| Stroke is a leading cause of morbidity and mortality in worldwide. Atherosclerosis is very important pathology of cerebrovascular disease. Most of the acute cerebrovascular accident was due to atherosclerotic vulnerable plaque rupture secondary thrombosis. An atherosclerotic plaque begins to develop as a result of damage/insult/hypoxia to the endothelial cells of the vascular system. As atherosclerosis progresses, reduced oxygen diffusion diminishes the nutrient supply reaching the arterial wall, resulting in hypoxia. Reactive physiologic compensation causes a thickening of the intima-media complex exceeding the oxygen diffusion threshold, inducing ischemia, which then triggers a continual release of angiogenic growth factors. It is believed that the absence of pericytes in some angiogenic vessels causes these immature vessels to "leak" potentially noxious and inflammatory plasma components into the extracellular matrix of the media/intima, increasing plaque volume. The ongoing deposit of plasma components appears to further reduce vessel wall oxygen diffusion, triggering continued growth of an- giogenesis. Ultimately, the plaque is enveloped in luxurious adventitial vasa vasorum and intraplaque neovascularization,a hallmark of symptomatic atherosclerosis. vulnerable plaque is easy to thrombosis and rupture. They have the following features:A thin layer of fibrous cap within the coverage of lipid core; a large number of inflammatory cells, less smooth muscle cells in it; surrounded by a wealth of nourishing blood vessels and angiogenesis. Vulnerable plaque is one of the important characteristics of neovascularization and is enveloped in luxurious adventitial vasa vasorum. The high lipid permeability of intraplaque neovascularization is one of the important deposited channels to make atherosclerotic plaque gradually increased, as in large fibrous cap covering the case, the plaque build-up can still be in the lipid. Neovascular inflammatory cells into the plaque also provided a channel. Inflammatory cells can produce cytokines, activate macrophages and smooth muscle cells and to generate the matrix metalloproteinases, which can degrade matrix, weaken the fibrous cap, leading to loss of stability of the plaque. Therefore, it is very important to detect intraplaque neovascularization.At present, MRI can be used to evaluate plaque neovascularization. As the fiber composition and lipid plaque components have different signal intensity area. So, MRI can diagnose vulnerable plaque. However, patients remain stationary longer period for inspection, any point moving in scanning region lead to the image dislocation, and their fees would be more expensive ultrasound examination. Advances in contrast material-enhanced ultrasonography(US) may allow for detection of neovascularization within atherosclerotic plaque. This technique takes advantage of the high spatial and temporal resolution of vascular US and of the properties of contrast agent microbubbles, which behave as pure intravascular tracers.Therefore, contrast-enhanced ultrasound examination can identify luxurious adventitial vasa vasorum and plaque neovascularization. Ultrasound can real-time observe the blood supply of the organization and provides a non-invasive examination methods for evaluating the stability of plaque. Although several histologic studies showed that more extensive plaque neovascularization is associated with clinically symptomatic disease, the association between the carotid plaque enhancement with contrast agent microbubbles and clinical symptoms is not fully understood. Therefore, our study was undertaken to correlate the degree of plaque enhancement obtained by using contrast agent microbubbles with clinical symptoms in patients with carotid atherosclerotic plaque. This study included three parts as follow: part 1 Correlation between plaque features and clinical symptomsThe purpose of this part to evaluated correlation between plaque features and clinical symptoms by two-dimensional plaque feature. Carotid US was performed with an ultrasound machine (Logiq 9; GE Healthcare,Milwaukee, Wis) by using a 9-L probe with transmission frequency of 6-8 MHz. Examination of 104 patients with carotid artery atherosclerotic plaque, including 35 patients with acute cerebrovascular disease,69 patients without acute cerebrovascular disease. Plaques were characterized by their appearance on standard US images and were classified according to widely used criteria as follows:(a) soft plaques, whose echogenicity was less than that of the surrounding adventitia for more than 80% of the plaque area, without acoustic shadowing; (b) hard plaques, whose echogenicity was greater than or equal to that of the surrounding adventitia for more than 80% of the plaque area, without acoustic shadowing; (c) calcified plaques, which contained more than 90% of circumferential calcification, showing as bright echoes within the plaque along with acoustic shadowing; or (d) mixed plaques, which contained less than 90% of circumferential calcification or had associating echodense and anechoic regions occupying less than 80% of the plaque area. plaque that was at least 2 mm deep and 2mm long and had a well-defined back at its base. Standard carotid US depicted 133 plaques in 104 patients.Multiple plaques were found in 27 patients. Plaque thickness did not significantly differ between symptomatic and asymptomatic patient (2.86mm±0.96vs3.00mm±0.88, p=0.45). The percentage of soft plaque in the symptomatic patients was significantly greater than that in the asymptomatic patients[(26 (74) vs26 (38) p=0.001)]. The percentage of plaque ulceration in the symptomatic group was not significantly different from that in the asymptomatic group [8 (23) vs11 (16) p=0.43)].part 2 Correlation between plaque echogenicity and intraplaque neovascularizationThe purpose of this part to evaluated correlation between plaque echogenicity and intraplaque neovascularization. Carotid US was performed with an ultrasound machine (Logiq 9; GE Healthcare,Milwaukee, Wis) by using a 9-L probe with transmission frequency of 6-8 MHz. Examination of 104 patients with carotid artery atherosclerotic plaque. Plaques were characterized by their appearance on standard US images and were classified according to widely used criteria as follows:(a) soft plaques, whose echogenicity was less than that of the surrounding adventitia for more than 80% of the plaque area, without acoustic shadowing; (b) hard plaques, whose echogenicity was greater than or equal to that of the surrounding adventitia for more than 80% of the plaque area, without acoustic shadowing; (c) calcified plaques, which contained more than 90% of circumferential calcification, showing as bright echoes within the plaque along with acoustic shadowing; or (d) mixed plaques, which contained less than 90% of circumferential calcification or had associating echodense and anechoic regions occupying less than 80% of the plaque area. Soft plaques had a significantly higher proportion of contrast enhancement compared with the other types of plaques (P<0.01). The enhanced intensity in the plaque (13.1dB±5.6) and the ratio in the soft plaques (0.51±0.20) were significantly higher than those in the other three types of plaques (all P values<0.05). No significant correlation was found between plaque thickness and enhanced intensity in the plaque (P =0.26) and the ratio of the enhanced intensity (P=0.13).Part 3 Correlation between contrast enhancement of plaque and symptomsTo evaluate the relationship between enhancement of carotid atherosclerotic plaques and the symptoms by contrast-enhanced ultrasonography with SonoVue.104 patients with carotid atherosclerotic plaques were examined with contrast-enhanced ultrasonography. The post-enhancement peak intensity in the plaque, ratio of enhanced intensity in the plaque to that in the lumen of the carotid artery were measured and calculated from the time-intensity curve. Receiver-operating characteristic curves were constructed to evaluate the accuracy of enhancement of atherosclerotic plaques in predicting acute cerebrovascular disease. Among the 104 patients,35 had transient ischemic attack and/or cerebrovascular ischemic stroke. Plaque enhancement was found in 28 (80%) of 35 symptomatic patients and in 21 (30%) of 69 asymptomatic patients (P<0.001). Enhanced intensity in the plaque (13.9 dB±6.4) and the ratio of enhanced intensity in the plaque to that in the lumen of the carotid artery (0.54±0.23) in symptomatic patients were significantly greater than those in asymptomatic patients (8.8 dB±5.2 [P<0.001] and 0.33±0.19 [P<0.001], respectively). Sensitivity and specificity were 74% and 62%, respectively, for enhanced intensity in the plaque (cutoff value,10.0 dB) and 74% and 75%, respectively, for ratio of enhanced intensity in the plaque to that in the lumen of the carotid artery (cutoff value,0.46). Conclusion:1. Contrast-enhanced carotid US allows assessment of neovascularization within plaque.2. Symptomatic patients had more intense contrast enhancement in plaque than asymptomatic patients,3. Contrast-enhanced carotid US may be used as method for plaque risk stratification...
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