Steal Phenomenon Research Articles

Association of Subclavian Steal Phenomenon with Prevalence of Contralateral Vertebral Artery Atherosclerotic Stenosis: A Hospital-Based Cohort Study.

It is uncertain if there is a connection between subclavian steal phenomenon (SSP) and atherosclerotic stenosis in the opposite vertebral artery (VA). We aimed to explore the association between SSP and the incidence of contralateral vertebral artery stenosis (VAS) in vivo. In this prospective registry study, we included patients diagnosed with ＞50% stenosis of proximal subclavian artery (SA) or innominate artery (INA) by digital subtraction angiography (DSA) from our comprehensive stroke center between 2011 and 2022. VAS and SSP was diagnosed by DSA in the resting state. Propensity score matching (PSM) was conducted among all participants and subgroups with a 1:1 ratio according to the presence of SSP. We further conducted sensitivity analysis by dividing all participants into subgroups according to the degree of stenosis and type of SSP. Binomial logistic regression analysis was applied to investigate the association of SSP with contralateral VAS. A total of 774 patients were included in this study and 309 (39.9%) were found with SSP. After PSM, presence of SSP was associated with lower prevalence of contralateral VAS among all participants (OR 0.45; 95% CI 0.31-0.65; p＜0.001). In subgroup analysis, the association was respectively found within left subclavian (LSA) stenosis group (OR 0.43; 95% CI 0.29-0.65; P＜0.001) and right subclavian artery (RSA) / INA stenosis group (OR 0.36; 95% CI 0.19-0.69; P=0.002). SSP is associated with lower prevalence of contralateral VAS.

Enhancing cerebral arteriovenous malformation analysis: Development and application of patient-specific lumped parameter models based on 3D imaging data

Objectives:Cerebral arteriovenous malformations (AVMs) present complex neurovascular challenges, characterized by direct arteriovenous connections that disrupt normal brain blood flow dynamics. Traditional lumped parameter models (LPMs) offer a simplified angioarchitectural representation of AVMs, yet often fail to capture the intricate structure within the AVM nidus. This research aims at refining our understanding of AVM hemodynamics through the development of patient-specific LPMs utilizing three-dimensional (3D) medical imaging data for enhanced structural fidelity. Methods:This study commenced with the meticulous delineation of AVM vascular architecture using threshold segmentation and skeletonization techniques. The AVM nidus’s core structure was outlined, facilitating the extraction of vessel connections and the formation of a detailed fistulous vascular tree model. Sampling points, spatially distributed and derived from the pixel intensity in imaging data, guided the construction of a complex plexiform tree within the nidus by generating smaller Y-shaped vascular formations. This model was then integrated with an electrical analog model to enable precise numerical simulations of cerebral hemodynamics with AVMs. Results:The study successfully generated two distinct patient-specific AVM networks, mirroring the unique structural and morphological characteristics of the AVMs as captured in medical imaging. The models effectively represented the intricate fistulous and plexiform vessel structures within the nidus. Numerical analysis of these models revealed that AVMs induce a blood shunt effect, thereby diminishing blood perfusion to adjacent brain tissues. Conclusion:This investigation enhances the theoretical framework for AVM research by constructing patient-specific LPMs that accurately reflect the true vascular structures of AVMs. These models offer profound insights into the hemodynamic behaviors of AVMs, including their impact on cerebral circulation and the blood steal phenomenon. Further incorporation of clinical data into these models holds the promise of deepening the theoretical comprehension of AVMs and fostering advancements in the diagnosis and treatment of AVMs.

Staged cerebral and brachiocephalic bypass in a patient with MCA and brachiocephalic steno-occlusion.

Background: Brachiocephalic steal is a rare phenomenon that may lead to hemodynamic abnormalities in the ipsilateral vertebral and carotid arteries. Current treatment includes management of vascular risk factors, endovascular stenting, and surgical management depending on the severity of symptoms. Case Information: We describe a patient with multiple vascular risk factors who presented with mild neurological symptoms and chronic right arm weakness associated with concurrent brachiocephalic steal and right MCA M1 stenosis on neuroimaging. Use of right superficial temporal artery to middle cerebral artery bypass and aorta-right subclavian bypass resulted in improved flow to the right hemisphere on quantitative magnetic resonance angiography and single-photon emission computed tomography, significantly lowering the risk of catastrophic ischemic stroke. Conclusion: Complex steal phenomena increase stroke risk. In cases of high-grade occlusion or advanced symptoms, endovascular or surgical management should be considered for optimal stroke prevention.

Acute Basilar Artery Tip Thrombosis Presenting as Basilar-Subclavian Steal Phenomenon on Transcranial Doppler

Acute basilar artery (BA) occlusion is a key etiology of devastating posterior circulation stroke, unless recanalization is performed early. Recanalization therapy is determined synthetically based on symptom onset time, stroke severity, and brain imaging. Herein, we report the case of a 72-year-old male patient presenting with minor neurological symptoms, but with thrombotic occlusion at the BA tip. Transcranial Doppler (TCD) showed systolic flow reversal along the vertebrobasilar arteries, and the patient benefited from endovascular thrombectomy. This case highlights the critical role of TCD in identifying hemodynamic insufficiency and determining the implementation of endovascular interventions to mitigate stroke progression.

Anomalous Left Coronary Artery from the Pulmonary Artery (ALCAPA) Syndrome: Pathophysiology, Clinical Manifestations, and Management Strategies

Anomalous Left Coronary Artery from the Pulmonary Artery (ALCAPA) syndrome is a rare congenital cardiac anomaly characterized by the abnormal origin of the left coronary artery from the pulmonary artery instead of the aortic root. This anomaly results in compromised myocardial perfusion, particularly under conditions of increased oxygen demand, leading to myocardial ischemia, left ventricular dysfunction, and potentially severe complications such as mitral regurgitation, heart failure, and sudden cardiac death. The pathophysiology of ALCAPA involves a complex interplay of coronary artery steal phenomenon, collateral vessel development, and ventricular remodeling. Early diagnosis is critical, often achieved through echocardiography, cardiac MRI, or coronary angiography, which helps in planning surgical intervention. The mainstay of treatment is surgical correction to re-establish a dual coronary artery system, with techniques including direct reimplantation of the anomalous coronary artery into the aorta or the creation of an intrapulmonary tunnel. This article provides a comprehensive review of the current understanding of ALCAPA syndrome, emphasizing its pathophysiology, clinical presentation, diagnostic modalities, and surgical management, along with outcomes and prognostic factors.

HEART FAILURE WITH PRESERVED EJECTION FRACTION (HFPEF) IN A PATIENT WITH RECENT TAVI AND NUMEROUS CORONARY FISTULAS OF THE LEFT CORONARY ARTERY DRAINING INTO THE VENTRICULAR CAVITY

Abstract Coronary fistula is a rare form of congenital heart disease and is defined as an abnormal connection between a coronary branch and a cardiac chamber or a large intrathoracic vessel without the interposition of the capillary circulation. The right coronary artery is the most common site of origin for coronary fistula. Other sites include the left anterior descending artery and left circumflex artery. The clinical presentation and the natural history can be extremely variable depending on the patient‘s age, fistula size, and anatomy. Small to medium–sized coronary fistulas may be asymptomatic. Large fistulas can manifest with angina pectoris due to myocardial ischemia secondary to the coronary steal phenomenon. Shunting through large fistulas can have hemodynamic consequences secondary to volume overload in the pulmonary or systemic circulation, leading to symptoms and signs of heart failure. We describe the case of an 83–year–old woman recently undergoing TAVI and suffering from primary myelofibrosis requiring periodic transfusions. Pre–TAVI coronary angiography showed coronary vessels free from significant hemodynamic lesions and multiple coronary–ventricular fistulas draining into the left ventricle. Total body aortic CT angiography did not reveal other abnormal vascular connections. One month after the aortic valve correction procedure, the patient presented with heart failure (HfpEF). At a recent follow–up visit, diuretic therapy was discontinued due to the successful correction of aortic valve disease and normal ejection fraction. Due to further anemization from the underlying hematologic condition, the patient underwent blood transfusion with worsening of dyspnea despite correction of hemoglobin levels. Discontinuation of diuretic therapy and transfusion of red blood cell units resulted in volume overload with worsening clinical condition. The presence of multiple coronary fistulas precluded an interventional approach, but therapeutic optimization and reintroduction of diuretic therapy restored the patient‘s hemodynamic compensation. Usually fistulas drain into the low–pressure venous circulation like right ventricle and right atrium. This case represents a rare instance of multiple left coronary fistulas draining into the left ventricle (only 3% of cases). Aortic valve correction may have further reduced left ventricular telediastolic pressures, worsening the shunt of coronary fistulas resulting in heart failure due to volume overload.

The volume of steal phenomenon is associated with neurological deterioration in patients with large-vessel occlusion minor stroke not eligible for thrombectomy.

A significant number of patients who present with mild symptoms following large-vessel occlusion acute ischemic stroke (LVO-AIS) are currently considered ineligible for EVT. However, they frequently experience neurological deterioration during hospitalization. This study aimed to investigate the association between neurological deterioration and hemodynamic impairment by assessing steal phenomenon derived from blood oxygenation-level dependent cerebrovascular reactivity (BOLD-CVR) in this specific patient cohort. From the database of our single-center BOLD-CVR observational cohort study (June 2015-October 2023) we retrospectively identified acute ischemic stroke patients with admission NIHSS < 6, a newly detected large vessel occlusion of the anterior circulation and ineligible for EVT. Neurological deterioration during hospitalization as well as outcome at hospital discharge were rated with NIHSS score. We analyzed the association between these two outcomes and BOLD-CVR-derived steal phenomenon volume through regression analysis. Additionally, we investigated the discriminatory accuracy of steal phenomenon volume for predicting neurological deterioration. Forty patients were included in the final analysis. Neurological deterioration occurred in 35% of patients. In the regression analysis, a strong association between steal phenomenon volume and neurological deterioration (OR 4.80, 95% CI 1.32-31.04, p = 0.04) as well as poorer NIHSS score at hospital discharge (OR 3.73, 95% CI 1.52-10.78, p = 0.007) was found. The discriminatory accuracy of steal phenomenon for neurological deterioration prediction had an AUC of 0.791 (95% CI 0.653-0.930). Based on our results we may distinguish two groups of patients with minor stroke currently ineligible for EVT, however, showing hemodynamic impairment and exhibiting neurological deterioration during hospitalization: (1) patients exhibiting steal phenomenon on BOLD-CVR imaging as well as hemodynamic impairment on resting perfusion imaging; (2) patients exhibiting steal phenomenon on BOLD-CVR imaging, however, no relevant hemodynamic impairment on resting perfusion imaging. The presence of BOLD-CVR derived steal phenomenon may aid to further study hemodynamic impairment in patients with minor LVO-AIS not eligible for EVT.

Stenting for subclavian steal phenomenon to restore cerebral perfusion due to acute carotid occlusion following carotid endarterectomy: a case report

BackgroundPerioperative symptomatic carotid artery occlusion after carotid endarterectomy is a rare complication. In this study, we present a case of symptomatic acute carotid artery occlusion that occurred after carotid endarterectomy in a patient with coexistent subclavian artery steal phenomenon, which was successfully treated with subclavian artery stenting.Case presentationA 57-year-old East Asian female presented with stenosis in the left common carotid artery and left subclavian artery along with subclavian steal. The proximal segment of the left anterior cerebral artery was hypoplastic, and the posterior communicating arteries on both sides were well-developed. Left internal carotid artery stenosis progressed during the follow-up examination; therefore, left carotid endarterectomy was performed. On the following day, symptoms of cerebral perfusion deficiency appeared due to occlusion of the left carotid artery. The stenotic origin of the left common carotid artery and the suspected massive thrombus in the left carotid artery posed challenges to carotid revascularization. Therefore, left subclavian artery stenting for the subclavian steal phenomenon was determined to be the best option for restoring cerebral blood flow to the whole brain. Her symptoms improved after the procedure, and the postprocedural workup revealed improved cerebral blood flow.ConclusionSubclavian artery stenting is safe and may be helpful in patients with cerebral perfusion deficiency caused by intractable acute carotid occlusion coexisting with the subclavian steal phenomenon. Revascularization of asymptomatic subclavian artery stenosis is generally not recommended. However, cerebral circulatory insufficiency as a comorbidity may be worth considering.

Transorbital embolization of a direct carotid-cavernous fistula with vascular steal phenomenon

Transorbital embolization of a direct carotid-cavernous fistula with vascular steal phenomenon

Should Coronary Artery Fistula Be Treated? A Review Throughout a Case Series

Background: Coronary artery disease (CAD) includes a wide spectrum of entities beyond the atherosclerotic disease. Coronary artery fistulas (CAF) represent an uncommon vascular abnormality that may cause several cardiovascular complications and symptoms, due to the coronary steal phenomena. Surgical or percutaneous closure should always be considered. The authors present a case series of patients with CAFs who developed cardiovascular manifestations, and underwent percutaneous closure safely and feasibly, with good clinical results. Case Summary: Five patients with CAFs were treated from 2021–2023; three were male (60%), the mean age was 59 years, the most common symptom was chest pain, and two patients presented in the context of unstable angina. The authors documented pulmonary hypertension in three patients, none of them with haemodynamic compromise of right ventricle. Two of the patients had documented ischaemia or haemodynamic significance due to the CAF. Finally, in two cases, no CAD was noted in coronary angiography. Percutaneous closure was done using a 6 Fr or 7 Fr sheath; guiding catheter 6 or 7 Fr through a workhorse guidewire, a microcatheter was placed in the coronary origin of the fistula, closure was done using a liquid embolisation system or delivering coils into the defect. The number and length of coils may vary depending on the fistula’s size. Discussion: The authors present five successful cases of percutaneous closure of symptomatic CAF, who presented with angina or dyspnoea as main symptoms. Once the diagnosis was made and further studies performed, the closure was decided based on the pulmonary hypertension or coronary steal phenomena.

Does Steal Phenomenon Exist in Multiple Neurotization?-An Experimental Rat Study.

Nerve transfers from one common donor nerve to recipient nerves with multiple target branches can yield slower and unpredictable recovery in the target nerves. Our hypothesis is that steal phenomenon exists when multiple nerve neurotization comes from one donor nerve. In 30 Sprague-Dawley rats, the left ulnar nerve (UN) was selected as the donor nerve, and the musculocutaneous nerve (MCN) and median nerve (MN) as the recipient target nerves. The rats were separated into three groups (10 rats in each): group A, UN-to-MCN (one-target); group B, UN-to-MN (one-target); and group C, UN-to-MCN and MN (two-target). The right upper limbs were nonoperative as the control group. Outcome obtained at 20 weeks after surgery included grooming test, muscle weight, compound muscle action potential, tetanic muscle contraction force, axon counts, and retrograde labeling of the involved donor and target nerves. At 20 weeks after surgery, muscles innervated by neurotization resulted in significant worse outcomes than the control side. This was especially true in two-target neurotization in the parameter of muscle weight and forearm flexor muscle contraction force outcome when compared to one-target neurotization. Steal phenomenon does exist because flexor muscle contraction force was significantly worse during two-target neurotization. This study proves the existence of steal phenomenon in multiple target neurotization but does not significantly affect the functional results. Postoperative rehabilitative measures (including electrical stimulation, induction exercise) and patient compliance (ambition and persistence) are other crucial factors that hold equivalent importance to long-term successful recovery.

Arteriovenous malformation presenting as complex regional pain syndrome: illustrative case.

Complex regional pain syndrome (CRPS) is typically described as a peripheral nerve disorder in which exaggerated allodynia and hyperalgesia follow a minor injury. Some researchers propose a central mechanism, although current evidence is lacking. A 14-year-old female presented with classic CRPS symptoms of left upper-extremity weakness and hyperalgesia after a bout of sharp pain in her thumb while shoveling snow. A possible seizure prompted magnetic resonance imaging, revealing a right frontal Spetzler-Martin grade II arteriovenous malformation (AVM) adjacent to the primary motor cortex. Brodmann areas 1, 3a, and 3b, which are responsible for localizing and processing burning and painful sensations, were also involved. The patient underwent transarterial Onyx embolization in two sessions and microsurgical resection, after which her CRPS symptoms completely resolved. To our knowledge, this is the first reported case of a cerebral AVM presenting as CRPS, which supports a central mechanism. The authors propose that rapid growth of the AVM led to a vascular steal phenomenon of surrounding parenchyma, which disrupted the patient's normal motor function and nociceptive processing. Further validation in other series is needed.

＜Editors' Choice＞ Thoracic endovascular aortic repair and spinal cord injury.

We previously reported that spinal cord injury following thoracic endovascular aortic repair for a thoracic aortic aneurysm is a micro embolism caused by a vulnerable mural thrombus. Conversely, patients who underwent thoracic endovascular aortic repair for aortic dissection develop spinal cord injury less frequently due to fewer mural thrombi. Paying attention to preserving blood flow toward the spinal cord, namely collateral circulation and steal phenomenon, prevents spinal cord injury following thoracic endovascular aortic repair for aortic dissection.

Exploring hemodynamic-induced crossed cerebellar diaschisis in large-vessel occlusion acute ischemic stroke patients: the role of BOLD cerebrovascular reactivity derived steal phenomenon

Exploring hemodynamic-induced crossed cerebellar diaschisis in large-vessel occlusion acute ischemic stroke patients: the role of BOLD cerebrovascular reactivity derived steal phenomenon

Occipital Steal Syndrome with Carotid Artery Occlusion–A Physiologic Study with Transcranial Doppler

Occipital or posterior steal syndrome is a constellation of signs and symptoms that arise from abnormal shunting of blood flow from the posterior cerebral circulation into its anterior counterpart leading to transient episodes of neurological deficits due to posterior circulation ischemia. A 45-year-old woman who experienced transient visual phenomena during breath holding was evaluated by transcranial Doppler sonography (TCD) for changes in cerebral blood flow. TCD revealed that the anterior cerebral vascular system was shunting blood away from its posterior counterpart in the setting of hypercapnia, resulting in visual symptoms. Using permissive blood pressure control, the steal phenomenon was resolved.

Subclavian steal phenomenon causing vertebral artery aneurysm and rupture

Subclavian steal phenomenon causing vertebral artery aneurysm and rupture

Abstract 096: Hypoperfusion Intensity Ratio Suggests Collateral Status, Stroke Mechanism, and Clinical Stability in Large Vessel Occlusion

Introduction Hypoperfusion Intensity Ratio (HIR), defined by the ratio of Tmax &gt;10s/Tmax &gt;6s on perfusion imaging, has been directly correlated with collateral status, stroke mechanism, and clinical outcomes in patients with acute large vessel occlusions [1,2]. We report a case of a patient with mild neurological symptoms despite an acute MCA M1 occlusion in which a very favorable HIR may have predicted clinical stability, extensive atherosclerotic burden, and compensatory leptomeningeal collaterals. Our aim was to provide support of the utility of HIR in quantifying collateral status and possibly predicting the underlying stroke mechanism and stroke progression of patients with acute large vessel occlusions. Methods Case report. Results A 61‐year‐old woman with a history of hypertension and hyperlipidemia, who is an active smoker with a known right extracranial carotid stenosis presented with acute left facial droop (NIHSS 1) upon awakening. CT head did not demonstrate early ischemic changes. CT angiogram demonstrated a right MCA M1 occlusion, marked narrowing of the right common carotid artery, and severe narrowing of the proximal innominate artery (Figure 1, Image A). CT perfusion demonstrated a Tmax &gt;6s delay of 41mL and HIR of 0, suggestive of robust collaterals (Figure 1, Image B). The patient was out of the window for tenecteplase administration. Thrombectomy was deferred due to a low NIHSS. MRI showed a right putamen and corona radiata infarct. DSA demonstrated crossed collateralization across the anterior communicating artery and robust right ACA‐MCA and PCA‐MCA leptomeningeal collaterals and retrograde filling of the brachiocephalic and right common carotid artery via the right vertebral artery. These findings were supported by quantitative MRA, which showed decreased blood flow in the right ICA, increased blood flow in right A2, increased blood flow in left A1, and retrograde right vertebral flow indicative of a brachiocephalic steal phenomenon. Her neurological exam remained stable upon discharge. She will be evaluated for brachiocephalic revascularization as an outpatient. Conclusion We present a patient with very mild symptoms due to an acute large vessel occlusion who remained clinically stable despite an acute MCA M1 occlusion, which was likely caused by ischemic conditioning related to chronic hypoperfusion secondary to severe brachiocephalic and right common carotid artery stenosis. Favorable HIR on perfusion imaging was predictive of robust collaterals, the underlying stroke mechanism, and the stable clinical course. Since clinical equipoise exists regarding the treatment of patients with low NIHSS in the setting of an acute large vessel occlusion, individualized selection remains paramount. HIR may serve as a quantitative radiographic marker to rapidly quantify collateral status and assist in decision‐making. Future studies exploring the role of HIR in predicting stroke progression are warranted.

Blood Oxygenation Level-Dependent Cerebrovascular Reactivity-Derived Steal Phenomenon May Indicate Tissue Reperfusion Failure After Successful Endovascular Thrombectomy.

In acute ischemic stroke due to large-vessel occlusion (LVO), the clinical outcome after endovascular thrombectomy (EVT) is influenced by the extent of autoregulatory hemodynamic impairment, which can be derived from blood oxygenation level-dependent cerebrovascular reactivity (BOLD-CVR). BOLD-CVR imaging identifies brain areas influenced by hemodynamic steal. We sought to investigate the presence of steal phenomenon and its relationship to DWI lesions and clinical deficit in the acute phase of ischemic stroke following successful vessel recanalization.From the prospective longitudinal IMPreST (Interplay of Microcirculation and Plasticity after ischemic Stroke) cohort study, patients with acute ischemic unilateral LVO stroke of the anterior circulation with successful endovascular thrombectomy (EVT; mTICI scale ≥ 2b) and subsequent BOLD-CVR examination were included for this analysis. We analyzed the spatial correlation between brain areas exhibiting BOLD-CVR-associated steal phenomenon and DWI infarct lesion as well as the relationship between steal phenomenon and NIHSS score at hospital discharge.Included patients (n = 21) exhibited steal phenomenon to different extents, whereas there was only a partial spatial overlap with the DWI lesion (median 19%; IQR, 8-59). The volume of steal phenomenon outside the DWI lesion showed a positive correlation with overall DWI lesion volume and was a significant predictor for the NIHSS score at hospital discharge.Patients with acute ischemic unilateral LVO stroke exhibited hemodynamic steal identified by BOLD-CVR after successful EVT. Steal volume was associated with DWI infarct lesion size and with poor clinical outcome at hospital discharge. BOLD-CVR may further aid in better understanding persisting hemodynamic impairment following reperfusion therapy.

Vertebro-Vertebral Fistula Occlusion Using a Woven EndoBridgeTM-Device.

Vertebro-vertebral fistulas (VVFs) are vascular lesions that may develop after trauma or spontaneously in association with connective tissue disorders. We present a rare case of a post-traumatic VVF in a young patient presenting with a painless swelling and a bruit in her left upper neck. Digital subtraction angiography showed an arteriovenous fistula between the left vertebral artery (VA) and the vertebral venous plexus with significant steal phenomenon. Endovascular therapy was performed using a Woven EndoBridgeTM (WEB)-device combined with coils that allowed preservation of the VA. The patient fully recovered from her symptoms and follow- up imaging showed stable occlusion. In conclusion, VVFs can be effectively treated using intrasaccular flow diverters such as the WEB-device, allowing for complete and stable occlusion while preserving the parent artery.

DIAGNOSTIC VALUE OF ADDITIONAL MARKERS FOR ACUTE KIDNEY INJURY IN PRETERM NEONATES WITH PATENT DUCTUS ARTERIOSUS

DIAGNOSTIC VALUE OF ADDITIONAL MARKERS FOR ACUTE KIDNEY INJURY IN PRETERM NEONATES WITH PATENT DUCTUS ARTERIOSUS