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Subclavian Steal Syndrome
Updated: Jul 24, 2009
Introduction
Background
Subclavian 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 1960,1 Reivich in 1961 first recognized the association between this phenomenon and neurologic symptoms.2 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.3
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.
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.
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.4,5,6,7
Pathophysiology
The 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).8 Another classification is based on vertebral artery hemodynamics as described by Branchereau and colleagues.9 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 subclavian steal syndrome (SSS).
Spontaneous resolution of vertebrobasilar symptoms may be related to the establishment of extracranial collaterals to the subclavian circulation.
Frequency
United States
The 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.10
International
The rate of subclavian steal phenomenon (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 subclavian steal syndrome (SSS) have an etiology of Takayasu arteritis, with atherosclerosis accounting for the remaining patients. Nonatherosclerotic etiologies are rare in whites.
Mortality/Morbidity
In subclavian steal syndrome (SSS) patients, risk of stroke is poorly documented but seems low. Bornstein and Norris prospectively followed 500 patients for 2-4 years, having documented subclavian steal phenomenon (SSP) in 45 (9%) of 500 persons.11 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. Fields 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.10
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.
- The presence of other extracranial arterial disease is a prerequisite to the development of symptoms. The reported incidence of associated extracranial stenotic disease is 24-80%.
- Neurologic symptoms, when they occur, more likely are related to other extracranial arterial disease than to vertebral artery flow reversal.
- Ackerman et al described a spontaneous remittence of vertebrobasilar symptoms that occurs in 50% of patients who were initially symptomatic.12 Only 15% of the initially asymptomatic patients experienced vertebrobasilar transient ischemic attacks during the follow-up period of at least 2 years.
Race
Subclavian steal syndrome (SSS) is most frequently described in whites 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.
Sex
Incidence 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.
Age
Subclavian steal syndrome (SSS) 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.
Anatomy
The ratio of left-sided to right-sided subclavian steal phenomenon (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 subclavian steal syndrome (SSS) by the territory from which blood is stolen as follows:
- Vertebro-vertebral
- Carotid-basilar
- External carotid-vertebral
- Carotid-subclavian (occurs only on the right side with right brachiocephalic occlusion)
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.
Presentation
History
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.
Subclavian steal syndrome (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 Examination
Color Doppler US is the preferred examination.
Limitations of Techniques
Color Doppler US is operator-dependent; direct examination of the proximal subclavian is compromised by overlying clavicle, ribs, and sternum.
Differential Diagnoses
Aorta, Dissection
Arteritis, Giant Cell
Arteritis, Takayasu
Embolization, Vascular Lesions
Other Problems to Be Considered
Causes of subclavian artery stenosis or occlusion include atherosclerosis, Takayasu arteritis, giant cell arteritis, tumor encasement, trauma, and previous surgical procedure, including aortic stent-graft placement for thoracic dissection or aneurysm. These stent grafts are being positioned intentionally across the left subclavian origin, leading functional subclavian occlusion with resultant subclavian steal phenomenon (SSP).
Causes of vertebrobasilar symptoms include cerebellar neoplasm, cerebellar degeneration, and multiple sclerosis.
Causes of arm symptoms include subclavian artery stenosis, neurologic factors, and atheroembolism.
More on Subclavian Steal Syndrome |
 Overview: Subclavian Steal Syndrome |
| Imaging: Subclavian Steal Syndrome |
| Follow-up: Subclavian Steal Syndrome |
| Multimedia: Subclavian Steal Syndrome |
| References |
| Further Reading |
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References
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Further Reading
Related eMedicine topics
Subclavian Steal Syndrome (Vascular Surgery)
Arteritis, Takayasu
Atherosclerosis
Subclavian Artery Thrombosis
Vertebrobasilar Atherothrombotic Disease
Embolization, Vascular Lesions
Keywords
subclavian steal syndrome, subclavian steal phenomenon, subclavian steal steno-occlusive disease, SSP, SSS, Takayasu arteritis
