PMC9168307_01
(a) Diffusion-weighted imaging at initial presentation showing a right frontal infarction. (b) Magnetic resonance angiography showing severe stenosis on the right side. (c) Preoperative angiography showing severe right internal carotid stenosis. (d) Angiography after carotid artery stenting.
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F1
Diffusion-weighted imaging revealed multiple small cerebral infarctions spreading cortically and a watershed area in the right brain hemisphere [Figure 1a]. Magnetic resonance angiography revealed severe stenosis of the right internal carotid artery [Figure 1b]. Angiography showed that the stenosis rate was 90%, according to the method used in the North American Symptomatic CEA Trial [Figure 1c]. Although a staged CAS was planned, plaque protrusion occurred just after PTA; therefore, we deployed a closed-cell stent (Carotid WallStent 10 x 24 mm, Boston Scientific, Marlborough, MA, USA) [Figure 1d].
(a) After carotid artery stenting (CAS), the postoperative carotid echography revealed no stenosis. The peak systolic velocity (PSV) was 62.3 cm/s. (b) A carotid echography 4 months after the first CAS showing in-stent restenosis (ISR). The PSV was over 300 cm/s. (c) Angiography showing ISR 4 months after the first CAS. (d) The angiography after percutaneous transcatheter angioplasty and a second CAS were performed.
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F2
Postoperative carotid echography revealed no plaque protrusion and the PSV was 83 cm/s [Figure 2a]. Four months after CAS, a carotid echography revealed that the PSV was over 300 cm/s [Figure 2b]. An open cell stent (Precise 6 x 30 mm, Cordis, Dublin, OH, USA) was deployed and poststenting PTA was performed [Figures 2c and d].
Worsening in-stent restenosis (ISR) after the second carotid artery stenting is shown. The carotid echography revealed peak systolic velocity changes from 139 cm/s (a) to 317 cm/s (b) 6 to 9 months after the second carotid artery stenting. (c and d) The angiography shows severe ISR. (e) The distal end of the stent location at the C2 level is shown.
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F3
Six to 9 months after the second CAS, ISR again worsened; the carotid echography revealed a PSV of 139-317 cm/s [Figures 3a and b]. ISR [Figures 3c-e]. ISR might have developed repeatedly in this patient, despite repeated CAS, and the thickness of the stent might cause ISR.
(a and b) The clear boundary between the plaque, including the stent, and the vessel wall is shown. Normal carotid endarterectomy was performed. (c) Insertion of an internal shunt after removed plaque is shown. (d) The vessel wall could be sutured as normal. (e and f) The stent and plaque are shown. Neointima formed inside the lumen of the stent, causing in-stent restenosis.
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F4
A normal CEA could be performed because the boundary between the plaque (including stent) and the vessel wall was clear [Figures 4a and b]. After the plaque was removed, an internal shunt was inserted [Figure 4c]. The internal shunt was removed and the insertion portion was sutured [Figure 4d]. Although there was atherosclerotic plaque around the stent [Figure 4e], the ISR was caused by neointima formation inside the lumen of the stent, not by plaque protrusion or atherosclerotic change [Figure 4f].