Prevalence and Clinical Characteristics of Subclavian Steal Phenomenon/Syndrome in Patients with Acute Ischemic Stroke

There are no published clinical studies regarding the prevalence of subclavian steal among acute ischemic stroke patients. The aim of this study was to evaluate the prevalence and clinical significance of subclavian steal among a large number of consecutive ischemic stroke patients. Materials and methods: We reviewed the medical records of 2192 consecutive cases of acute ischemic stroke at a tertiary neurology clinic in Targu Mures, Romania, between 2018 and 2020. In total, 47 patients (2.2%) were diagnosed with subclavian steal phenomenon/syndrome. Results: Stroke patients with associated steal phenomenon were significantly younger (64.2 ± 11.1 versus 70.2 ± 12.8, p = 0.005) and predominantly male (68.1%). From among the 47 patients with subclavian steal phenomenon, nine (19.1%) presented stroke symptomatology in the vertebrobasilar territory. Overall, 83.3% of the stroke patients with associated steal phenomenon presented cerebral infarction and 16.7% presented TIA. There was no difference between groups regarding the affected vascular territory (VB versus carotid). Large artery atherosclerosis was more frequent in the stroke group with associated steal phenomenon (81.3% versus 43.5%, p = 0.0033). The NIHSS score at admission was higher in the patient group with associated steal phenomenon, but there was no difference in mRS at discharge. Associated carotid artery occlusion was more frequent in the stroke group with steal phenomenon (p < 0.01). Smoking and peripheral arteriopathy were more frequent in the patient group with associated steal phenomenon. Of the nine symptomatic patients, five underwent revascularization treatment. Conclusions: The prevalence of subclavian steal phenomenon among acute ischemic stroke patients was not higher than in other cohorts with heterogenous peripheral vascular pathologies. Similar to the general population, in acute ischemic stroke patients, the associated subclavian steal behaved like a benign hemodynamical condition, without severe consequences.

Abstract 1122‐000050: Arterial Steal in AVM: An Etiology of Ischemic Stroke

Introduction : Arteriovenous malformations (AVM) are rare congenital malformations in the brain, often presenting with cerebral hemorrhage. Unruptured AVMs usually remain asymptomatic, or they can present with headache, seizure, or focal neurological deficits. “Arterial steal” is one of the mechanisms which can lead to focal neurological deficits. The idea of vascular steal through high flow shunting within brain AVMs is not a new concept. There is, however, debate about whether the vascular steal phenomenon indeed exists empirically. In a study focused on vascular reserve in patients with cerebral AVMs (utilizing acetazolamide augmentation and perfusion CT methods), decreased hemodynamic reserve was noted in 27% of parenchymal regions of interest close to the AVM and in 17% of parenchymal regions of interest far from the AVM. Other imaging modalities have shown abnormal blood regulation around AVM however there exists a level of discordance between various modalities which questions whether vascular steal exists in vivo. We present an ischemic stroke caused by “arterial steal” phenomenon. Methods : Case report Results : 63‐year‐old male with past medical history of seizure, hypertension presented with confusion and dysarthria for 3 weeks. On exam he was found to have right upper quadrantanopia. CT head without contrast and MRI of brain revealed an evolving infarct in the left posterior cerebral artery (PCA) territory. CT angiogram showed possible occlusion in the left PCA P2 segment which correlated to the previously described stroke and in addition showed evidence of left thalamic AVM. Evaluation for cardioembolic or atheroembolic sources was unrevealing. A diagnostic cerebral angiogram showed a 1.3 mm AVM fed through anterior choroidal branches as well as posterior choroidal branches through left posterior communicating artery. There was delayed filling in the left PCA territory likely due to steal phenomenon which might be the etiology of the stroke. Conclusions : In our case, as demonstrated on angiogram, vascular steal phenomenon through high flow shunting of AVM is the likely explanation for the ischemic stroke.

Coronary steal phenomenon following right ventricle decompression and revascularization of atretic left coronary ostium: case report

Background Coronary steal phenomenon and myocardial ischemia is a complication following decompression of a hypertensive right ventricle in patients with left coronary-cameral fistulae. Case presentation We present a 12-year-old girl with a complex heart defect successfully operated on using a hybrid surgical-interventional approach to decompress the ventricle, embolize the fistula and reconstruct the atretic left coronary ostium. Conclusions A novel hybrid strategy is the best solution for coronary-cameral fistulas reliant on high ventricular pressure at high risk for coronary steal phenomenon.

Coronary steal phenomenon following right ventricle decompression and revascularization of atretic left coronary ostium - case report

BackgroundCoronary steal phenomenon and myocardial ischemia is a complication following decompression of a hypertensive right ventricle in patients with left coronary-cameral fistulae.Case presentationWe present a 12-year-old girl with a complex heart defect successfully operated on using a hybrid surgical-interventional approach to decompress the ventricle, embolize the fistula and reconstruct the atretic left coronary ostium.ConclusionsA novel hybrid strategy is the best solution for coronary-cameral fistulas reliant on high ventricular pressure at high risk for coronary steal phenomenon.

Competition (‘Steal’ Phenomenon) betwe en [68Ga]Ga-PSMA-11 Uptake in Prostate Tumor Tissue Versus Healthy Tissue

We aimed to clarify whether a steal ‘phenomenon’ exists by investigating if uptake of ‘prostate specific membrane antigen’ (PSMA) in prostate tumor tissue correlates with the uptake in healthy tissue. Patients with prostate cancer referred for a [68Ga]Ga-PSMA-11 PET/CT were identified retrospectively. Semi-automated quantitative image analysis was performed; fractional healthy tissue [68Ga]Ga-PSMA-11 uptake volume (HT-PSMA (SUV*cm3)) in the lacrimal, submandibular, and parotid glands, and kidneys, and the fractional total lesion [68Ga]Ga-PSMA-11 uptake volume (TL-PSMA (SUV*cm3)) of prostate cancer were used. Ninety-two patients, age 78 ± 8 years, were analyzed. Median TL-PSMA was 703.37 SUV*cm3 (IQR 119.56–2778.20), median HT-PSMA of the lacrimal, submandibular, and parotid glands, and kidneys was: 13.69 (IQR 7.29–19.06), 194.75 (IQR 133.67–276.53), 552.54 (IQR 379.98–737.16), and 8092.75 SUV*cm3 (IQR 5793.02–11385.86), respectively. A significant (p-value ≤ 0.001) but weak–moderate correlation was found between the TL-PSMA and HT-PSMA of the parotid- and submandibular glands, and kidneys (correlation coefficient of −0.447,−0.345, and −0.394, respectively). No correlation was found between TL-PSMA and HT-PSMA of the lacrimal glands. The existence of a ‘steal’ phenomenon cannot be confirmed in this study. Healthy tissue uptake of [68Ga]Ga-PSMA-11 is only partially influenced by TL-PSMA. Thus, modification of therapeutic PSMA activity should not be adjusted based on TL-PSMA alone.

Ipsilateral hypoperfusion caused by intracerebral steal phenomenon after carotid artery stenting: a case report

Background Abnormal hypoperfusion on the surgical side after carotid artery stenting is rare. Neurological deterioration caused by it is deceptive, which can easily lead to misdiagnosis. The mechanism of hypoperfusion has rarely been demonstrated. We present here a fully studied case with a high probability of intracerebral steal phenomenon. Case presentation A 68-year-old male with severe right internal carotid artery stenosis and left internal carotid artery occlusion underwent right stenosis stent implantation. Restlessness and left limb hemiplegia occurred within 24 h after the procedure, which was similar to hyperperfusion syndrome. However, postoperative computerized tomography perfusion (CTP) revealed abnormal hypoperfusion in the right hemisphere. Transcranial Doppler (TCD) also showed decreased flow velocity in the right middle cerebral artery, and increased flow velocity in the right anterior cerebral artery. We considered that intracerebral steal phenomenon might be the cause, then hypervolemic therapy was accepted and the symptoms completely resolved after 3 days. Conclusions Ipsilateral hypoperfusion is rarely seen after carotid artery stenting. Intracerebral steal phenomenon may be the underlying mechanism. CTP or TCD is helpful for the early detection of this adverse event.