Duplex Ultrasound Surveillance After Carotid Stent Angioplasty

 When to Follow Up and What to Look for

Duplex ultrasonography, developed by Dr. Eugene Strandness, Jr. at the University of Washington in the 1970s, has evolved to become the primary noninvasive diagnostic technique for the evaluation of the extracranial carotid artery.^1,2 By utilizing B-mode imaging to detail arterial anatomy and pulsed Doppler velocity spectra to assess blood flow characteristics, duplex ultrasound scanning provides a safe and accurate method to detect and grade the severity of atherosclerotic internal carotid artery (ICA) stenosis, both prior to and following intervention. Carotid duplex testing after surgical endarterectomy or stent-angioplasty permits assessment of the technical success by documenting a non-stenotic patent repair, and through serial testing, the detection of restenosis or occlusion.

Carotid endarterectomy (CEA) was shown to be superior to the “best” medical therapy for stroke prevention in patients with severe atherosclerotic ICA stenosis in both the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the Asymptomatic Carotid Atherosclerosis Study (ACAS),^3,4 and is currently being compared to carotid stent-assisted angioplasty (CAS) in the Carotid Revascularization Endovascular Stent Trial (CREST).⁵ Until the CREST study outcomes are known, the option for CAS is being applied selectively to treat a patient cohort judged to be high-risk for surgical repair.The endovascular approach removes much of the surgical morbidity associated with “high-risk” conditions, such as ischemic cardiomyopathy, prior neck irradiation, and re-do endarterectomy.

The efficacy of both CEA and CAS is highly dependent on achieving low (6–10 Procedural duplex scanning can immediately confirm technical success of CEA or CAS repairs by imaging for residual stenosis, platelet-thrombus, or pulsed Doppler spectra, indicating abnormal flow characteristics before leaving the operating room or angiography suite.^7,8 When the intraprocedural duplex scan is normal, the likelihood of repair-site thrombosis is extremely low ( 50% diameter residual, or recurrent stenosis.^9,10 The incidence of duplex-detected “high-grade” stenosis, i.e. in the > 75–80% diameter-reduction (DR) stenosis classification, is much lower (3–5%). The management of “high-grade” stenosis after both CEA and CAS is controversial, as the patients are typically asymptomatic and the natural history of these lesions has not clearly delineated. Certainly, the embolic potential of myointimal hyperplasia restenosis is less than an atherosclerotic lesion. In general, clinicians recommend re-intervention when a progressive repair site stenosis is demonstrated and confirmatory imaging studies (digital subtraction angiography, computed tomography angiography) indicate a > 80% DR stenosis. This stenosis severity threshold has been shown to progress to occlusion, and if functional patency of the Circle of Willis is abnormal, stroke can occur.

Duplex ultrasound surveillance in our patients has demonstrated a similar incidence of intervention for “high-grade” stenosis following CEA (7%) and CAS (10%). Treatment of contralateral ICA disease progression was more common than intervention for restenosis of a CEA or CAS site. Routine ultrasound surveillance is recommended to our patients with consideration for reintervention when a duplex-detected > 75% DR stenosis is identified. Essentially, all of these patients are asymptomatic when the lesion is detected, but repair most commonly by endovascular stent angioplasty, has been associated with continued ICA patency and a low ( Carotid Duplex Testing Protocol The interpretation of duplex testing after CAS should include review of the pre-stent angioplasty duplex study for ICA plaque characteristics (calcification, acoustic shadowing) as well as the severity of contralateral ICA disease, especially if occluded. These variables can influence velocity spectra (peak systolic velocity [PSV] and end-diastolic [EDV]) values recorded from the stented ICA segment. Calcified atherosclerotic plaques can inhibit nitinol stent expansion with time and compensatory flow as a result of severe, contralateral ICA stenosis or occlusion can contribute to elevations of PSVs, and thus the overdiagnosis of stent stenosis. The technique of duplex testing after CAS mimics the imaging protocol and pulsed Doppler flow pattern interrogation used for the diagnosis of extracranial carotid occlusive disease. A bilateral examination using a high-resolution 7 MHz linear array transducer was performed with sagittal and transverse scan planes from the proximal CCA to distal ICA. The common carotid artery was initially imaged low in the neck, and vessel scanning continued to the carotid bifurcation to include the external (ECA) and internal (ICA) carotid artery origins, and the ICA as distal as possible. Ultrasound imaging of the CCA should yield results similar to pre-stent findings, but PSV and EDV values may be increased as a result of ICA stenosis correction. Often the carotid stent will traverse the ECA origin, but flow through stent is typically present and sufficient to maintain patency. The stented carotid segment should be imaged in multiple planes to confirm lumen expansion at the ICA plaque site, and stent apposition to the artery wall along its entire length. Mid-stream pulsed Doppler velocity spectra, using a small sample volume and 60-degree Doppler angle to vessel wall, are recorded from multiple sites, including the proximal and distal CCA, in the proximal, middle, and distal stent, and from the ICA distal to the stent. Stent diameter should be measured and residual lumen assessed when in-stent intimal thickening is identified. Power Doppler imaging is useful to image the stent lumen and the stent transition flow into the ICA, and an excellent technique to demonstrate both the severity and extent of instent restenosis. From the pulsed Doppler velocity spectra recordings, the maximum PSV from the stent is calculated, as are the PSV ratio along the stent, and PSVSTENT to proximal PSVCCA ratio. These parameters are used in the carotid duplex interpretation and estimating of stent stenosis severity. Testing is performed within 1 month of CAS and every 6 months thereafter for 1 to 2 years, then annually if duplex testing demonstrates Interpretation of Carotid Duplex Testing following Stent Angioplasty Stent implantation across a stenotic ICA segment delivers radial forces to expand the lumen and maintain a larger diameter. After stent delivery, both positive (stent expansion) and negative (wall recoil, myointimal hyperplasia) remodeling occurs, with corresponding changes in lumen caliber. The remodeling of the stented ICA is a dynamic process occurring over months and involves a biologic response to the arterial wall injury and the stent.^12–16 For several months after deployment, stent expansion occurs — approximately a 20–40% diameter increase — but this positive remodeling can be inhibited in the presence of extensive plaque calcification. Also during this time period, neointimal hyperplasia is also developing within the stent, and can be demonstrated by high-resolution B-mode imaging as a homogenous, concentric intimal thickening. Typically, by 3-months, the anatomic changes produced by neointimal hyperplasia exceeds that of stent expansion, yielding the net result of stent lumen reduction and the hemodynamics of an increase in stent PSV with time.¹⁵ The extent and rate of neointimal hyperplasia development is varied, including lesions that develop rapidly within the first 6 months after CAS to stenotic lesions that can regress, i.e., negative remodeling, from > 50% DR to Duplex testing of “normal” stent imaging and hemodynamics is associated with a smooth, widely patent lumen with nondisturbed flow and a PSV of less 150 cm/s. The PSVSTENT ratio along the stent length should be less than 2, as should PSV changes at the proximal and distal stent ends. On transverse imaging, the stent should be apposed to the artery wall circumferentially and the lumen patent without anatomic or flow defect. An audit duplex testing of 65 CAS procedures, with completion angiograms confirming The biomechanical properties of the stented ICA segment is altered by a decrease in wall compliance compared to the adjacent non-stented artery producing a compliance mismatch at the stent ends.^18–20 Stent flow has similarity to flow in a rigid tube and may account for the elevated velocities compared to a surgical endarterectomy site. The PSV level in the stent is also related to the stent’s diameter and the balloon size used for final dilation after stent deployment. Residual stent stenosis as a result of incomplete calcified plaque expansion is a common cause for an increased PSVSTENT. Tapered stents deployed from the distal CCA to the ICA will also have a progressive increase in PSV along the stent length, due to the decrease in stent diameter.

Presently, the clinical interpretation of an in-stent PSV in the 150–200 cm/s range is a subject of debate. Blood flow velocity in this range is not associated with a pressure gradient and thus, would not affect cerebral circulation. Interpretation of instent stenosis should be based on both imaging and PSV criteria. Scanning with high-resolution (7–10 MHz) B-mode linear array transducer perpendicular to the stent will accurately determine the presence of myointimal thickening or stent deformation. These regions should be carefully interrogated to assess changes in the velocity spectra, including focal spectral broadening (turbulence) and changes in PSV. In the absence of an anatomic abnormality, a PSV as high as 200 cm may be measured and the interpretation of stenosis severity in the The reported PSV threshold for > 50% diameter-reduction stent stenosis varies in the literature, with several vascular groups recommending a higher (150–200 cm/s) value than the 125 cm/s threshold recommended in the University of Washington criteria for carotid bulb atherosclerotic lesions and used in the CREST clinical trial. Our group utilizes multiple criteria when reporting on the presence of > 50% stent stenosis, including lumen reduction on stent imaging, disturbed stent flow with color Doppler aliasing, a PSV value >150 cm/s, and a PSVSTENT ratio > 2. For severe (> 75% DR) stent stenosis, the hemodynamic criteria of a PSV > 300 cm/s, PSVstent ratio > 4, and EDV > 125 cm/s are used. Power Doppler imaging should indicate a Duplex Ultrasound Surveillance after CAS A retrospective review of duplex surveillance after 114 CAS procedures performed in 111 patients demonstrated on both initial testing and during follow-up the majority (70%) of the stent-angioplasty repairs, had findings of 50% DR to the 75% DR) in-stent stenosis. Angiography confirmed > 75% DR CAS stenosis in all 6 patients, resulting in balloon angioplasty (n = 3), stent angioplasty (n = 2), and in one patient stent removal with endarterectomy. Three patients developed nondisabling, reversible neurologic events (30, 45, and 120 days), and duplex testing detected no CAS stenosis in two and > 50% DR (PSV = 185 cm/s) in one patient. Two of the three events were minor, involving visual symptoms, and one involved contralateral extremity weakness that resolved fully in 72 hours. The yield of duplex surveillance for high-grade CAS stenosis was 5% (6 of 114 CAS sites) — no stent occluded. Angiography confirmed > 75% DR CAS stenosis in all 6 patients, resulting in balloon angioplasty (n = 3), stent angioplasty (n = 2), and in one patient stent removal with endarterectomy. After 30 days, no patient with > 50% CAS stenosis on initial testing, or who demonstrated stenosis progression to > 50% DR, developed ipsilateral neurological symptoms. No CAS or stroke-related deaths were observed during follow-up.

Our experience of CAS surveillance has allowed us to conclude that testing intervals of 6 months are sufficient to detect CAS site stenosis, and follow 50–75% stenotic lesions for progression. However, surveillance is also important to detect contralateral ICA stenosis progression. Of the 19 patients, 5 with 50–75% DR ICA stenosis progressed to > 75% DR without symptoms and underwent carotid endarterectomy. Imaging the CAS site within 1 month is useful to exclude residual stenosis and reconfirm the severity of contralateral disease. If duplex testing demonstrates 50% DR ipsilateral or contralateral ICA stenosis. The development of hemispheric symptoms in the presence of > 50% DR ICA or CAS stenosis, or asymptomatic disease progression to a high-grade stenosis (> 75–80% DR, end-diastolic velocity >140 cm/sec), should prompt a recommendation of surgical or endovascular (stent-assisted angioplasty) intervention in appropriate patients.

Duplex surveillance after CAS identified a 5% procedural failure rate, due to the development of high-grade in-stent stenosis, a higher clinical yield than CEA surveillance.6 Both progression and regression of stent stenosis severity was observed on serial testing, but the majority (70%) of CAS sites demonstrated velocity spectra consistent with 75% DR stenosis. Our policy of duplex ultrasound surveillance and reintervention for high-grade stenosis was associated with sustained stent patency and infrequent neurologic events. Although the PSV of CAS sites may be increased compared to CEA sites, the development of moderate (50–75%) stenosis is not clinically worrisome, but progression to high-grade (>75%) stenosis may lead to occlusion. Currently, we recommend angiographic confirmation to these patients who have been asymptomatic, followed by endovascular repair if a high-grade stenosis is verified.