35 Endothelial Damage
35.1 Case Description
35.1.1 Clinical Presentation
A 59-year-old female inpatient under the care of cardiology developed a sudden-onset aphasia, right hemiplegia, and neglect. Her National Institutes of Health Stroke Scale (NIHSS) score was 28. Three days previously, the patient had undergone ablation procedure for atrial fibrillation, complicated by left atrial perforation and pericardial tamponade, and followed by ministernotomy and surgical repair. Anticoagulation was on hold. In addition to the history of atrial fibrillation, comorbidities included hypertension, which was well controlled. There were no other cardiovascular risk factors.
35.1.2 Imaging Workup and Investigations
Noncontrast computed tomography (NCCT) of the brain obtained 90 minutes from symptom onset (Fig. 35.1a–c) demonstrated already loss of gray-white matter differentiation in the left insular region and lentiform nucleus in keeping with early infarction. Elsewhere, gray-white matter differentiation was preserved. There was hyperdensity consistent with thrombus in the left carotid termination and proximal middle cerebral artery (MCA; Fig. 35.1a).
CT angiography (CTA) demonstrated absence of contrast opacification of the left supraclinoid internal carotid artery (ICA), carotid terminus, M1 segment of left MCA, and proximal M2 branches (Fig. 35.1d, e). Left MCA branches in the sylvian fissure filled through leptomeningeal collaterals. The left A1 segment (Fig. 35.1e, arrow) and more distal anterior cerebral artery (ACA) was patent, opacified by contrast from the contralateral side through the anterior communicating artery.
Cardioembolic occlusion of the left carotid terminus in the setting of atrial fibrillation off anticoagulation.
In view of the high NIHSS score, presentation clearly within the time window, relative lack of early change on CT (other than left lentiform and insular region infarction), and the presence of large artery occlusion on CTA, a decision was made to proceed with intervention.
Intravenous tissue plasminogen activator (IV-tPA) was contraindicated in view of the recent surgery and therefore not administered. The patient was transferred directly to the neurointerventional suite.
8-Fr short angiographic sheath.
8-Fr MERCI balloon guide catheter.
5-Fr VTK slip catheter.
0.035 angled hydrophilic wire.
Trevo 18 microcatheter.
Trevo ProVue 4 × 20 mm stent retriever.
8-Fr Angio-Seal closure device.
Intervention was performed with conscious sedation and local anesthetic. A single-wall, left common femoral artery (CFA) puncture was performed, and the 8-Fr short vascular access sheath inserted. The right femoral artery had been recently accessed for cardiac intervention. The 8-Fr balloon guide catheter was advanced to the midcervical level of the left ICA over a 5-Fr VTK slip catheter with the aid of an angled Terumo guidewire using roadmap guidance. Left ICA angiography in frontal (Fig. 35.2a) and lateral (Fig. 35.2b) views showed slow filling of the left carotid artery to the level of the supraclinoid segment, where there was distal sharp cutoff with meniscus sign at the proximal clot face. There was no anterograde flow and no opacification of the MCA or ACA. Contrast stagnation and layering was noted in the cervical and supraclinoid ICA. A Trevo 18 microcatheter was navigated across the occluded carotid terminus and left M1 segment of MCA, and into an opercular branch of the superior division of MCA. Microcatheter injection (not shown) confirmed position distal to thrombus in a good caliber M2 branch. A Trevo ProVue 4 × 20 mm stent-retriever device was then deployed from the proximal M2 segment back to the supraclinoid segment of the ICA.
Control angiography with the stent in situ (Fig. 35.2c, d) showed some antegrade flow through the deployed stent, with filling defect consistent with thrombus in the supraclinoid ICA and carotid terminus region. The stent was left in situ for 5 minutes to allow incorporation of thrombus and then retrieved with flow arrest and suction. Some small clot fragments were retrieved in the stent; however, there was no back bleeding through the guide catheter, even with aspiration. The guide catheter was removed and flushed on the angiography table. Three large pieces of thrombus were flushed from the guide catheter. Total retrieved thrombus length was approximately 2 cm. The catheter was cleaned thoroughly and flushed. Using the same coaxial approach as before, the guide catheter was again placed in the left ICA. Control angiography showed complete recanalization of the left ICA, MCA, and now filling of left ACA from the carotid injection (Fig. 35.2d, e). There was complete reperfusion of the distal territory, with no evidence of distal clot migration or distal emboli, and no evidence of narrowing or spasm at site of thrombectomy.
All devices were removed. Hemostasis of the femoral artery puncture site was achieved by insertion of an 8-Fr Angio-Seal.
The patient demonstrated on-table improvement following recanalization and reperfusion, with improved power in the right arm and leg, along with improvement of aphasia and neglect. She was transferred to the neuro high-dependency unit (HDU) in stable condition for further monitoring and care. NCCT of the head performed 24 hours postprocedure demonstrated infarction in the left lentiform nucleus, caudate, insula, and small-volume patchy left frontal lobe infarction, with no evidence of hemorrhage. Following CT, the patient was commenced on IV heparin infusion for anticoagulation. Subsequently, anticoagulation with apixaban was commenced.
MRI with time of flight (TOF) MRA and vessel wall imaging were performed at 3 Tesla 5 days postthrombectomy. Diffusion-weighted imaging showed diffusion restriction in a pattern similar to previous postprocedural CT (Fig. 35.3a, b), involving left lentiform nucleus posteriorly, caudate, insular region, and small-volume infarction in the left frontal lobe, with sparing otherwise of basal ganglia, internal capsule, and most of the left MCA territory. MRA (Fig. 35.3c) showed normal appearance to the left ICA, carotid terminus, MCA, and ACA with no evidence of luminal irregularity or narrowing. Vessel-wall imaging was performed (Fig. 35.4a–f) with the following protocol: pre- and postcontrast T1 FLAIR and T2-weighted images in axial, coronal, and sagittal oblique planes with slice thickness of 2 to 3 mm and matrix size 512 × 512. There was no evidence of intrinsic T1 hyperintensity to suggest intramural thrombus on precontrast imaging (Fig. 35.4a, c). Gadolinium-enhanced T1 FLAIR showed concentric wall thickening and enhancement of the left M1 and proximal M2 segment of MCA (Fig. 35.4b, f), and enhancement of the left supraclinoid ICA and ICA termination (Fig. 35.4d, e). This corresponded to the location of deployment of the stent retriever.
There was continued clinical improvement throughout her in-patient stay, and she was discharged to rehabilitation 7 days following the thrombectomy procedure; 2 weeks later, she was discharged home. On the 3-month follow-up in the clinic, the patient was well, with no residual motor or sensory deficits, and complete resolution of language difficulties (modified Rankin scale score of 0).
Acute ischemic stroke due to intracranial large artery occlusion is independently associated with poor functional outcomes and high-mortality rates. Broadly speaking, the underlying cause for intracranial arterial occlusion can be either embolic, or, less commonly, related to diseases of the occluded vessel itself such as atherosclerosis. IV thrombolysis is an established treatment for acute ischemic stroke presenting within the 4.5 hour thrombolysis window. However, intracranial large arterial occlusion has been shown to be relatively resistant to treatment with IV thrombolytic therapy, and recent randomized controlled trials such as MR CLEAN, ESCAPE, EXTEND-IA, and SWIFT-PRIME have proven beneficial for mechanical thrombectomy over IV thrombolytic therapy alone in patients with large artery occlusive stroke. Mechanical thrombectomy is now the standard of care for such patients.
Little is currently known regarding the aftereffects of mechanical thrombectomy on the arterial wall in human subjects, as this has not been extensively studied to date. There is, however, some evidence from animal studies with regard to histopathological correlation that mechanical thrombectomy can result in arterial wall damage. In addition, there are some emerging studies in human subjects on angiographic follow-up postthrombectomy, showing delayed development of luminal narrowing/stenosis at the site of previous intracranial thrombectomy.
High-resolution 3-Tesla MRI can be used to study the wall of intracranial arteries, and can give valuable information regarding underlying abnormality. The MRI appearance of the arterial wall in disease states such as atherosclerosis and vasculitis is now well reported. Recently, this imaging technique has also been used to study the wall of intracranial arteries following stent retriever thrombectomy.
In this illustrative case, the patient presented with cardioembolic occlusion of the left carotid terminus in the setting of atrial fibrillation off anticoagulation. Mechanical thrombectomy was performed. MRI of the vessel wall subsequently showed abnormality of the intracranial arterial wall at the site of the deployed stent retriever.