INTRODUCTION — The term "subclavian steal" refers to a phenomenon of flow reversal in the vertebral artery ipsilateral to a hemodynamically significant stenosis or occlusion of the prevertebral subclavian artery [1-3]. In most cases, subclavian steal is asymptomatic (ie, subclavian steal phenomenon), does not warrant invasive evaluation or treatment, and represents an appropriate physiological response to proximal arterial disease. Subclavian steal syndrome implies the presence of significant symptoms due to arterial insufficiency in the brain (ie, vertebrobasilar insufficiency) or upper extremity, which is supplied by the subclavian artery (figure 1).
The physiology, diagnosis, and treatment of subclavian steal will be reviewed here. General considerations for patients with symptoms of vertebrobasilar ischemia are discussed in detail elsewhere. (See "Posterior circulation cerebrovascular syndromes".)
The clinical presentations and diagnosis of upper extremity ischemia (eg, exertional pain, digital ischemia, gangrene) are reviewed in detail separately. (See "Overview of upper extremity ischemia", section on 'Clinical presentation'.)
DEFINITION AND PHYSIOLOGY
Classic subclavian steal — Subclavian artery occlusion or a hemodynamically significant stenosis proximal to the origin of the vertebral artery results in lower pressure in the distal subclavian artery [4,5]. As a result, blood flows from the contralateral vertebral artery to the basilar artery and may flow in a retrograde direction down the ipsilateral vertebral artery, away from the brainstem (figure 2) [6,7]. Reversed vertebral artery flow, although it may have deleterious neurologic effects, serves as an important collateral artery for the arm in this setting.
Coronary-subclavian steal — A coronary-subclavian steal phenomenon has been described in patients who have undergone prior coronary artery bypass surgery (CABG) using the internal mammary artery (IMA) [8-10]. The prevalence of subclavian artery stenosis is 2.5 to 4.5 percent in patients referred for coronary artery bypass grafting [11]. In the presence of a hemodynamically significant subclavian artery stenosis proximal to the origin of the ipsilateral IMA, flow through the internal mammary artery may reverse and "steal" flow from the coronary circulation. This may be exacerbated during upper extremity exercise (figure 3). Coronary and graft angiography may demonstrate retrograde flow in the involved IMA during selective catheterization of the grafted coronary artery [12].
Simultaneous coronary and cerebrovascular ischemia has also been reported [10,13]. Identification of a significant subclavian artery stenosis prior to CABG can prevent this important problem. Those patients with a high-grade subclavian artery stenosis should be treated (percutaneously or surgically) prior to CABG [14]. For patients with symptomatic subclavian lesions who require coronary artery bypass, no differences were seen for complications, mortality, or symptom recurrence, using a combined or staged approach to revascularization [15].
EPIDEMIOLOGY AND RISK FACTORS — The incidence/prevalence of subclavian steal syndrome is not well defined. Among individuals with documented peripheral artery disease, the prevalence of upper extremity atherosclerotic disease is much lower compared with lower extremities. Approximately 30 percent of such patients have subclavian artery stenosis; however, only a minority develop symptoms, predominantly because of the extensive collateral network of vessels around the shoulder (figure 4) [7]. (See "Overview of upper extremity peripheral artery disease".)
In a large study of extracranial arterial disease, the incidence of subclavian/innominate stenosis/occlusion was 17 percent, but only 2.5 percent fulfilled the criteria for subclavian steal [16]. A later study identified subclavian stenosis/occlusion in 432 of 7881 patients presenting for ultrasound exam of the extracranial neck vessels; among these, 38 (8.8 percent) experienced symptoms [17]. Therefore, subclavian steal syndrome occurs in only a minority of patients with subclavian stenosis [18]. (See 'Duplex ultrasound' below.)
Risk factors — Atherosclerosis is the most common cause of subclavian artery stenosis. The risk factors associated with atherosclerosis are discussed elsewhere. (See "Overview of established risk factors for cardiovascular disease".)
Males are more commonly affected compared with females. Subclavian stenosis and therefore subclavian steal occurs more commonly on the left side (>75 percent), possibly due to a more acute origin of the left subclavian artery, resulting in accelerated atherosclerosis from increased turbulence [4,17,19-22].
Other conditions that increase the risk for subclavian stenosis that may lead to subclavian steal include:
●Takayasu arteritis [23]. These patients present at a younger age. (See "Clinical features and diagnosis of Takayasu arteritis".)
●Compression of the subclavian artery in the thoracic outlet (figure 5). The site of arterial compression in thoracic outlet syndrome is most often distal to the origin of the vertebral artery. Therefore, the potential for symptomatic steal is low. However, these patients can have posterior circulation strokes due to retrograde propagation of thrombus. Athletes, such as baseball pitchers, cricket bowlers, and swimmers, are the most likely to be affected due to neurovascular compression as the subclavian artery crosses over the first rib. (See "Overview of thoracic outlet syndromes", section on 'Arterial TOS'.)
●Following surgical repair of coarctation of the aorta [24]. (See "Clinical manifestations and diagnosis of coarctation of the aorta".)
●Following surgical repair of tetralogy of Fallot with a Blalock-Taussig anastomosis [25]. (See "Management and outcome of tetralogy of Fallot".)
●Congenital abnormalities such as right aortic arch with isolation of the left subclavian artery and anomalies of the brachiocephalic arteries [26-29]. (See "Vascular rings and slings".)
CLINICAL FEATURES — The incidence of the subclavian/innominate stenosis and the subclavian steal phenomenon is much higher than that of the symptomatic clinical syndrome. (See 'Epidemiology and risk factors' above.)
Clinical presentations
Asymptomatic — Most patients with subclavian artery stenosis are asymptomatic. In many patients, subclavian artery occlusive disease is found incidentally by noting a blood pressure discrepancy between arm pressures or on ultrasound testing of patients with carotid or coronary artery disease. A careful history and physical examination may identify subtle findings. For the majority of patients, the finding of "angiographic steal" is clinically insignificant and is not associated with an increased risk of vertebrobasilar ischemia [17,30].
A steal phenomenon is apparent on duplex scanning in approximately 6 percent of patients with asymptomatic neck bruits, but in one series, none of the patients developed symptoms during a two-year follow-up period [31]. Even when reversed flow occurs in the vertebral artery, antegrade basilar arterial flow persists and may even be increased.
In one prospective study, 500 patients with asymptomatic neck bruits were followed over a four-year period [31]. Of these patients, 9 percent had severe subclavian stenosis, and over one half of these patients (64 percent) had a steal phenomenon. None of the patients had symptoms as a result of arm exercise.
Symptomatic — When symptoms occur, they are most often due to arm ischemia, but this is uncommon as well. Symptoms of vertebrobasilar ischemia are also uncommon and tend to develop only when there are concurrent cerebrovascular lesions. Anomalies of the circle of Willis (figure 1), the most important collateral route in the cerebrovascular circulation, occur with increased frequency in patients with symptomatic subclavian steal [32].
Upper extremity ischemia — Symptoms, when they occur, are due mainly to ischemia of the ipsilateral upper extremity. Exercise-induced arm pain, fatigue, coolness, paresthesias, or numbness, occurs in approximately one third of patients, but chronic ischemic and trophic changes are rare. A large pressure difference (>40 mmHg) between the arms is more commonly associated with symptoms and the need for intervention [17].(See "Overview of upper extremity ischemia".)
Ischemic symptoms may also result from embolism of atherosclerotic or thrombotic debris from the subclavian lesion. (See "Embolism to the upper extremities".)
Neurologic symptoms — Less often, neurologic symptoms can be caused by vertebrobasilar ischemia of the brainstem.
However, whether the steal phenomenon is the principal cause of cerebral ischemic symptoms remains controversial. This is based upon a number of observations:
●Reestablishment of antegrade blood flow may not relieve symptoms.
●Exercise rarely provokes cerebral symptoms.
●Occlusive arterial disease in the other extracranial arteries is often present and may be a confounding source of symptoms.
●Retrograde flow in the vertebral arteries is commonly identified with duplex ultrasound and is often not associated with neurologic symptoms [18].
Symptoms and signs of vertebrobasilar ischemia may include the following (see "Posterior circulation cerebrovascular syndromes"):
●Dizziness
●Vertigo
●Ataxia
●Dysequilibrium
●"Drop attacks"
●Diplopia
●Nystagmus
●Graying of vision
●Hemianopia
●Bilateral visual blurring
●Syncope
●Tinnitus
●Hearing loss
●Bilateral brachial diplegia
Upper extremity exercise, which increases blood flow to the arm and decreases arterial resistance, can precipitate central nervous system symptoms. The presence of collateral blood supply and the capacity to increase collateral flow may be the principal determinants of which patients develop neurologic symptoms in this setting.
Vertebral artery compression and neurologic symptoms can also occur with head movements, usually rotation of the face toward the opposite side [17]. This association can usually be detected by a careful history.
Although patients with documented subclavian steal have a very low incidence of posterior circulation ischemic events, these patients are more likely to develop hemispheric ischemia due to concurrent progressive carotid disease [18]. Collateral pathways are usually compromised in symptomatic patients, placing them at increased risk, principally from carotid territory cerebrovascular events.
Bilateral vertebral flow reversal may be associated with an increased risk of nonlateralizing cerebral ischemia. In one study, brainstem dysfunction from upper extremity exercise was seen only in patients with bilateral reversed flow [33]. However, persistent retrograde flow in the basilar artery, with collateral blood supply from the internal carotid arteries, has been reported in a patient without any neurologic or upper extremity symptoms [34].
Physical examination — On examination, there is usually a difference in brachial systolic blood pressure between the affected and normal arm of at least 15 mmHg. In addition, simultaneous palpation of both radial artery pulses will usually disclose a decrease in amplitude and delay in arrival on the affected side (waveform 1).
The carotid arteries should be carefully examined, using palpation and auscultation, for evidence of occlusive arterial disease. Auscultation over the suboccipital region for vertebral artery bruits should also be performed. It is important to examine the subclavian arteries in the supraclavicular fossa using palpation (pulse character and thrills) and auscultation for paraclavicular bruits.
Other parts of the physical examination should include:
●Performance of thoracic outlet maneuvers to exclude other causes of a subclavian stenosis. (See "Brachial plexus syndromes", section on 'Thoracic outlet syndrome'.)
●All major pulses should be palpated. The presence of multiple pulse deficits (subclavian and carotid) raises the possibility of Takayasu's disease. (See "Clinical features and diagnosis of Takayasu arteritis".)
●The skin of the hands and nail beds of the affected extremity should be thoroughly examined. Atheroembolism from atherosclerotic lesions of the subclavian artery may result in blue fingers, livedo reticularis, digital ischemia, or ulceration or splinter hemorrhages under the nail beds. (See "Embolism to the upper extremities".)
DIAGNOSIS — A difference in upper extremity pressures in a patient with appropriate symptoms suggests subclavian steal syndrome; however, imaging confirmation is necessary to definitively establish the diagnosis.
Noninvasive imaging of the cerebrovascular and upper extremity arterial circulation demonstrates the lesion and appropriate physiology. Duplex ultrasound is the first-line imaging modality for the detection of the subclavian stenosis causing subclavian steal phenomenon. However, due to inherent limitations, ultrasound cannot reliably evaluate the origin of the aortic branches. Consequently, arteriography, typically magnetic resonance (MR) or computed tomographic (CT) angiography, is needed to confirm and grade the subclavian artery stenosis.
Catheter-based cerebral angiography (image 1) is generally not needed to establish a diagnosis, but when performed prior to endovascular intervention, concurrent intracranial atherosclerotic disease and anomalies of the circle of Willis can also be identified.
Duplex ultrasound — Duplex ultrasound (combined two-dimensional ultrasound and pulsed-wave Doppler) can readily diagnose and semiquantify proximal subclavian artery stenoses and demonstrate reversal of flow, if present, in the ipsilateral vertebral artery (image 2). A subclavian artery peak systolic velocity >240 cm/second is predictive of a significant (>70 percent) subclavian artery stenosis [35]. Duplex ultrasound is limited in the evaluation of the origin of the vertebral artery for evidence of occlusive disease due to its intrathoracic location, but is extremely accurate for the assessment and identification of significant extracranial carotid artery occlusive disease. (See "Noninvasive diagnosis of upper and lower extremity arterial disease", section on 'Duplex ultrasound'.)
When severe stenosis (>80 percent narrowing) of the proximal subclavian artery is present, 65 percent of patients have permanent flow reversal in the ipsilateral vertebral artery, and 30 percent have intermittent flow reversal (ie, "to and fro" waveform pattern on duplex) [18,36]. In patients with moderate subclavian artery stenosis (approximately 50 percent narrowing), flow reversal in the vertebral artery is permanent in 56 percent and intermittent in 36 percent.
While not commonly needed or performed on a routine basis, a reactive hyperemia type test can be performed to uncover occult or intermittent subclavian steal [37-39]. To do this, a blood pressure cuff is applied to the ipsilateral extremity and inflated at least 20 mmHg above systolic pressure for three to four minutes. This produces ischemia and compensatory vasodilation distal to the cuff. After deflation of the cuff, blood flow will increase in the upper extremity, and for patients with an otherwise asymptomatic subclavian stenosis, reversal of blood flow in the ipsilateral vertebral artery may provoke symptoms. During these maneuvers, retrograde flow can be observed with the concomitant use of ultrasound [40].
Magnetic resonance angiography — MR angiography is an accurate and reliable imaging modality for patients with suspected subclavian steal syndrome [41]. Contrast-enhanced MR angiography combined with phase-contrast MR imaging enables visualization and characterization of the majority of supraaortic arteries, with excellent image quality and diagnostic values comparable to CT angiography or conventional catheter-based arteriography for detection of arterial stenoses [42,43]. In addition to evaluation of the extracranial vessels, MR also provides detailed anatomic information of the intracranial cerebrovascular circulation.
Flow reversal in the vertebral artery ipsilateral to a subclavian stenosis is inferred from presence of vertebral artery patency on three-dimensional contrast-enhanced MR but absence of flow on time-of-flight localizer images [44].
Pitfalls in using MR to evaluate the subclavian artery include the possibility of overestimating stenosis severity and the inability to discriminate between near-complete and complete arterial occlusion.
CT angiography — Multidetector CT angiography can confirm and grade subclavian artery stenosis, as well as reveal other pathology involving the subclavian artery. CT angiography is indicated in patients with subclavian steal syndrome who have abnormal or nondiagnostic findings on duplex ultrasound to identify and characterize the underlying pathology and any anatomic abnormalities [17,45]. CT angiography can detect arterial stenosis, thrombosis, occlusion, aneurysm formation, and vasculitis within the subclavian artery [46].
Transcranial Doppler — When flow reversal of the vertebral artery is identified, some authors have suggested the use of transcranial Doppler (TCD) to evaluate the direction of flow in the basilar artery [39]. A finding of reversed flow at the level of the basilar artery is more predictive of symptoms than reversal of flow in the vertebral artery only. In one study of patients with flow reversal of the vertebral artery ipsilateral to a subclavian stenosis/occlusion, 76 percent had antegrade flow in the basilar artery [36]. Patients with antegrade flow in the basilar artery are not likely to have symptoms.
DIFFERENTIAL DIAGNOSIS — The diagnosis of subclavian steal includes vascular pathologies that may also cause occlusion of the proximal subclavian artery, which may or may not have symptoms of upper extremity ischemia, as well as other predominantly neurologic conditions that lead to symptoms associated with basilar insufficiency. (See "Overview of upper extremity ischemia" and "Overview of upper extremity peripheral artery disease" and "Posterior circulation cerebrovascular syndromes".)
There is a subset of patients with primary proximal subclavian artery lesions who embolize through the ipsilateral vertebral artery, leading to symptoms of transient vertebrobasilar ischemia that is not due to the steal phenomenon. (See "Posterior circulation cerebrovascular syndromes".)
MANAGEMENT
Risk modification — Subclavian stenosis/occlusion is a marker for atherosclerotic disease (eg, carotid, coronary, lower extremity arteries) and future adverse cardiovascular events. Subclavian artery stenosis is associated with an increased risk of both overall mortality and mortality related to cardiovascular disease (CVD). In a study of 157 patients with subclavian artery stenosis (diagnosed as brachial systolic pressure difference ≥15 mmHg), the presence of subclavian stenosis was significantly associated with increased total mortality and CVD mortality (hazard ratios 1.40 and 1.57, respectively) after adjusting for other demographic and CVD disease risk factors [47].
Thus, the detection of subclavian stenosis identifies patients who may benefit from secondary prevention measures such as the following:
●Control of hypertension
●Treatment of dyslipidemia
●Glycemic control in diabetes
●Smoking cessation
●Antithrombotic therapy
●Lifestyle changes
The importance of these risk reduction strategies for secondary prevention of CVD and stroke is discussed in detail separately. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk" and "Overview of secondary prevention of ischemic stroke".)
INTERVENTION — The approach to therapy of subclavian steal associated with symptoms varies with the clinical setting. In many patients, symptoms improve over time without treatment. Interventional treatment is not usually warranted in patients with asymptomatic subclavian stenosis/occlusion.
Patients with unacceptable surgical risk or anatomy unfavorable for intervention can be treated with antiplatelet therapy (and possibly oral anticoagulation), but no prospective trials have evaluated the effectiveness of this option.
Open surgical bypass — Symptomatic patients with an ulcerated lesion in the subclavian artery as a cause of distal embolization can be successfully treated by surgical exclusion of the lesion from the circulation, usually accomplished by arterial bypass or carotid transposition [48,49]. (See "Surgical and endovascular techniques for aortic arch branch and upper extremity revascularization", section on 'Open surgical repair'.)
Extra-anatomic revascularization (eg, carotid-subclavian bypass, carotid transposition) is the most common form of surgical correction for symptomatic subclavian artery stenosis. Overall patency rates of 95 percent at one year, 86 percent at three years, and 73 percent at five years have been reported [33]. Procedures using the common carotid artery as the donor vessel generally have high patency rates at five years compared with those using the contralateral subclavian or axillary arteries (83 versus 46 percent) [33]. Axillo-axillary bypass is an alternative method of extra-anatomic revascularization that can be used in high-risk surgical patients [50].
Surgical treatment for patients with a subclavian steal and coexisting severe carotid stenosis is controversial. Because a significant percentage of patients with subclavian steal have concomitant severe extracranial atherosclerotic disease, carotid artery endarterectomy should generally be performed first, and, if the patient's symptoms improve, other treatment may not be necessary [51]. (See "Management of symptomatic carotid atherosclerotic disease" and "Carotid endarterectomy".)
Endovascular intervention — Endovascular intervention (with embolic protection) for embolism related to proximal subclavian artery is appropriate for patients with appropriate anatomy (short proximal stenosis or occlusion). If percutaneous treatment will jeopardize the integrity of the vertebral artery, we prefer surgical revascularization. (See "Surgical and endovascular techniques for aortic arch branch and upper extremity revascularization".)
Although data are limited and no randomized trials are available, retrospective observational studies suggest that endovascular intervention is safe with low morbidity and mortality (3.6 percent combined stroke and death rate in one study [52]) [53]. Immediate technical success is achieved in greater than 93 percent of patients, with failures usually related to an inability to cross occlusive lesions [54-56]. Five-year primary patency rates are approximately 85 percent [55]. In a single-center retrospective review of 167 patients with left subclavian artery stents who were being evaluated for coronary artery bypass, stent patency rates were 75.2 percent at 10 years [57]. Freedom from reintervention for the target vessel and sustained resolution of ischemic symptoms is observed in most patients (>95 percent) [52,55,56,58-60].
Whether angioplasty alone has inferior outcomes compared with angioplasty and stenting depends on the nature of the lesion being treated [23,61]. This issue is discussed separately. (See "Surgical and endovascular techniques for aortic arch branch and upper extremity revascularization", section on 'Angioplasty/stenting'.)
Symptoms due to significant (>70 percent) recurrent stenosis or obstruction occur in approximately 10 percent of patients and are typically treated with repeat angioplasty; however, surgery may be required in up to 5 percent of patients [52]. Patients with a continuous (compared with intermittent) subclavian and coronary artery steal may have a higher risk of subclavian artery restenosis following endovascular intervention [62].
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Occlusive carotid, aortic, renal, mesenteric, and peripheral atherosclerotic disease".)
SUMMARY AND RECOMMENDATIONS
●Subclavian steal – Subclavian steal refers to a phenomenon of flow reversal in the vertebral artery ipsilateral to a hemodynamically significant stenosis or occlusion of the prevertebral subclavian artery. Subclavian steal represents an appropriate physiological compensation to proximal subclavian artery disease. Subclavian steal syndrome refers to the presence of significant symptoms due to arterial insufficiency. (See 'Introduction' above.)
●Pathophysiology – A hemodynamically significant stenosis proximal to the origin of the vertebral artery results in lower pressure in the distal subclavian artery. As a result, blood flows from the contralateral vertebral artery to the basilar artery, and blood may flow in a retrograde direction down the ipsilateral vertebral artery, away from the brainstem (figure 2). In patients with an internal mammary artery bypass graft to the heart, proximal ipsilateral stenosis relative to the graft may reverse and "steal" flow from the coronary circulation during upper extremity exercise (ie, coronary-subclavian steal syndrome) (figure 3). (See 'Definition and physiology' above.)
●Symptoms – Most patients with subclavian artery stenosis are asymptomatic. For many, subclavian artery occlusive disease is found incidentally. When symptoms occur, they are most commonly due to arm ischemia or symptoms of vertebrobasilar ischemia. (See 'Clinical features' above.)
●Physical examination – Pulse examination and duplex ultrasound evaluation of the cerebrovascular and upper extremity arterial circulation establish the diagnosis in most patients. On examination, the patient often has a significant difference in brachial systolic blood pressure (>15 mmHg differential) between the affected and normal arm. Duplex ultrasound can readily diagnose and semiquantify proximal subclavian artery stenoses and demonstrate reversal of flow in the ipsilateral vertebral artery, if present. If needed, arteriography that includes the aortic arch vessels and intracranial vessels can be accomplished with magnetic resonance angiography, CT angiography, or occasionally catheter-based arteriography. (See 'Diagnosis' above.)
●Risk modification – Subclavian stenosis/occlusion is a marker for atherosclerotic disease (eg, carotid, coronary, lower extremity arteries) and is associated with an increased risk of morbidity and mortality related to cardiovascular disease. Patients with atherosclerosis benefit from secondary prevention measures (ie, treatment of modifiable cardiovascular risk factors). (See 'Risk modification' above.)
●Treatment – We treat patients with subclavian steal syndrome. The choice of intervention (surgical, endovascular) depends upon the patient's specific anatomy, the presence of concomitant ipsilateral carotid disease, and the patient's overall medical status. Patients with subclavian steal syndrome who are not candidates for intervention are treated with antithrombotic therapy. For asymptomatic patients, the emphasis is on secondary prevention. (See 'Management' above and "Surgical and endovascular techniques for aortic arch branch and upper extremity revascularization".)
ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledges Peter C Spittell, MD, who contributed to an earlier version of this topic review.
