This article includes discussion of subclavian steal, brachio-basilar insufficiency syndrome, brachio-vertebral syndrome, subclavian suction syndrome, vertebral grand larceny, carotid steal, cerebral steal (intracranial steal; reversed Robin Hood syndrome), congenital subclavian steal, coronary steal (cardiac steal), subclavian steal phenomenon, subclavian steal syndrome, Takayasu arteritis, and vascular access steal (dialysis-associated steal). The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
With subclavian artery stenosis proximal to the takeoff of the vertebral artery, there is a compensatory shunting of blood from the ipsilateral vertebral artery to supply the arm, thus, “stealing” blood from the vertebrobasilar system. In most patients with subclavian steal, the steal is asymptomatic (subclavian steal phenomenon), but a minority may have ischemic symptoms referable to the posterior circulation or the arm. In a minority of cases, neurologic symptoms may be precipitated by ipsilateral arm exercise, head turning, or standing up. The key signs of a subclavian steal are markedly diminished, delayed, or absent radial pulses on the affected side; supraclavicular systolic bruits; and asymmetric brachial blood pressures, with the lower systolic pressure on the affected side, and generally with a minimum difference of 20 mm Hg. Asymptomatic cases should be managed conservatively with regard to vascular risk factor modification and antiplatelet therapy. Endovascular stenting and extrathoracic surgical bypass or transposition (eg, carotid-subclavian) are safe and lasting therapeutic options for selected cases of subclavian steal syndrome, particularly among those with disabling symptoms.
Historical note and terminology
In 1960, Cortorni described angiographic findings of retrograde flow in the vertebral artery and stenosis of the proximal subclavian artery in a patient with an absent radial pulse but without neurologic symptoms (Contorni 1960). In 1960, James F Toole suggested that proximal subclavian artery stenosis or occlusion might cause vertebrobasilar insufficiency, and the following year Reivich, Holling, Roberts, and Toole reported 2 patients with evidence of cerebral ischemia and reversal of blood flow through the vertebral artery; they provided experimental results in dogs that confirmed the clinical observations (Reivich et al 1961; Patel and Toole 1965; Anazawa et al 1969; Toole and McGraw 1975). An anonymous editorial in the New England Journal of Medicine designated the syndrome as “the subclavian steal,” and this label served to popularize the condition (Anonymous 1961); it was apparently C Miller Fisher (1913-2012) who coined the term “the syndrome of the subclavian steal” (Fisher 1962; Patel and Toole 1965). Toole and colleagues were instrumental in the subsequent elaboration of understanding of various steal syndromes as well as the evaluation and management of affected patients (Toole 1964a; Toole 1964b; Conrad et al 1965; Patel and Toole 1965; Toole and Tulloch 1966; Anazawa et al 1969; Toole and McGraw 1975). Because steals are often asymptomatic, Vollmar suggested in 1971 that the term “steal syndrome” be reserved for situations in which shunting occurs with symptoms of deficient blood flow, and “steal phenomenon” (or “steal effect”) should be used for asymptomatic steals (Vollmar 1971). Vollmer's suggestion has subsequently been adopted.
Various synonyms for subclavian steal have been used in the past, but none of these older terms gained acceptance and none are current terminology. These include brachio-basilar insufficiency syndrome, brachio-vertebral syndrome, subclavian suction syndrome, and vertebral grand larceny.
Since the initial description of subclavian steal, various other steal phenomena have been described. Cerebral steal can occur in the setting of focal cerebral ischemia if the patient's blood pressure drops, if the patient is given a vasodilator, or if the patient is hypoventilated (PaCO2 increases and pH decreases), causing arterioles in nonischemic brain to dilate and, thereby, shunting blood flow from the ischemic areas that require oxygen (Dyken 1971-1972; Toole and McGraw 1975; Alexandrov et al 2007). This has been called the “reversed Robin Hood syndrome” on the basis that it serves to “rob the poor to feed the rich” (Alexandrov et al 2007). Intracranial steal phenomena also occur with angiomas and arteriovenous fistulas (Mosmans and Jonkman 1980; Schwartz and Hennerici 1986). Similarly, coronary steal (cardiac steal) occurs when a coronary vasodilator is used in the setting of narrowing of the coronary arteries, causing blood to be shunted away from the coronary vessels supplying the ischemic areas and, thereby, causing further ischemia; this phenomenon is used diagnostically in drug-based cardiac stress tests. Coronary-subclavian steal syndrome is a rare but well-recognized complication of coronary artery bypass graft surgery when a left internal mammary artery (LIMA) graft is used and proximal left subclavian artery stenosis is either present or develops subsequently; the result is retrograde flow from the LIMA graft to the distal subclavian artery to perfuse the left arm, causing accentuation of, rather than relief from, cardiac ischemia (Costa et al 2007; Potter and Pinto 2014; Kilic et al 2015). Vascular access steal (or dialysis-associated steal) refers to vascular shunting resulting from a surgically created arteriovenous fistula or synthetic vascular graft-AV fistula (Eicke et al 1998; Schenk 2001; Bron et al 2010); vascular access steal syndrome is associated with pain distal to the fistula as well as pallor, depressed pulses distal to the fistula, necrosis, a decreased wrist-brachial index (below 0.6), and rarely with neurologic manifestations of vertebrobasilar insufficiency (Schenk 2001; Kargiotis et al 2016). Axillo-femoral bypass stead due to subclavian artery stenosis has also been reported (Shigyo et al 2016).
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