28 Hyperacute Extracranial Angioplasty and Stenting: When and How
28.1 Case Description
28.1.1 Clinical Presentation
A 69-year-old male presented initially to the emergency department of an outside center with chest pain, dyspnea, and right arm pain. He was diagnosed with bilateral pulmonary emboli on computed tomography pulmonary angiography (CTPA), and was also noted to be in atrial fibrillation. Oral aspirin had already been administered in view of presentation with chest pain. Anticoagulation with low molecular weight heparin was commenced. Later in the same day, there was a sudden onset of left hemiparesis including left facial weakness and dysarthria. Noncontrast computed tomography (NCCT) of brain was performed, but no evidence of hemorrhage was found.
The patient was transferred as a code stroke to our regional stroke center for further evaluation and treatment. At the time of assessment, he was 2 hours from symptom onset. The left hemiparesis had improved significantly during transfer, with residual mild left upper limb drift, mild left facial weakness, and mild dysarthria remaining (National Institutes of Health Stroke Scale [NIHSS] score of 3).
Past medical history was significant for cigarette smoking, and dyslipidemia treated with lipid-lowering medication. There were no other known cardiovascular risk factors at the preadmission stage, and the only regularly administered preadmission medication was rosuvastatin 5 mg once daily.
28.1.2 Imaging Workup and Investigations
NCCT of brain (Fig. 28.1a–c) demonstrated subtle loss of gray-white matter differentiation in the right basal ganglia. No other early or established ischemic change was observed. There was no evidence of hemorrhage. Computed tomography angiography (CTA) performed from the level of the aortic arch demonstrated right carotid artery (RCA) stenosis with soft ulcerated plaque (Fig. 28.1d). The caliber of the right internal carotid artery (ICA) distal to the stenosis was reduced compared to the contralateral side, indicating critical stenosis. A small nonocclusive thrombus was visualized in the midportion of the right M1 segment, along the superior wall of the vessel (Fig. 28.1e, f). No other intracranial thrombus or intracranial arterial occlusion was observed on CTA. A patent anterior communicating artery (AComm) was identified on the CTA (Fig. 28.1e, f), while a right-sided posterior communicating artery (PComm) could not be appreciated.
Right ICA critical stenosis.
Intravenous (IV) tissue plasminogen activator was contraindicated, as therapeutic dose of low molecular weight heparin had been recently administered. The patient had demonstrated significant clinical improvement (NIHSS score of 3). An emergency multidisciplinary discussion took place regarding the best approach to management. As the right M1 thrombus was very small and nonocclusive, it was felt that immediate endovascular intervention and mechanical thrombectomy was not required. Supporting this, there was already loss of gray-white matter differentiation in the basal ganglia, suggesting early infarction. It was considered very likely, given the configuration of the carotid plaque and the degree of stenosis, that the intracranial thrombus was embolic from the ICA rather than cardioembolic related to the atrial fibrillation. There was consensus that the RCA should be urgently revascularized. Risks and benefits of carotid stenting versus urgent endarterectomy were discussed, in particular taking into consideration the already administered antiplatelet agent, low molecular weight heparin, and the diagnosis of bilateral pulmonary emboli which would require continuation of anticoagulation treatment. Following discussions, a decision was taken to proceed with urgent carotid stenting.
Once decision was made to proceed with stenting, a loading dose of 300 mg Plavix was administered, as well as 162 mg aspirin, and the patient was transferred to the neurointerventional suite.
8-Fr short angiographic sheath.
6-Fr 80-cm Shuttle sheath.
5-Fr Berenstein catheter.
0.035 angled hydrophilic wire.
Angioguard RX Emboli Capture Guidewire System.
Synchro 14 microguidewire.
Mini Trek RX PTA balloon catheter 2 mm × 15 mm.
Mini Trek RX PTA balloon catheter 3 mm × 15 mm.
Aviator Plus PTA balloon catheter 5 mm × 20 mm.
Carotid WALLSTENT 9 mm × 40 mm.
8-Fr Angio-Seal closure device.
Intervention was performed with conscious sedation and systemic heparinization. Local anesthetic was administered at the puncture site. A single-wall, right common femoral artery (CFA) puncture was performed. An 8-Fr short angiographic sheath was placed for vascular access. A 6-Fr 80-cm Shuttle was advanced to the right common carotid artery (CCA) over a 5-Fr Berenstein catheter. Right common carotid angiography confirmed the presence of irregular ulcerated plaque involving the ICA bulb, with stenosis of the right ICA just beyond its origin. The external carotid artery (ECA) led over the ICA. Distally, the cervical portion of the ICA was patent, but of reduced caliber, in keeping with a critical stenosis (Fig. 28.2a).
Based on the caliber of the distal vessel, a 5-mm Angioguard distal protection device was chosen. Predilation of the stenosis was necessary to allow passage of the Angioguard. The stenosis was crossed with a Synchro-14 microguidewire using roadmap guidance (Fig. 28.2b). Over this, a 2 mm × 15 mm Mini Trek balloon dilatation catheter was advanced and placed across the stenosis. Angioplasty with the 2-mm balloon was not sufficient to allow passage of the Angioguard across the stenosis, therefore a second single inflation angioplasty was performed with a 3 mm × 15 mm Mini Trek balloon dilatation catheter. Following this, the Angioguard device was successfully advanced across the stenosis, and deployed in a straight segment of distal cervical ICA (Fig. 28.2c, arrow). Angioguard deployment resulted in further reduction of flow in the ICA, and the following steps were rapidly undertaken: A 9 × 40 mm carotid Wallstent was chosen. Further prestenting angioplasty was required to allow passage of the stent, and this was performed using a 5 mm × 20 mm Aviator Plus balloon, utilizing rapid exchange maneuver. The Wallstent was then optimally positioned and deployed across the stenosis (Fig. 28.2d, e). A weight-calculated bolus of ReoPro (0.25 mg/kg) was administered immediately once the stent was deployed to bridge, while the administered antiplatelet agents achieved full effect. The Angioguard distal protection device was then recaptured uneventfully and removed.
Poststenting angiography (Fig. 28.2f, g) showed improved caliber of the ICA, with mild residual waisting at the level of the stenosis, improved distal flow in the ICA, and improved perfusion of the right hemisphere, with ICA now leading over ECA. The previously noted filling defect in the M1 segment of middle cerebral artery (MCA) was no longer evident (Fig. 28.3a). A right MCA distal branch occlusion with slow flow, and distal cutoff observed in an inferior parietal M3 branch was noted, possibly representing distal passage of the small right M1 segment thrombus (Fig. 28.3b). This was too distal for stent-retriever thrombectomy, and in the late arterial to parenchymal phase, leptomeningeal collaterals could be seen filling the territory of the occluded branch. The patient was examined, and since the clinical condition was unchanged from the start of the procedure, no further intervention was performed. All devices were retrieved, and an 8-Fr Angio-Seal closure device placed in the right CFA for hemostasis.
The patient’s clinical condition remained unchanged throughout the procedure, with no change in neurological status pre- and postprocedure. Strict blood pressure control was maintained postprocedure for 24 hours, with systolic blood pressure (SBP) maintained below 140 mm Hg in order to avoid hyperperfusion injury.
The patient remained well and continued with an oral dose of 75 mg clopidogrel and 81 mg aspirin daily. In view of the diagnosis of bilateral pulmonary emboli and atrial fibrillation, anticoagulation was continued, initially with low-molecular-weight heparin, with subsequent transition to apixaban 2.5 mg orally twice daily on discharge.
NCCT of the brain was performed 24 hours postprocedure (Fig. 28.4a, b). This demonstrated evolving infarct in the right basal ganglia, with a small region of central petechial hemorrhagic change and without significant mass effect, and also no evidence of infarction elsewhere. The patient showed further neurological improvement, with left upper limb returning to normal power. He was discharged home 6 days postprocedure with mild residual left facial weakness and mild dysarthria remaining.
ICA stenoses are most commonly atherosclerotic in etiology. Extracranial ICA stenosis accounts for 15 to 25% of ischemic stroke, with an incidence that may be as high as 10% in patients older than 80 years. Ipsilateral high-grade ICA stenosis or occlusion is present in approximately 10 to 20% of patients presenting with acute large vessel occlusion stroke which further complicates endovascular access and may lead to a delay in recanalization of the target vessel occlusion. The risk of stroke in patients with extracranial ICA stenosis is associated with the degree of narrowing; for asymptomatic patients with less than 75% stenosis, the risk of stroke is less than 1%/year, but the risk increases to 2 to 5%/year for patients with greater than 75% stenosis. In symptomatic patients (previous transient ischemic attack [TIA] or stroke), the risk is considerably higher; nearly 10% in the first year and 30 to 35% over the next 5 years for patients with stenoses larger than 70%. Currently, the three major treatments for extracranial ICA stenosis are medical management, carotid endarterectomy (CEA), and carotid angioplasty with stenting.
28.2.2 Workup and Diagnosis
In an acute setting, it may be difficult for the neurointerventionalist to gather information regarding relevant medical history expeditiously. This information may already have been obtained by emergency department staff or the stroke physician/neurologist. Patients with carotid disease (or their family members) may report a history of prior stroke or TIAs either as a result of thromboemboli or related hypoperfusion of watershed regions. Since atherosclerosis is a systemic disease, a history of coronary artery disease or peripheral vascular disease may also be elicited.
Risk factors for atherosclerotic disease may be present, including smoking, diabetes, hypertension, and hyperlipidemia.
Examination and Investigations
Findings on physical examination will depend on the ischemic or hypoperfused territory. Neurologic deficits may also be present from previously infarcted territories. A bruit may be heard on auscultation over the cervical ICA.
ICA stenosis will be apparent on CTA performed in the hyperacute or acute stroke workup; therefore, it should be performed from the level of the aortic arch. Accurate estimation of the degree of stenosis and characterization of the plaque may be performed with CTA and/or MRA. CTA has the benefit of higher spatial resolution than MRA and will more reliably depict calcifications. In addition, MRA occasionally also suffers from inability to reliably differentiate slow flow or critical stenosis from a complete occlusion. Flow-related artifacts are less common with contrast-enhanced MRA compared to time-of-flight (TOF) MRA. In the nonacute setting, the use of precontrast, T1-weighted, high-resolution MRI of the carotid wall at 3 Tesla may also identify intraplaque hemorrhage, which can be helpful in risk stratification of patients regardless of percentage of stenosis.
Although advances in noninvasive CTA and MRA imaging have eliminated routine use of digital subtraction angiography (DSA) for carotid stenosis quantification in the nonemergent setting, when endovascular therapy is being considered in the acute setting (e.g., mechanical thrombectomy, carotid angioplasty, or stenting), DSA remains the gold standard for measurement of percentage stenosis.
Carotid Doppler ultrasongraphy is of limited utility in the acute setting. It should be reserved as a screening tool in the nonemergent setting, as it suffers from interoperator variability, artifacts due to calcified atherosclerotic plaques, and difficulties distinguishing pseudo-occlusion from complete occlusion.
28.2.3 Imaging Findings
NCCT or MRI of the head may demonstrate old or recent embolic infarcts in the territory of the ipsilateral anterior circulation or infarcts in the MCA–posterior cerebral artery (PCA) and/or anterior cerebral artery (ACA)–MCA watershed regions. CTA from the aortic arch to the vertex of the skull, which is performed as part of hyperacute stroke workup, will demonstrate ICA stenosis as an area of caliber narrowing in the artery. MRA will also show an area of narrowing; however, MRA suffers from lower spatial resolution and may overestimate the degree of stenosis. Furthermore, in the setting of critical ICA stenosis, the slow flow of contrast beyond the stenosis may result in absence of signal distal to the stenosis, and mislead the reader into thinking the ICA is occluded just beyond the stenosis (pseudo-occlusion). Maximum-intensity projections and multiplanar reconstructions are helpful in evaluating the morphology and extent of stenosis. The presence and size of the AComm and PComm arteries should be noted. MRI of carotid plaques may also demonstrate high-risk features such as the presence of intraplaque hemorrhage, inflammation, large lipid core, and/or ulcerations.
Patients presenting with significant ICA stenosis may demonstrate CT perfusion asymmetry (with elevated time to peak/mean transit time, decreased relative cerebral blood flow, and preserved or reduced relative cerebral blood volume) in the arterial territory distal to the stenosis, or confined to the ACA–MCA and/or MCA–PCA watershed regions. If an extracranial carotid occlusion is present, no contrast will be seen distal to the occlusion on CTA. The proximal extent of the intracranial and/or extracranial occlusion may be difficult determine on CTA, as the slow or stagnant contrast column within the ipsilateral ICA may not opacify the face of the clot.
DSA remains the gold standard in the diagnosis of ICA stenosis or occlusion, differentiation from pseudo-occlusion, and characterization of extent and morphology of the stenosis. Percentage stenosis should be calculated according to the formula set forth in the North American Symptomatic Carotid Endarterectomy Trial (NASCET): % ICA stenosis = (1– [narrowest ICA diameter/diameter normal distal cervical ICA]) × 100. A critical stenosis may be identified as “string sign,” or a small thread of contrast, visible within a stenosis in association with a diffusely and smoothly narrowed caliber of the remainder of the extracranial ICA due to downregulation. In the setting of a critical stenosis, percentage stenosis calculated using NASCET criteria will be “falsely” lowered due to the smaller caliber of the distal ICA, resulting in a smaller denominator. It is helpful to look at the contralateral extracranial ICA for more accurate estimation of the true ICA diameter. Normally, the ICA should fill before the ECA territories when CCA injections are performed. On DSA, patients with long-standing severe or critical ICA stenosis may demonstrate well-developed, pial-pial collaterals in the ACA–MCA and/or MCA–PCA watershed regions of the brain on angiography.
28.2.4 Decision-Making Process
A number of randomized controlled trials published in 2015 have proven to be beneficial for endovascular intervention over medical treatment alone in large artery occlusive stroke. The clinical presentation and imaging findings in this case would not fit the inclusion criteria for these trials. The patient’s presenting symptoms had improved to a NIHSS score of 3 and there was no large vessel occlusion on the CTA. Immediate mechanical thrombectomy was thus not indicated.
Urgent revascularization is, however, indicated, given the presence of a significant stenosis of the extracranial carotid artery and the presenting stroke. In general, patients with preocclusive carotid stenosis, as in this case, are considered for emergency intervention, whereas those with lesser degrees of stenosis could initially be managed medically with urgent, but not emergency intervention. A number of randomized clinical trials have demonstrated the benefit of carotid revascularization within the first 2 weeks after stroke or TIA. Numerous clinical trials have compared CEA versus carotid artery stenting (CAS). Based on the results of these trials, as discussed further in later sections, current combined consensus statements from neurosurgical, neurology, interventional neuroradiology, cardiology, and vascular surgery societies state that in a majority of cases where there is a need for revascularization of symptomatic extracranial carotid stenosis, CEA is recommended over CAS unless contraindications to surgery are present, or in other specific situations as outlined later in the discussion section.
In the present case, the patient had been anticoagulated with low-molecular-weight heparin for the treatment of acute pulmonary emboli. Furthermore, anticoagulation would also be needed after revascularization for the medical management of atrial fibrillation. The need for anticoagulation places the patient at higher surgical risk for neck hematoma from CEA. In addition, data from a pooled analysis of the three major CEA trials demonstrated no significant benefit of CEA with near occlusion of the ICA, as with this patient, where the absolute risk reduction was negative. Proceeding with CAS is justified on the basis of these considerations.
Medical management of extracranial carotid atherosclerotic disease is by far the most commonly used treatment and includes aspirin 81 to 325 mg PO daily. It is the only modality that is considered an essential aspect of management for any patient with a noncardioembolic acute infarct, and is used either alone or in conjunction with more invasive treatments. However, aspirin generally should not be given for the first 24 hours following treatment with IV or IA thrombolytic therapy. Alternatives to aspirin for patients with aspirin intolerance include clopidogrel or ticlopidine, although the effectiveness of these antiplatelets in acute stroke setting is not established. The use of dual-antiplatelet therapy remains largely unproven, with the exception that short-term treatment with clopidogrel plus aspirin appears to be beneficial for high-risk TIA and minor stroke in Asian populations.
Beyond the acute phase of an acute ischemic stroke or TIA, long-term antiplatelet therapy for secondary stroke prevention should be continued.
Major treatable atherosclerotic stroke risk factors including hypertension, diabetes, smoking, and dyslipidemia should also be addressed.