Contralateral middle cerebral artery embolization following transradial vertebral artery stenting: a case report

Abstract

Background

Transradial vertebral artery (VA) stenting is an effective, and relatively safe treatment for symptomatic extracranial VA stenosis—the main cause of posterior circulation ischemia. Still, rare non-target anterior circulation cerebral embolisms can occur intraoperatively.

Case presentation

A 63-year-old male with prior cerebral infarction (NIHSS score 0, mRS score 1) presented with recurrent dizziness. Pre-admission CTA imaging confirmed severe (> 70%) bilateral VA ostial stenosis. The patient underwent right transradial VA stenting. Ten minutes post-procedure, he developed altered consciousness, mixed aphasia, and right hemiplegia (NIHSS score 16). Angiography confirmed acute occlusion in the M2 segment of the left middle cerebral artery (MCA). Mechanical thrombectomy was attempted but terminated due to severe vascular tortuosity, with no recanalization achieved. Immediate postoperative CT revealed contrast extravasation (CE) in the left frontoparietal sulci, rather than intracranial hemorrhage. The patient received tirofiban, dual antiplatelet therapy, and early rehabilitation. By discharge on day 7, he had achieved partial recovery (NIHSS score 9, mRS score 4).

Conclusion

Despite its extremely low incidence, the risk of anterior circulation cerebral embolism persists during transradial posterior circulation interventions. Gentle manipulation and emboli monitoring may mitigate this risk. Intraoperative neuromonitoring and rapid imaging are critical, and precise diagnosis and treatment can facilitate functional recovery.

Background

Symptomatic extracranial vertebral artery (VA) stenosis is a major cause of posterior circulation ischemia, and endovascular stenting has emerged as an effective treatment. Transradial VA stenting carries periprocedural risks including access site hematoma, in-stent thrombosis, vascular dissection, and distal embolization [1]. Embolic stroke typically occurs within the territory of the manipulated vessel (posterior circulation) [2]; however, accidental plaque disruption during interventions on the aortic arch (AA) or supra-aortic vessels can rarely lead to non-target anterior circulation embolization, a potentially devastating complication [3]. This case report describes contralateral middle cerebral artery (MCA) embolization during transradial VA stenting, highlighting critical clinical implications for practice.

Case presentation

A 63-year-old male with hypertension and a 6-year history of cerebral infarction presented with recurrent dizziness over two months. On admission, his National Institutes of Health Stroke Scale (NIHSS) score was 0 and modified Rankin Scale (mRS) score was 1. He had been consistently compliant with Optimal Medical Therapy (OMT), including daily oral aspirin (100 mg) and atorvastatin (20 mg), along with strict hypertension control, yet the dizziness persisted. Pre-admission computed tomography angiography (CTA) revealed severe stenosis (> 70%) at the bilateral VA ostia (Fig. 1A). Upon hospital admission, magnetic resonance imaging (MRI) indicated that the prior infarcted lesions, which initially involved the right frontoparietal region, right corona radiata, and left cerebellar hemisphere, had evolved into encephalomalacia foci (Fig. 1B, C, D). Consequently, the patient immediately received dual antiplatelet therapy (DAPT) with aspirin and clopidogrel, combined with atorvastatin calcium.

Fig. 1.

A Pre-admission CTA revealing severe stenosis at the bilateral VA origins. B Admission MRI: prior right frontoparietal and corona radiata infarcts exhibited central hypointensity with peripheral hyperintensity on Fluid-Attenuated Inversion Recovery (FLAIR), consistent with encephalomalacia and perifocal gliosis. C, D The prior left cerebellar hemisphere infarct showed FLAIR hypointensity, representing encephalomalacia foci

On the fifth hospital day, cerebral angiography and stenting were performed via right transradial access (TRA) under local anesthesia. A 5 F Sidewinder II catheter (Cordis, Miami Lakes, USA) was advanced into the descending aorta over a 0.035-inch J-type Radifocus hydrophilic guidewire (Terumo, Tokyo, Japan). By leveraging the apex of the catheter’s curve and the anatomical configuration of the aortic arch, the catheter was manipulated through a combination of advancement, withdrawal and torque maneuvers to achieve proper shaping of the Sidewinder II catheter. After shaping, the catheter was used to sequentially engage the bilateral subclavian artery (SA) for diagnostic angiography, confirming severe bilateral VA ostial stenosis. Subsequently, the 5 F Sidewinder II catheter was exchanged for a 6 F Chaperon guiding catheter (Terumo, Tokyo, Japan) positioned in the right SA. Under roadmap guidance, a 0.014-inch Asahi Sion guidewire (Asahi Intecc, Aichi, Japan) was navigated across the right VA ostial lesion, followed by deployment of a 4.0 × 13 mm Bridge vertebral artery rapamycin-targeted drug-eluting stent (MicroPort NeuroTech, Shanghai, China). Post-stenting angiography of the right VA showed resolution of stenosis with restored antegrade flow (Fig. 2A, B); subsequent intracranial angiography revealed an absence of the P1 segment of the left posterior cerebral artery (PCA) (Fig. 2C).

Fig. 2.

Digital Subtraction Angiography (DSA) findings. A Pre-intervention severe right VA ostial stenosis (white arrow). B Post-stenting patent vessel lumen (white arrow). C Post-stent implantation, right VA intracranial angiography: no visualization of left PCA (blue arrow). D, E Acute left MCA M2 segment occlusion (red arrow); left PCA visualized via left posterior communicating artery (PCoA), consistent with complete fetal-type posterior cerebral artery (CFPCA) (blue arrow)

Ten minutes post-procedure, the patient developed acute cough followed by altered consciousness, mixed aphasia, and inability to follow commands. Neurological examination revealed spontaneous movements in the left extremities but no withdrawal to painful stimuli on the right side. His NIHSS score increased to 16. Emergent left internal carotid artery (LICA) angiography was performed via right femoral access using a 5 F TEMPO catheter (Cordis, Miami Lakes, USA), revealing occlusion in the M2 segment of the superior division of the left MCA (Fig. 2D, E). Intra-arterial tirofiban (6 ml of a 50 µg/ml solution) was administered via the LICA, followed by a continuous intravenous infusion of tirofiban at 3 ml/h. After family consultation, mechanical thrombectomy (MT) was attempted. Under the guidance of a J-type Radifocus guidewire and with the assistance of a 5 F Chaperon inner catheter (Terumo, Tokyo, Japan), a 6 F 105 cm support catheter (HeartCare, Shanghai, China) was advanced to the proximal segment near the origin of the LICA within the common carotid artery. Subsequently, using a 0.014 inch × 200 cm hydrophilic Traxcess 14 guidewire (MicroVention, Aliso Viejo, USA) and a 2.7 F × 150 cm XT-27 microcatheter (Stryker, Kalamazoo, USA) as coaxial systems, the support catheter was navigated to the C3 segment of the LICA. Under roadmap fluoroscopy, repeated attempts to traverse the occluded M2 segment of the left MCA with the Traxcess 14 guidewire proved unsuccessful due to severe vascular tortuosity. Given the high risk of intracranial hemorrhage with forced manipulation, the procedure was terminated without recanalization.

Immediate postoperative head Computed Tomography (CT) showed linear hyperdensities in cerebral sulci suggestive of contrast extravasation (CE) (Fig. 3A, B). The patient was transferred to the Intensive Care Unit (ICU) for intensive monitoring and received dual antiplatelet therapy with aspirin and clopidogrel, statin treatment for plaque stabilization, as well as hydration and fluid supplementation. By postoperative day 1, he regained consciousness but persisted with aphasia and right hemiplegia. Follow-up CT at 48 h demonstrated near-complete absorption of CE and new left frontoparietal infarction (Fig. 3C, D). Following early aggressive bedside rehabilitation, the patient achieved partial language recovery, could speak fragmented words, and exhibited improved motor function (muscle strength in the right upper and lower limbs respectively of grade 2 and grade 3, assessed using the Medical Research Council (MRC) scores.) when discharged on day 7. His final NIHSS score was 9.

Fig. 3.

A, B Emergency postoperative CT showing left frontoparietal sulcal hyperdensities (240 HU) consistent with CE (yellow arrow). C, D 48-hour follow-up CT showing CE resolution (yellow arrow) and new left frontoparietal infarct (red arrow)

Discussion

This patient presented with recurrent dizziness for over two months despite strict adherence to secondary prevention measures, including daily aspirin, atorvastatin, and rigorous blood pressure control following a previous cerebral infarction 6 years ago. MRI revealed infarct encephalomalacia, and angiography confirmed severe bilateral VA ostial stenosis (> 70%), which indicated that revascularization was reasonable according to the Chinese Expert Consensus (symptomatic stenosis ≥ 50% in patients who fail OMT) [4]. Meanwhile, the European Society for Vascular Surgery (ESVS) 2023 guidelines recommend against routine stenting for asymptomatic or stable patients; however, they suggest that revascularization may be considered (Class IIb, Level B) for patients with recurrent vertebrobasilar symptoms despite OMT [5]. In this case, the lesion involved the extracranial VA origin, which is fundamentally different in pathophysiology and procedural risk from the intracranial stenosis studied in SAMMPRIS [6]; therefore, the high-risk results of that trial do not apply here. Given the severe bilateral VA ostial stenosis and persistent vertebrobasilar ischemic symptoms refractory to OMT, endovascular intervention was deemed clinically appropriate to restore perfusion and prevent further disabling stroke. Importantly, the patient had adhered to DAPT for 5 days prior to the procedure, fulfilling the requirement for adequate platelet inhibition [4, 5].

Compared with the transfemoral approach, the TRA significantly reduces not only major bleeding but also various access-site vascular complications such as pseudoaneurysm, arteriovenous fistula, and retroperitoneal hematoma, while shortening hospital stays and improving patient comfort due to early ambulation [7]. Therefore, based on these advantages, we selected the TRA for stenting of the VA origin.

However, while TRA is generally safe with a periprocedural stroke risk of 0%-0.8% [8], this case illustrates a rare but severe complication: acute left MCA M2 embolization following right VA stenting. Although symptomatic, large-vessel anterior circulation embolism explicitly attributed to VA stenting is exceedingly rare, prior studies have shed light on the risk of non-target embolization during posterior circulation interventions. Previous studies evaluated 16 patients undergoing VA origin stenting using diffusion-weighted imaging (DWI) and found that 7 cases (43%) developed new postoperative DWI hyperintensities, with one case exhibiting isolated anterior circulation abnormalities involving the left MCA territory (frontal and parietal lobes) [9]. Similarly, in a clinical series involving 58 patients treated with ostial VA stenting, although most periprocedural neurological complications were posterior circulation events, one case (1.7%) of definitive anterior circulation stroke was documented [10].

Although the embolic mechanism remains theoretical, competing hypotheses exist. One possibility involves emboli generated during right VA stenting (via BCT manipulation or balloon angioplasty [3, 11]), which could theoretically reach the left MCA via a patent posterior communicating artery (PCoA). However, imaging revealed a left complete fetal-type posterior cerebral artery (CFPCA) with an absent P1 segment (Fig. 2C-E), anatomically excluding this retrograde pathway. Consequently, the source most likely originated from the aortic arch. During Sidewinder II shaping and selective cannulation, repeated torque and tractive maneuvers likely scraped atherosclerotic plaques near the left common carotid artery orifice, directly embolizing the left MCA [12]. Nevertheless, this mechanism remains speculative, as preprocedural high-resolution CTA or vessel wall imaging of the aortic arch was not performed; thus, the presence of vulnerable plaque at the left common carotid artery ostium could not be confirmed.

To mitigate these risks, preoperative and intraoperative strategies may be optimized as follows: (1) Preoperative Assessment: Adherence to contemporary guidelines emphasizes the necessity of OMT [4, 5]. It also mandates preoperative evaluation of plaque vulnerability (arch/ostial) [13] and hemodynamic compensation, such as Doppler ultrasound assessment of VA flow dynamics, which has been shown to correlate with ischemic stroke risk and aid in tailoring operative caution [14]. (2) Refined Catheter Technique and Device Selection: Meticulous, gentle torque and tractive maneuvers are paramount, especially during Sidewinder II shaping and aortic arch (AA) navigation, to avoid scraping atherosclerotic plaques at the AA or supra-aortic ostia [15]. Utilizing soft-tipped, pre-shaped dedicated radial access systems that integrate diagnostic and interventional capabilities can minimize repeated catheter exchanges and traumatic aortic arch contact [16]. (3) Emboli Monitoring and Protective Adjuncts: Transcranial Doppler (TCD) monitoring for microembolic signals allows intraoperative detection of emboligenic maneuvers, prompting immediate technique adjustment [17]. In anatomically complex or high-risk cases, proximal flow arrest/occlusion techniques may be cautiously considered. While distal embolic protection devices (EPDs) have demonstrated efficacy in reducing perioperative embolic signals during VA stenting [17, 18], their routine clinical adoption remains challenging due to vessel tortuosity and potential spasm at the VA origin [19].

Furthermore, rapid identification of intraoperative embolism relies on vigilant neuromonitoring. Here, acute neurological deficits prompted immediate emergency protocols. Following exclusion of hemorrhage, hyperacute left MCA M2 occlusion was confirmed angiographically. Given intraoperative heparinization, MT was performed immediately as the definitive reperfusion strategy [2]. Although recanalization failed, the expedited response minimized delays. Notably, postoperative imaging excluded hemorrhage—evidenced by marked high attenuation (240 HU) and rapid resolution inconsistent with hyperacute bleed (60–80 HU) [20]—confirming CE due to ischemia-induced blood-brain barrier disruption. Intraoperative tirofiban inhibited platelet aggregation [21], followed by postoperative dual antiplatelet therapy and early rehabilitation [22], resulting in significant neurological recovery despite the failed recanalization.

In conclusion, this rare case highlights that anterior circulation embolic risks persist during posterior transradial interventions. Intraoperative neuromonitoring and rapid imaging are critical.

Abbreviations

AA

Aortic Arch

BCT

Brachiocephalic Trunk

CE

Contrast Extravasation

CFPCA

Complete Fetal-type Posterior Cerebral Artery

CTA

Computed Tomography Angiography

CT

Computed Tomography

DAPT

Dual Antiplatelet Therapy

DSA

Digital Subtraction Angiography

EPD

Embolic Protection Device

LICA

Left Internal Carotid Artery

ICU

Intensive Care Unit

MCA

Middle Cerebral Artery

MRC

Medical Research Council

MRI

Magnetic Resonance Imaging

MT

Mechanical Thrombectomy

mRS

Modified Rankin Scale

NIHSS

National Institutes of Health Stroke Scale

OMT

Optimal Medical Therapy

PCA

Posterior Cerebral Artery

PCoA

Posterior Communicating Artery

SA

Subclavian Artery

TCD

Transcranial Doppler

TRA

Transradial Access

VA

Vertebral Artery

Authors’ contributions

JS Tu, W Qiu: manuscript conception, design, writing and editing, and clinical care of the patient. WS Deng, H Peng, QH Liu: review of the article and clinical care of the patient. XY Gao: critical review of the manuscript.

Funding

No specific funding was provided for this case report.

Data availability

The data used to support the findings of this study are available from the corresponding author upon request.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Written informed consent for publication of the clinical details and/or clinical images was obtained from the patient’s wife. A copy of the consent form is available for review by the Editor of this journal.

Competing interests

The authors declare no competing interests.