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Subclavian Steal Syndrome
Updated: Oct 29, 2009
Introduction
The term subclavian steal has been used to describe retrograde blood flow in the vertebral artery associated with proximal ipsilateral subclavian artery stenosis or occlusion. This phenomenon may occur when the subclavian artery is occluded proximal to the origin of the vertebral artery. Although retrograde blood flow in the vertebral artery associated with ipsilateral subclavian artery occlusion is not unusual, neurological symptoms following ipsilateral arm exercise in this setting are uncommon. Most patients with significant arterial occlusive lesions in the proximal subclavian artery are asymptomatic; therefore, the term subclavian steal syndrome should really be reserved for those patients who develop neurological symptoms as a consequence of brain ischemia that occurs during or immediately following exercise of the ipsilateral arm.
Retrograde blood flow from the left vertebral artery into the left subclavian artery in a patient with subclavian steal syndrome.
History of the Procedure
In 1960, Contorni published the first report of blood flowing in a retrograde direction in the vertebral artery associated with a proximal ipsilateral subclavian artery occlusion.1 The following year, Reivich et al reported the first patient with symptoms and retrograde vertebral blood flow.2 However, in 1961, Fisher was the first to use the term subclavian steal syndrome to describe the neurologic symptoms associated with arm exercise.3 Surgical treatment for this syndrome was first reported in 1964, when Parrott described the technique of subclavian artery transposition.4 Percutaneous transluminal angioplasty for subclavian steal syndrome was first reported in 1980.
Problem
A definition of subclavian steal syndrome must include the following criteria:
- Neurological symptoms due to cerebral ischemia that are initiated by ipsilateral arm exercise
- Diminished blood pressure in the ipsilateral arm secondary to hemodynamically significant stenosis or occlusion of the subclavian artery proximal to the origin of the vertebral artery
Even if retrograde blood flow in the vertebral artery occurs in the presence of proximal subclavian artery stenosis or occlusion, subclavian steal syndrome is not present without symptoms and signs of cerebral ischemia initiated by ipsilateral arm exercise.
Frequency
Although peripheral arterial disease affects about 20-25% of Americans older than 70 years, the vessels of the upper extremity are affected much less often than those of the lower extremity. Since most patients do not seek medical advice unless symptoms occur, the prevalence of subclavian artery occlusive disease and subclavian steal syndrome is unknown.
The left subclavian artery is the most common aortic arch branch vessel affected by atherosclerosis; therefore, it is not surprising that the left subclavian artery is involved with subclavian steal 3 times more frequently than the right. In the Joint Study of Extracranial Arterial Occlusion, Fields and Lemak found that 17% of 6534 patients admitted to the study had arteriographic evidence of subclavian and/or innominate stenosis of greater than 30% or occlusion.5 However, only 168 patients had symptoms of subclavian steal syndrome. Berguer and associates found that only half of patients with significant subclavian occlusive lesions manifest reversal of blood flow in the ipsilateral vertebral artery.6
Etiology
The most common cause of proximal subclavian artery occlusive lesions is atherosclerosis. The risk factors for developing atherosclerotic plaques have been recognized for some time and are categorized as nonmodifiable and modifiable. Nonmodifiable risks include age, male sex, and family history. The modifiable risk factors are cigarette smoking, hypercholesterolemia, diabetes mellitus, hypertension, and hyperhomocysteinemia.
Although retrograde blood flow in the vertebral artery is usually noted angiographically in association with proximal ipsilateral subclavian artery occlusion, subclavian steal may also occur with hemodynamically significant subclavian artery stenosis (see Image 1).
Other less common causes of subclavian steal syndrome have been recognized. Arteriopathies, such as Takayasu disease, temporal arteritis, and congenital lesions of the aortic arch or subclavian artery, are unusual causes. Finally, subclavian steal syndrome has been documented following surgical sacrifice of the subclavian artery to perform the Blalock-Taussig procedure for tetralogy of Fallot.
Pathophysiology
Subclavian steal produces symptoms by flow-related phenomena rather than embolic. When an atherosclerotic lesion in the proximal subclavian artery progresses to cause hemodynamically significant stenosis, collateral vessels from the subclavian artery gradually enlarge. The upper extremity becomes dependent on these large collateral blood vessels that originate from the subclavian artery distal to the obstruction.
The collateral vessels serve as points of re-entry for blood flowing retrograde into the arm from the head, shoulder, and neck, thereby providing the extremity with adequate perfusion. When the arm is exercised, the blood vessels dilate to enhance perfusion to the ischemic muscle, thus lowering the resistance in the outflow vessels. Blood is siphoned from the head, neck, and shoulder through collateral vessels to supply this low-resistance vascular bed, satisfying increased oxygen demand by the exercising muscles of the upper extremity.
When arm exercise ceases, the resistance in the outflow vessels of the arm increases, thereby reducing retrograde blood flow in the vertebral artery.
Despite retrograde flow through the vertebral artery away from the brain, symptoms are not produced unless cerebral ischemia occurs. When cerebral ischemia from retrograde vertebral blood flow occurs, occlusive lesions in the other cerebral vessels are commonly present. Arterial lesions are present in the contralateral vertebral and/or carotid arteries in up to 80% of patients with subclavian steal symptoms.
Presentation
Patients who demonstrate retrograde blood flow in a vertebral artery are usually asymptomatic. In addition, with few exceptions, proximal subclavian stenosis or occlusion usually causes no symptoms of arm ischemia. Muscle cramping due to ischemia in the upper extremity typically occurs in laborers who perform vigorous work, often with their arms elevated above their heads. If arm exercise exceeds the ability of collateral vessels to provide sufficient blood flow to meet increased oxygen demand, then cerebral ischemia may occur as more blood is siphoned from the brain through the vertebrobasilar system.
Numerous symptoms are associated with posterior circulation cerebral ischemia. Symptoms of dizziness or vertigo occur in more than half of patients, and syncope and dysarthria have been noted in 18% and 12.5%, respectively. Visual symptoms secondary to vestibular dysfunction and/or nystagmus include a sensation of objects moving or the inability to focus as well as monocular or binocular visual loss. Diplopia occurs in 19% of cases. Fortunately, these transient ischemic episodes seldom progress to cause cerebral infarction.
An invariable finding in the patient with symptoms of subclavian steal is a difference (on average, 45 mm Hg) in the upper extremity pulses and brachial systolic blood pressures between the patient's arms.
Indications
Patients with atherosclerotic occlusive plaques in the subclavian artery are usually asymptomatic and therefore require no treatment. However, if either vertebrobasilar symptoms or exercise-induced arm pain occurs, a search for subclavian artery occlusive disease should be undertaken. If the ischemic symptoms are due to retrograde vertebral artery blood flow, surgical or interventional (ie, subclavian angioplasty/stent) treatment is indicated.
Relevant Anatomy
True subclavian steal syndrome cannot occur without retrograde blood flow in a vertebral artery associated with proximal ipsilateral subclavian artery stenosis or occlusion. In a healthy individual, blood pressures in both arms should be similar. Without a significant difference in blood pressure between the patient's arms, proximal subclavian stenosis or occlusion cannot be present.
Therefore, with a simple physical examination, the clinician can effectively eliminate significant subclavian arterial lesions without the need for angiography or duplex ultrasonography. The internal mammary artery arises from the inferior aspect of the proximal subclavian artery, opposing the origin of the vertebral artery. Recurrent symptoms of angina pectoris following otherwise successful coronary revascularization using a left internal mammary artery (LIMA) graft may also indicate a hemodynamically significant proximal left subclavian stenosis.
Atherosclerotic lesions (stenosis or occlusion) of the proximal vertebral artery may produce similar symptoms. Occlusive disease of the vertebral artery should be considered if posterior circulation symptoms occur with normal blood pressures in the affected arm.
Contraindications
Surgical treatment should not be offered to treat subclavian artery stenosis or occlusion in the absence of symptoms related to either cerebral or ipsilateral arm ischemia. Symptoms (eg, ataxia, dysarthria, diplopia, muscle cramping in the arm) must be associated with exercise and resolve quickly following cessation of exercise.
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References
Contorni L. Il circolo collaterale vertebro-vertebrale obliterazione dell'arteria succlavia alla origine. Minerva-Chir. 1960;15:268-71.
Reivich M, Holling E, Roberts B et al. Reversal of blood flow through the vertebral artery and its effect on cerebral circulation. N Engl J Med. Nov 2 1961;265:878-85. [Medline].
Fisher CM. A new vascular syndrome: "The Subclavian Steal". N Engl J Med. 1961;265:912-13.
Parrot JD. The subclavian steal syndrome. Arch Surg. 1969;88:661-5.
Fields WS, Lemak NA. Joint Study of extracranial arterial occlusion. VII. Subclavian steal--a review of 168 cases. JAMA. Nov 27 1972;222(9):1139-43. [Medline].
Berguer R, Higgins R, Nelson R. Noninvasive diagnosis of reversal of vertebral-artery blood flow. N Engl J Med. Jun 12 1980;302(24):1349-51. [Medline].
Moghazy KM. Value of color Doppler sonography in the assessment of hemodialysis access dysfunction. Saudi J Kidney Dis Transpl. Jan 2009;20(1):35-43. [Medline].
Bachman DM, Kim RM. Transluminal dilatation for subclavian steal syndrome. AJR Am J Roentgenol. Nov 1980;135(5):995-6. [Medline].
Baker R, Rosenbaum A, Caplan L. Subclavian steal syndrome. Contemporary Surgery. 1974;4:96.
Bornstein NM, Norris JW. Subclavian steal: a harmless haemodynamic phenomenon?. Lancet. Aug 9 1986;2(8502):303-5. [Medline].
Caplan LR. Vertebrobasilar occlusive disease. Stroke: Pathophysiology, Diagnosis and Management. 1986;549.
Caplan LR, Wityk RJ. Transient Ischemic Attacks and Stroke in the Distribution of the Vertebrobasilar System: Clinical Manifestations. Surgery for Cerebrovascular Disease. 1996;85-86.
Cherry KJ Jr. Arteriosclerotic Occlusive Disease of Brachiocephalic Arteries. Rutherford RB (ed) Vascular Surgery. 2000;2:1154-60.
Crawford ES, Stowe CL, Powers RW Jr. Occlusion of the innominate, common carotid, and subclavian arteries: long-term results of surgical treatment. Surgery. Nov 1983;94(5):781-91. [Medline].
Deriu GP, Milite D, Verlato F, et al. Surgical treatment of atherosclerotic lesions of subclavian artery: carotid-subclavian bypass versus subclavian-carotid transposition. J Cardiovasc Surg (Torino). Dec 1998;39(6):729-34. [Medline].
Erbstein RA, Wholey MH, Smoot S. Subclavian artery steal syndrome: treatment by percutaneous transluminal angioplasty. AJR Am J Roentgenol. Aug 1988;151(2):291-4. [Medline].
Farina C, Mingoli A, Schultz RD, et al. Percutaneous transluminal angioplasty versus surgery for subclavian artery occlusive disease. Am J Surg. Dec 1989;158(6):511-4. [Medline].
Graor RA, Gray BH. Peripheral Vascular Disease. In: Young JR, Graor RA, Olin JW et al (eds):. Interventional treatment of peripheral vascular disease. Mosby Year Book; 1991:111-33.
Hebrang A, Maskovic J, Tomac B. Percutaneous transluminal angioplasty of the subclavian arteries: long-term results in 52 patients. AJR Am J Roentgenol. May 1991;156(5):1091-4. [Medline].
Hennerici M, Klemm C, Rautenberg W. The subclavian steal phenomenon: a common vascular disorder with rare neurologic deficits. Neurology. May 1988;38(5):669-73. [Medline].
Henry M, Amor M, Henry I, et al. Percutaneous transluminal angioplasty of the subclavian arteries. J Endovasc Surg. Feb 1999;6(1):33-41. [Medline].
Lochaya S, Kaplan B, Shaffer AB. Pseudocoarctation of the aorta with bicuspid aortic valve and kinked left subclavian artery: a possible cause of subclavian steal. Am Heart J. Mar 1967;73(3):369-74. [Medline].
Mehigan JT, Buch WS, Pipkin RD, et al. Subclavian-carotid transposition for the subclavian steal syndrome. Am J Surg. Jul 1978;136(1):15-20. [Medline].
Moran KT, Zide RS, Persson AV, et al. Natural history of subclavian steal syndrome. Am Surg. Nov 1988;54(11):643-4. [Medline].
Motarjeme A, Keifer JW, Zuska AJ, et al. Percutaneous transluminal angioplasty for treatment of subclavian steal. Radiology. Jun 1985;155(3):611-3. [Medline].
Olin JW, Young JR, Graor RA, et al. Role of the cardiologist in peripheral vascular disease. J Am Coll Cardiol. Jan 1992;19(1):235-6. [Medline].
Perler BA, Williams GM. Carotid-subclavian bypass--a decade of experience. J Vasc Surg. Dec 1990;12(6):716-22; discussion 722-3. [Medline].
Piccone VA Jr, LeVeen HH. The subclavian steal syndrome. Ann Thorac Surg. Jan 1970;9(1):51-75. [Medline].
Pollock M, Blennerhassett JB, Clarke AM. Giant cell arteritis and the subclavian steal syndrome. Neurology. Jun 1973;23(6):653-7. [Medline].
Riles TS, Imparato AM. Indications for repair of the brachiocephalic trunks. In: Surgery for Cerebrovascular Disease. 2nd ed. WB Saunders Co; 1996:590-594.
Solti F, Iskum M, Papp S, et al. The regulation of cerebral blood circulation in subclavian steal syndrome. Circulation. Dec 1970;42(6):1185-91. [Medline].
Sueoka BL. Percutaneous transluminal stent placement to treat subclavian steal syndrome. J Vasc Interv Radiol. May-Jun 1996;7(3):351-6. [Medline].
Sullivan TM, Gray BH, Bacharach JM, et al. Angioplasty and primary stenting of the subclavian, innominate, and common carotid arteries in 83 patients. J Vasc Surg. Dec 1998;28(6):1059-65.
Vitti MJ, Thompson BW, Read RC, et al. Carotid-subclavian bypass: a twenty-two-year experience. J Vasc Surg. Sep 1994;20(3):411-7; discussion 417-8. [Medline].
Walker PM, Paley D, Harris KA, et al. What determines the symptoms associated with subclavian artery occlusive disease?. J Vasc Surg. Jan 1985;2(1):154-7. [Medline].
Wholey MH, Postoak D, Suri R, et al. Tools of the subclavian trade. Endovascular Today. April 2006;5(4):24-33.
Further Reading
Keywords
subclavian steal syndrome, subclavian, subclavian vein, retrograde vertebral artery blood flow, proximal ipsilateral subclavian artery stenosis, proximal ipsilateral subclavian artery occlusion, atherosclerosis, atherosclerotic plaque, tobacco




Overview: Subclavian Steal Syndrome