PMC2911585_01
(a) B-mode ultrasound with color flow Doppler image on the longitudinal display of the carotid plaque with irregular surface. (b) The transverse display of the plaque at the carotid bifurcation. (c) 123I-IMP SPECT transaxial slices of a patient with right ICA stenosis. MR angiography ((d) submental vertical projection; (e) lateral projection) with a hypoplastic or absent anterior and posterior communicating arteries.
SRT2010-602642.001.jpg
PMC2911585_01_SRT2010-602642.001.jpg
fig1
Carotid Doppler ultrasonography demonstrated hypoechoic plaques with an irregular surface at the carotid bifurcation extending to the proximal ICA with stenosis of 83% (by area method) and peak systolic flow velocity at 1.89 m/s (Figures 1(a) and 1(b)). Resting single photon emission CT (SPECT) showed severe hypoperfusion in the right ICA territory (Figure 1(c)), presumably due to less prevalence of collateral flow via the anterior or posterior communicating artery (Figures 1(d) and 1(e)).
(a) Peroperative common carotid angiogram (lateral projection) of a 64-year-old asymptomatic patient with a 60% stenosis of the right ICA by NASCET criteria (arrow). (b) Postoperative MR angiography confirmed disappearance of the stenosis. (c) Axial diffusion-weighted MR imaging of the brain immediately after the occurrence of neurologic events following the DSA. Ipsilateral hyperintense lesions are appreciable at the cortical-subcortical junction of right front-parietal lobes. (d) Postoperative diffusion-weighted imaging indicative of no ischemic lesions associated with CEA. Postoperative MR imagings ((b) and (d)) were performed on the next day after CEA.
SRT2010-602642.002.jpg
PMC2911585_01_SRT2010-602642.002.jpg
fig2
Diffusion-weighted MR imaging showed multiple, small hyperintense lesions in the distal ICA territory of the right front-parietal lobe indicative of an embolic origin from the carotid plaques (Figure 2(c)). The postoperative course was uneventful and the stenosis had improved significantly on follow-up MRA (Figure 2(b)) with no apparent distal embolization (Figure  2(d)).
(a) An intraoperative view of an atheromatous plaque originating from the proximal ICA during CEA with a shunt. (b) Magnified image revealing the sharp laceration of the plaque surface (black arrow) and intraplaque hemorrhage (white arrow). (c) Elastica-Masson stain matching histology cross section of the carotid plaque showing a large lateralized atheroma and intraplaque hemorrhage. A ditch shown in blue arrow suggests a part of the lacerating injury. Asterisks indicate the lumen.
SRT2010-602642.003.jpg
PMC2911585_01_SRT2010-602642.003.jpg
fig3
Fragile atherosclerotic plaque with sharp surface laceration, somewhat different from atheromatous plaque rupture, accompanied by intraplaque hemorrhage was observed at the proximal ICA close to the bifurcation (Figures 3(a) and 3(b)). Microscopic examination of the endarterectomy specimen revealed a large atheromatous plaque with fibrous hypertrophy and intraplaque hemorrhage filled with recent hemorrhagic debris that stained red to brown with Elastica-Masson stain, cholesterol crystal formation, and speckled calcification (Figure 3(c)).