent absence of left vertebral artery opacification. With delayed imaging on the same patient (right image), the left vertebral artery fills retrogradely to supply the left subclavian artery, confirming left subclavian steal phenomenon secondary to a severe stenosis of the proximal left subclavian artery. | |
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| Media file 2: Selective arteriogram (same patient as shown in Image 1) shows a severe proximal subclavian stenosis proximal to left internal mammary artery. The patient presented with angina having had a left internal mammary artery-left anterior descending coronary graft 12 months previously. Note nonopacification of the left vertebral artery and the filling defect consistent with in situ thrombus. | |
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| Media file 3: Thrombolysis was considered before angioplasty. As no antegrade left vertebral flow was demonstrated on the original digital subtraction arteriogram, thrombolysis was not performed. This line of treatment was determined in the belief that if any clot embolized to the coronary or vertebral circulations after percutaneous transluminal angioplasty (also a risk of thrombolysis alone), thrombolysis could then be performed with selective catheterization. After administration of vasodilators and anticoagulants, angioplasty with a 7-mm balloon restored antegrade flow to the left vertebral artery. The patient has had sustained relief from angina without embolic complication to either vertebral or coronary circulations. Both radial and ulnar pulses improved post angioplasty. | |
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| Media file 4: Gadolinium-enhanced magnetic resonance angiography maximum intensity projection image shows left subclavian artery occlusion in a patient with left subclavian steal phenomenon and aberrant right subclavian artery. The patient had no neurologic or arm symptoms, but the subclavian lesion eliminated the left internal mammary artery as a coronary bypass graft option. | |
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| Media file 5: Gadolinium-enhanced magnetic resonance angiogram (MRA) of right carotid-subclavian subclavian steal phenomenon. This tangential aortic arch maximum intensity projection view shows innominate artery occlusion and severe left proximal subclavian artery steno-occlusive lesion. Two-dimensional time-of-flight MRA confirmed retrograde flow in the right vertebral but not in the left vertebral artery. MRA tends to exaggerate the severity of steno-occlusive disease. While this MRA suggests a short occlusion of the left proximal subclavian, a severe stenosis rather than occlusion was documented on conventional catheter arteriography. | |
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| Media file 6: Conventional arteriogram in a 70-year-old man who previously had a carotid-subclavian bypass for dizziness related to subclavian steal syndrome. The bypass is occluded and a severe stenosis of the proximal subclavian artery is apparent. Note poor filling of right vertebral artery caused by retrograde flow documented on Doppler ultrasound; note also the bovine arch with common origin of right brachiocephalic trunk and left common carotid artery. | |
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| Media file 7: After stent placement, antegrade flow is restored in the right vertebral artery. Primary stenting was chosen because of theoretical risk of embolism to the left vertebral artery territory; however, there appears to be a time lag before restoration of antegrade vertebral artery flow after proximal subclavian revascularization that protects against this embolism risk. Other techniques to decrease the risk of vertebral artery embolism include decreasing peripheral resistance in the ipsilateral upper extremity (eg, with intra-arterial vasodilators or temporary blood pressure cuff inflation above systolic pressure) to promote vertebral artery retrograde flow during angioplasty or stenting. | |
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| Media file 8: Patient presented with cardiac ischemia after a left internal mammary artery-left anterior descending coronary graft and multiple coronary artery vein grafts. Subclavian steal cannot occur in this patient, as the left subclavian stenosis is distal to the left vertebral artery origin. Note antegrade flow in the left vertebral artery. | |
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| Media file 9: Postangioplasty with a 9-mm balloon. The pressure gradient across the mid subclavian stenosis was reduced from 60 to 0 mm Hg. | |
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| Media file 10: Normal antegrade right vertebral artery flow on Doppler ultrasound. With cephalad direction of insonation, the negative Doppler scale reading is consistent with flow going away from the direction of insonation in a normal cephalad antegrade fashion. | |
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| Media file 11: Doppler ultrasound shows reversed flow in the left vertebral artery consistent with left subclavian steal phenomenon. Doppler scale reading shows a negative deflection again; however, this time the direction of insonation is caudad, thus a negative scale Doppler reading indicates flow in a caudad direction and flow reversal in the left vertebral artery. | |
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Subclavian Steal Syndrome excerpt
Article Last Updated: Feb 15, 2007