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Subclavian steal syndrome as a cause of a transient ischemic attack


Authors: D. Kouřil 1;  Z. Kunc 1;  J. Vinklárek 2;  J. Štefela 2;  M. Cviková 2;  J. Brichta 2;  V. Všianský 2;  M. Haršány 2,3;  R. Herzig 4,5;  V. Bárková 6;  P. Aulický 7;  P. Filip- 8-10;  O. Škoda 11,12;  V. Červeňák 13;  V. Weiss 2
Authors‘ workplace: Neurologické oddělení, Nemocnice, Blansko 1;  I. neurologická klinika, LF MU a FN u sv. Anny v Brně 2;  International Clinical Research Centre, FN u sv. Anny v Brně 3;  Neurologická klinika, Komplexní, cerebrovaskulární centrum, FN Hradec, Králové 4;  Neurologická klinka LF UK v Hradci, Králové 5;  Nemocniční lékárna, oddělení klinické, farmacie FN u sv. Anny v Brně 6;  Oddělení anesteziologie, resuscitace, a intenzivní medicíny, Nemocnice, Milosrdných bratří Brno 7;  Neurologická klinika 1. LF UK a VFN, v Praze 8;  Katedra kybernetiky, České vysoké učení, technické v Praze 9;  Center for Magnetic Resonance, Research (CMRR), University, of Minnesota, Minneapolis, MN, USA 10;  Neurologické oddělení, Nemocnice, Jihlava 11;  Neurologická klinika 3. LF UK a FNKV, Praha 12;  Klinika zobrazovacích metod, LF MU a FN u sv. Anny v Brně 13
Published in: Cesk Slov Neurol N 2025; 88(4): 249-252
Category: Letter to Editor
doi: https://doi.org/10.48095/cccsnn2025249

This is an unauthorised machine translation into English made using the DeepL Translate Pro translator. The editors do not guarantee that the content of the article corresponds fully to the original language version.

 

Dear Editor,

We would like to present atypical subclavian steal syndrome (SSS) as a cause of transient ischemic attack. SSS is a hemodynamic phenomenon typically characterized by retrograde or alternating blood flow in the vertebral artery (VA) due to significant stenosis or occlusion of the proximal part of the ipsilateral subclavian artery (SA) or brachiocephalic trunk (BCT). Although SSS is usually asymptomatic, it can manifest as neurological deficit from the ipsilateral AV basin or, rarely, as ischemia of the upper limb. Hemodynamically significant stenosis of the AS (exceeding 60% of the artery diameter) causes a reduction in filling pressure distal to the lesion, which gradually leads to a reversal of flow in the ipsilateral AV, which, as a significant collateral, begins to contribute to ensuring adequate blood supply to the affected upper limb. Collateral blood supply is primarily provided from the unaffected contralateral AS through the contralateral AV (Fig. 1A). Clinical manifestation is typically triggered by physical exertion of the affected arm and/or sudden sharp turning of the head toward the affected side [1].

The symptoms of SSS can be varied. Ischemia of the upper limb manifests as pain, paresthesia, or fatigue accentuated by exercise. Symptoms from the left cerebral circulation include paroxysmal vertigo, diplopia, ataxia, dysarthria, syncope, and cerebellar syndrome. The prevalence of SSS in the general population ranges from 0.6 to 6.4% [2]. Atherosclerotic involvement of large arteries is considered the most common etiology of SSS. Other causes include vasculitis, thoracic outlet syndrome, and iatrogenic interventions [3]. To diagnose SSS, it is necessary to detect retrograde or alternating flow in the AV, which is why duplex ultrasound is considered a very accurate non-invasive diagnostic modality with a sensitivity and specificity of 94% in detecting ≥ 70% stenosis of the AS or TB.

Significant stenosis is predicted by a peak systolic velocity (PSV) of AS greater than 240 cm/s. Clinical examination also often reveals a significant difference in blood pressure between the upper limbs (> 20 mmHg) and reduced or absent radial artery pulsation [4]. Changes in the flow curve during AV examination can be assessed in three stages. The first stage, known as presteal, is characterized by noticeable systolic deceleration of AV flow, but with preserved cranial flow direction. The second degree is referred to as pendulum steal, which is characterized by a more severe disruption of AV hemodynamics with regular changes in flow during the cardiac cycle and detection of retrograde flow in the systolic phase. The most advanced stage is described as fully developed steal with retrograde flow in both the systolic and diastolic phases [5]. To verify the diagnosis and decide on a possible intervention strategy, it is usually necessary to supplement the sonological examination with complementary examinations, namely MRA or CTA. These methods can also describe the anatomical features of subclavian artery stenosis or occlusion in more detail. DSA is usually performed as part of endovascular treatment of AS stenosis, and it also serves as the gold standard for definitive assessment of stenosis and anatomical conditions [6]. Asymptomatic AS stenosis rarely requires interventional therapy, even if retrograde flow in the AV is sonographically proven. In patients with mild symptoms, drug therapy and regular follow-up are appropriate, as symptomatic improvement usually occurs even without interventional procedures and the risk of developing complete ischemic stroke is very low. These patients benefit from consistent compensation for secondary risk factors [6,7]. In the past, symptomatic AS stenosis was treated with bypass surgery. In recent years, however, percutaneous transluminal angioplasty (PTA) has come to the fore and is considered effective and safe. Endovascular treatment of AS stenosis involves either angioplasty alone or angioplasty combined with stenting. The results of observational studies suggest a greater benefit of stenting after PTA than angioplasty alone for maintaining arterial patency after one year, with no significant number of complications in either procedure [8–10]. In the differential diagnosis of SSS, it is necessary to consider upper limb arterial occlusion, cerebral infarction from the vertebrobasilar basin of a different etiology than SSS, and cardiac causes, including aortic stenosis [6].

A 73-year-old female patient began rehabilitation after a fracture of the distal radius of her left upper limb. She had previously been treated for arterial hypertension, dyslipidemia, type 2 diabetes mellitus, and ischemic heart disease. During rehabilitation involving repeated squeezing of a balloon in her left upper limb, she developed temporary nausea without any other observed symptoms. Rehabilitation therapy was continued to alleviate the symptoms, but during hydrotherapy with the left upper limb immersed in warm water, nausea reappeared, this time accompanied by vomiting, collapse, dysarthria, and a central lesion of the left facial nerve. The patient was referred for an acute neurological examination, where no focal deficit was observed in the objective neurological findings. During the clinical examination, no pulsations were palpable in the left upper limb ( ). When measuring blood pressure in the upper limbs, the systolic pressure on the left side was 60 mmHg lower than on the right side. Ultrasound ruled out arterial occlusion of the left radial or ulnar artery. Native CT of the brain showed no recent ischemia or other pathological densities. CTA of the cerebral arteries was performed, revealing a short hemodynamically significant stenosis of the left AS proximal to the AV origin (Fig. 1B). further, in the contralateral right AV, there was a lack of filling over a length of approximately 35 mm, and a collaterals supplying the distal section of the right AV was also described (Fig. 1C). As part of secondary prevention, the patient was treated with acetylsalicylic acid (ASA) and a lipid-lowering agent (rosuvastatin 20 mg). A neurosonological examination revealed a pendulum steal phenomenon in the intervertebral segment of the left AV2, which changed to a fully developed phenomenon after loading the left upper limb (Fig. 1D, E). The patient was indicated for interventional surgery. After DSA and subsequent PTA, a stent was inserted into the stenotic area of the left AS (Fig. 2A–C). The procedure was performed without complications, with normalization of the lateral difference in measured pressures and clinically palpable pulsations of the arteries of the left upper limb. The objective neurological findings continued to show no focal deficit. A follow-up neurosonological examination showed no evidence of steal phenomenon. The patient was placed on dual antiplatelet therapy (ASA and clopidogrel) for 3 months.

The remarkable feature of this case report is the developed SSS in hemodynamic AS stenosis on the left with angiographic and sonographic evidence of contralateral proximal occlusion (V0–V2) of the AV. CTA examination reveals collateral flow supplying the distal segment of the right AV. It can therefore be assumed that left AS stenosis alone could be considered clinically insignificant. The manifestation was largely due to proximal occlusion of the contralateral right AV and insufficient collateral capacity to supply the vertebrobasilar basin. (Fig. 2D) When evaluating the clinical manifestation of the steal phenomenon and considering an interventional solution, it is therefore necessary to assess not only the demand side, in this case the degree of stenosis of the ipsilateral AS, but also the supply side, i.e., the contralateral AV, AS, and possibly other sources of collateral circulation.

 

Conflict of interest

The authors declare that they have no conflict of interest in relation to the subject of the study.

 


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Paediatric neurology Neurosurgery Neurology

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Czech and Slovak Neurology and Neurosurgery

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