Right Extracranial Internal Carotid Artery Stenosis
A 70-year-old man presented to the emergency department with a sudden onset of numbness in his left arm. He had a history of cigarette smoking (but had discontinued smoking 10 years before admission), arterial hypertension, hyperlipoproteinemia, peripheral arterial occlusive disease with femoral artery stenting several years prior, and a 50% right-sided internal carotid artery (ICA) stenosis (NASCET criteria) diagnosed 1 year prior. The patient was being treated with metoprolol, simvastatin, and aspirin/dipyridamole. His neurologic examination on admission was within normal limits and thrombolysis was therefore not performed.
Initial cranial CT showed no signs of ischemia (not shown).
Right-hemispheric transient ischemic attack (TIA) in the right middle cerebral artery (MCA) territory with transient sensory deficits of the left arm.
- Was it possible to confirm the 50% (NASCET criteria) right ICA stenosis?
- Was there any stenosis progression?
- If so, what was the grade of stenosis?
Extracranial Duplex Sonography
B-mode sonography revealed generalized atherosclerotic vessel wall thickening. The color-flow image of the right ICA showed a lumen reduction distal to the carotid bifurcation caused by a large anechoic mass. Doppler spectrum analysis in the narrowing revealed a raised flow velocity of 225/99 cm/s with mild flow turbulence. Cross-sectional insonation confirmed a marked reduction of the vessel diameter. Distal of the stenosis, the ICA Doppler spectrum almost normalized (flow velocity: 109/33 cm/s). Blood flow in the common carotid arteries (CCA) was regular and comparable on both sides. There were no pathologic findings in the left ICA (Fig. B1.1, Fig. B1.2, Fig. B1.3, Fig. B1.4, Fig. B1.5; see also Video B1.1).
Contrast-enhanced Harmonic Imaging
For advanced plaque analysis, contrast harmonic imaging was performed. 1 mL SonoVue was injected intravenously into an antecubital vein and the pattern of contrast arrival was analyzed in a longitudinal and cross-sectional imaging plane. Imaging revealed a marked irregular surface within the stenosis with several circumscribed ulcerations which were visible as contrast traces extending into the plaque material (Fig. B1.6 and Video B1.2). (For further reading about contrast-enhanced harmonic imaging see Chapter 1, “Harmonic Imaging and Ultrasound Contrast Agents” under “Imaging Modalities, Parameters, and Settings.”)
Transcranial Duplex Sonography
All detectable intracranial vessels including the ophthalmic arteries (OAs) revealed normal and symmetric flow signals (not shown).
Nearly unchanged right ICA stenosis of 50–60% according to the NASCET criteria (equaling 70–75% using ECST criteria) directly above the carotid bifurcation. The anechoic stenotic material was thought to be a smooth-surfaced “soft plaque” and not a fresh, unorganized intravascular thrombus.
Diffusion-weighted MRI sequences showed an acute right-sided partial territorial MCA infarct of assumed embolic origin within the region of the sensory cortex. No old ischemic lesions were seen. MR angiography (MRA) was not performed (Fig. B1.7).
CT angiography (CTA) showed segmental ICA narrowing with an ulcerated surface directly above the bifurcation. The stenotic segment extended ~2 cm. The calculated grade of stenosis was 73% according to ECST criteria (local stenosis grade) and 54% according to the NASCET criteria (Fig. B1.8, Fig. B1.9, Fig. B1.10). There were no pathologic findings in the distal ICA or the MCA on the affected side.
Fig. B1.1 Extracranial duplex, longitudinal plane. Normal flow signal in the left ICA (flow velocity 62/22 cm/s).
Fig. B1.2 Extracranial duplex, transversal plane, color-mode image. Cross-sectional imaging of the right ICA with marked segmental narrowing caused by nonechogenic material. Left: Diameter reduction assessment, bulb diameter 8.8 mm, residual perfused diameter 2.1 mm resulting in a calculated 76% local-grade stenosis. Right: Identical image but area reduction assessment, bulb area 55 mm2, residual perfused area 10 mm2, resulting in a calculated 82% stenosis.
Fig. B1.3 Extracranial duplex, longitudinal plane, color-mode image. Right ICA with lumen narrowing over a distance of ~2 cm. Note the intrastenotic color aliasing phenomenon, indicating locally raised flow velocity.
Fig. B1.4 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the right ICA with intrastenotic flow velocity of 225/99 cm/s.
Considering the clinical event during best medical treatment, the anechoic high-grade stenosis identified using ultrasound, and the demarcation of a hyperacute ischemia in the corresponding distal intracranial vascular territory, a symptomatic stenosis requiring interventional treatment was diagnosed. Two days after admission, the patient underwent carotid endarterectomy (CEA). Intraoperatively, a soft plaque with an irregular surface was removed (Fig. B1.11). There was no evidence of a fresh thrombus. The operation and postoperative clinical course were uneventful. No further ischemic attacks occurred. Transthoracic echocardiography and a 24-hour electrocardiogram (ECG) were normal.
Symptomatic right-sided high-grade ICA stenosis with a lumen reduction of 70–80% (ECST criteria), corresponding to 50–60% (NASCET criteria) caused by anechoic plaque.
Fig. B1.5 Extracranial duplex, longitudinal plane. Distal right ICA segment with normal flow signal and velocity (109/34 cm/s).
Fig. B1.6 Extracranial duplex, harmonic imaging mode. Left: Longitudinal plane. Right: Cross-sectional plane. White lines delineate the vessel borders. Dotted lines delineate the plaque surface. Note the irregular plaque surface and additional contrast traces reaching into the plaque formation, considered to be additional circumscribed plaque ulcerations (arrows).
Fig. B1.7 MRI, diffusion-weighted imaging, axial imaging plane. Fresh right cortical MCA infarction mainly in the left postcentral gyrus.
Fig. B1.8 CT angiography, sagittal image plane displaying both carotid bifurcations. (A) Left carotid bifurcation with minor vessel wall irregularities without stenosis. (B) Right carotid bifurcation with marked hypodense plaque formation at the bulb of the ICA (arrow).
Clinically, our patient had a transient numbness of his left arm suggestive of a TIA. Though the initial CT scan did not show ischemic infarct demarcation, MRI revealed a fresh embolic territorial MCA infarction assumed to be caused by an artery-to-artery embolism from the right-sided high-grade ICA stenosis.
Symptomatic ICA Stenosis
Atherosclerosis of the ICA is thought to be responsible for ~8% of all ischemic strokes (Flaherty et al 2013). The risk of ischemic stroke increases proportionally with the grade of carotid stenosis. In patients with a symptomatic carotid stenosis >70% (NASCET), the annual risk has been calculated to range from 10% to 15% based on 1990s medical therapy (Barnett et al 1998). Surgical revascularization, first performed in the mid-1950s, is recommended if ICA stenosis is 70% or higher based on the results of two large randomized clinical trials—the North American Symptomatic Carotid Endarterectomy Trial (Barnett et al 1998, NASCET Collaborators 1991) and the European Carotid Surgery Trial (ECST Collaborative Group 1991, 1998). These trials compared CEA with medical treatment. Both trials reported similar results after adjusting for the different stenosis grading methods (Rothwell et al 2003a, 2003b) (for further reading see also Chapter 5, “Grading of ICA Stenosis by Digital Subtraction Angiography” under “Extracranial Pathology”). According to these two trials, which included 5,950 patients with symptomatic ICA stenosis, the number needed to treat (NNT) for preventing one ipsilateral disabling ischemic stroke or death over 2–6 years follow-up was 15 for the >70% (NASCET) or >80% (ECST) ICA stenosis, and 21 for the 50–69% (NASCET) or 70–79% (ECST) ICA stenosis. Patients with milder stenosis did not benefit and the NNT to have a postsurgical disabling stroke or death was 45 (Cina et al 2000).
Fig. B1.9 CT angiography, enlarged image of the right ICA stenosis. (A) Cross-sectional image of the maximal lumen narrowing, corresponding well with the ultrasound derived cross-sectional image in Fig. B1.2. ICA diameter 9.3 mm, residual lumen 2.57 mm, resulting in a calculated local narrowing of 73% (ECST criteria, local stenosis grade). (B) Cross-sectional image of the distal right ICA. Diameter 5.57 mm, resulting in a calculated NASCET lumen reduction of 54%. (C) Longitudinal plane, rotated 90° counterclockwise to correspond with the ultrasound images in Fig. B1.5 and Fig. B1.6. Note the small calcified spots within the plaque (arrows) and contrast undermining the plaque surface (arrowhead), comparable to the ulceration visualized by ultrasound contrast harmonic imaging in Fig. B1.6.
Fig. B1.10 CT angiography. (A) Lateral maximal intensity projection (MIP) reconstruction demonstrating the plaque-induced lumen reduction of the right ICA. (B) Color-inversion and digital removal of surrounding tissue signal, leaving a vessel signal similar to what would have been obtained if digital subtraction angiography (DSA) had been performed. The DSA lumen reduction is 70% according to the ECST criteria (referring to the estimated lumen reduction—dotted line), 50–60% according to the NASCET criteria. Note that the real dimensions of the carotid bulb (continuous line) are larger than estimated. (C) 3D reconstruction of the stenosis.
Fig. B1.11 (A) Intraoperative findings of the right carotid bifurcation before opening of the vessel. (B) Opened bifurcation with visualization of the large soft plaque in situ. (C) Removed plaque formation, the original position illustrated by schematic drawing of the carotid bifurcation. Note the largely irregular plaque surface of the specimen. (D) Final operative findings after patching and vessel closure. (Intra- and postoperative images with kind permission from Dr. Kasper, Department of Vascular Surgery, Charité—Universitätsmedizin Berlin, Germany.)