PDF(Pubmed)
Abstract：
Background/Objectives: The underlying mechanism of the potential involvement of inflammatory crosstalk between pericarotid fat and vascular layers in atherosclerosis pathogenesis is unclear. We investigated the association between pericarotid fat density and positive remodeling and inflammatory markers in carotid stenosis. We hypothesized that pericarotid fat density might serve as a marker of plaque inflammation in a clinical setting. Methods: We evaluated the stenosis degree and pericarotid fat density in 258 patients with carotid plaques. Plaque composition was examined, and the correlation between pericarotid fat density and expansive remodeling was investigated. Pearson\'s product-moment correlation coefficient was used to examine the relationship between pericarotid fat density and the expansive remodeling ratio. We also evaluated the relationship of pericarotid fat density with plaque composition, degree of stenosis, and macrophage and microvessel counts by. The subgroup analysis compared these factors between symptomatic mild carotid stenosis. Results: The pericarotid fat density was -63.0 ± 11.1 HU. The carotid fat densities were -56.8 ± 10.4 HU in symptomatic and -69.2 ± 11.4 HU in asymptomatic lesions. The pericarotid fat density values in intraplaque hemorrhage, lipid-rich necrotic core, and fibrous plaque were -51.6 ± 10.4, -59.4 ± 12.8, and -74.2 ± 8.4 HU, respectively. Therefore, the expansive remodeling ratio was 1.64 ± 0.4. Carotid fat density and expansive remodeling ratio were correlated. Immunohistochemistry showed high macrophage and microvessel levels (143.5 ± 61.3/field and 121.2 ± 27.7/field, respectively). In symptomatic mild carotid stenosis, pericarotid fat density was correlated with other inflammatory factors. The pericarotid fat density and expansive remodeling ratio (2.08 ± 0.21) were high in mild stenosis (-50.1 ± 8.4 HU). Conclusions: Pericarotid fat and intraplaque components were well correlated. Carotid fat density may be a marker of plaque inflammation in carotid plaques.
摘要：
背景/目的：颈动脉周围脂肪和血管层之间的炎性串扰可能参与动脉粥样硬化发病的潜在机制尚不清楚。我们研究了颈动脉狭窄中颈动脉周围脂肪密度与阳性重塑和炎症标志物之间的关系。我们假设在临床环境中，颈动脉周脂肪密度可能作为斑块炎症的标志。方法:对258例颈动脉斑块患者的颈动脉狭窄程度及颈动脉周围脂肪密度进行评估。检查斑块成分，探讨颈动脉周围脂肪密度与扩张性重构的相关性。采用皮尔逊积矩相关系数检验颈动脉周脂肪密度与膨胀重构率的关系。我们还评估了颈动脉周围脂肪密度与斑块组成的关系，狭窄程度,巨噬细胞和微血管计数。亚组分析比较了症状性轻度颈动脉狭窄之间的这些因素。结果：颈动脉周围脂肪密度为-63.0±11.1HU。有症状的颈动脉脂肪密度为-56.8±10.4HU，无症状病变为-69.2±11.4HU。斑块内出血的颈动脉周围脂肪密度值，富含脂质的坏死核心，纤维斑块分别为-51.6±10.4、-59.4±12.8和-74.2±8.4HU，分别。因此,膨胀重塑率为1.64±0.4。颈动脉脂肪密度与扩张性重构率相关。免疫组化显示巨噬细胞和微血管水平较高（143.5±61.3/场和121.2±27.7/场，分别)。在有症状的轻度颈动脉狭窄中，颈动脉周围脂肪密度与其他炎症因子相关。轻度狭窄（-50.1±8.4HU）时，颈动脉周围脂肪密度和膨胀重塑率（2.08±0.21）较高。结论：颈动脉周围脂肪与斑块内成分有很好的相关性。颈动脉脂肪密度可能是颈动脉斑块炎症的标志。
