PMC10400896_01
Brain MRI on admission shows hyperintense lesions on diffusion-weighted imaging in the territories of the left middle cerebral artery, including the left putamen, corona radiata, and posterior lobe (A, arrows). Although 3D time-of-flight MRA of his brain does not show any occluded vessel, the intensities of the left middle cerebral artery are decreased (B). 3D time-of-flight MRA of his neck shows severe stenosis at the origin of the left internal cerebral artery with intraplaque high intensities (C, arrows). MRI with T1-weighted black blood methods shows high intensities in the plaques at the left ICA suggesting the presence of intraplaque hemorrhages (D: axial view and E: longitudinal view, arrowheads). ICA: internal carotid artery
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On admission, diffusion-weighted imaging (DWI) of brain MRI showed hyperintense lesions in the left temporal lobe, occipital lobe, putamen, and corona radiata (Fig. 1A). MRA did not show any occluded vessel in his brain, there was severe stenosis at the origin of his left ICA with intraplaque high intensities (Fig. 1B and 1C). MRI with T1-weighted black blood methods showed high intensities in the plaques at the left ICA suggesting intraplaque hemorrhages components (Fig. 1D and 1E). Trial angiography method (Supplementary Fig. 1). Carotid ultrasonography showed severe stenosis, with area stenosis of 98% and peak systolic velocity of greater than 4 m/s at the origin of the left ICA (Supplementary Fig. 2A-2C), and the characteristics of the plaques were hypoechoic, suggesting the presence of soft plaques. Thus, he was diagnosed with atheromatous cerebral embolism due to severe stenosis of the left ICA.
Frontal views during CAS. After the balloon of the 9-Fr Optimo balloon guiding catheter located in the distal left CCA (A) is inflated (B), a FilterWire EZ embolic protection system is advanced to the distal ICA (B, arrow). Pre-stent dilation is performed using a Sterling balloon dilatation catheter 4.0 mm x 40 mm (B). The first stent, Carotid WALLSTENT 6 mm x 22 mm, is placed to cover the stenotic lesion (C). The second stent, CASPER Rx 9 mm x 30 mm, is placed from the ICA to the distal CCA covering the Carotid WALLSTENT (D). An enlarged figure of the stents shows smaller free cell areas by overlapped stents compared with those of CASPER alone (E). Postoperative angiography shows enough dilation of the left ICA with no in-stent plaque protrusion or acute stent thrombosis (F). CAS: carotid artery stenting; CCA: common carotid artery; ICA: internal carotid artery
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Trial angiography method (Supplementary Fig. 1). Carotid ultrasonography showed severe stenosis, with area stenosis of 98% and peak systolic velocity of greater than 4 m/s at the origin of the left ICA (Supplementary Fig. 2A-2C), and the characteristics of the plaques were hypoechoic, suggesting the presence of soft plaques. Thus, he was diagnosed with atheromatous cerebral embolism due to severe stenosis of the left ICA. A 9-Fr Optimo balloon guiding catheter (Tokai Medical Products, Aichi, Japan) was placed in the left CCA via a left femoral artery approach (Fig. 2A). Then, a FilterWire EZ embolic protection system (Boston Scientific, Natick, MA, USA) was carefully navigated to the distal ICA through the stenotic lesion using road-mapping guidance (Fig. 2B). Pre-stent dilation of the stenotic lesion was performed with a Sterling balloon dilatation catheter, 4.0 mm x 40 mm (Boston Scientific) (Fig. 2B). Scientific) was placed to cover the stenotic lesion (Fig. 2C). Second, a double-layer micromesh stent CASPER Rx 9 mm x 30 mm (Terumo, Tokyo, Japan) was deployed from the ICA to the CCA covering the Carotid WALLSTENT from the proximal ICA to the distal CCA (Fig. 2D and 2E). Postoperative angiography showed enough dilation of the left ICA with no in-stent plaque protrusion or acute stent thrombosis (Fig. 2F).
DSA 6 months after the operation shows no in-stent restenosis (A: frontal view and B: lateral view). There is no dislocation between the two stents or migration of the stents (C: frontal view and D: lateral view).
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MRI on postoperative day 1 showed no additional cerebral embolic lesion (Supplementary Fig. 3). The patient's postoperative course was uneventful, and he was discharged without any neurological sequelae on postoperative day 14 on maintenance DAPT with prasugrel 3.75 mg and aspirin 100 mg, and he did not develop any further ischemic events or in-stent restenosis on DSA 6 months after the operation (Fig. 3A-3D).