Three patients had a combination of the symptoms. Mean NIHSS on admission was 4 (min: 0, max: 8). Cerebral Magnetic Resonance Imaging with diffusion-weighted sequences documented the presence of ischemic areas in 7 patients in the corresponding omolateral carotid territory.

All patients presented hemodynamic internal carotid stenosis consistent with the clinical symptoms. Heterogeneous, mostly hypoechoic, complicated plaques were detected find more in all cases. Moreover, high-resolution B-Mode imaging performed with high frequency probes and spatial compound to better visualize plaque surface and texture, demonstrated an extensive rupture of the surface with structure fissurations (Fig. 1), intraoperatively confirmed. Ultrasound B-Mode imaging also allowed the detection of an abnormal motion of the soft parts of the plaques, in particular nearby the sites of plaque rupture. In two cases, real-time B-Mode imaging demonstrated an endothelial floating flap represented by the ruptured cap of the plaque, mobile

in the lumen, and thus confirming the high potential embolic risk of these lesions (Fig. 2). Mobile clots were also visualized from the surface at the site of plaque rupture in two cases (Fig. 3). Contrast ultrasound imaging detected a high density of microvessels in the plaque tissue consisting with relevant neoangiogenesis, as already described elsewhere [2] and [3] in acute symptomatic plaques. Furthermore, contrast ultrasound allowed a better visualization of the plaque extension and surface, better demonstrating INK 128 price the rupture extended deeply from the surface to the core of the plaque. In one

case, a small ulceration with a mobile clot was also identified. All patients were immediately and successfully submitted to CEA: mean NIHSS at discharge was 2 (min: 0, max: 4). Stroke remains a leading cause of disability and death worldwide [4]. About one-third of ischemic strokes arise from carotid atherosclerotic GPX6 plaques, embolization representing the main pathophysiological explanation. For this reason, the identification of vulnerable lesions represents the fundamental step to select patients at risk of cerebrovascular ischemic events from carotid disease where the surgical procedure is indicated. This is a particularly relevant hot topic in literature since optimal management of asymptomatic carotid stenosis still remains controversial [5], while the beneficial effect of CEA is recognized worldwide in symptomatic patients for hemodynamic stenosis. However, the timing of surgery in acute cerebrovascular events is still controversial. At present, early CEA is indeed the most appropriate strategy to prevent further carotid cerebrovascular events.