双侧颈动脉钙化与区域脑葡萄糖代谢相关:心血管风险因素患者 PET/CT 成像的启示

Eric M. Teichner, Robert C. Subtirelu, Shiv Patil, Omar Al-Daoud, Chitra Parikh, Linh Nguyen, Jordan Atary, Andrew Newberg, P. Høilund-Carlsen, Abass Alavi
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引用次数: 0

摘要

背景:心血管疾病是全球疾病和死亡的主要原因,主要是由于动脉粥样硬化。这种疾病会减少器官的血流量和氧气输送,如果影响到颈动脉,就会导致认知障碍和痴呆症。我们对 104 人进行了研究,其中既有健康对照组,也有因已知风险因素而罹患心血管疾病(CVD)的高危人群。我们使用 18F- 氟脱氧葡萄糖(FDG)正电子发射计算机断层成像技术评估脑葡萄糖代谢,并使用 18F- 氟化钠(NaF)正电子发射计算机断层成像技术检测动脉粥样硬化钙化。我们的统计分析表明,健康人和高危人群在特定脑区的代谢活动存在明显差异。在楔回(β = -0.030,SE = 0.014,p = 0.035)、枕中回(β = -0.032,SE = 0.011,p = 0.005)和扣带回后部(β = -0.032,SE = 0.015,p = 0.044)等区域,大脑中的 18F-FDG 摄取与心血管风险的临床评估呈反向变化。相比之下,包括桥基(β = 0.025,SE = 0.012,p = 0.038)和桥脑(β = 0.034,SE = 0.013,p = 0.008)在内的区域表现出直接相关性。值得注意的是,颈动脉 18F-NaF 摄取与小脑(β = -0.825,SE = 0.354,p = 0.021)、延髓(β = -0.888,SE = 0.405,p = 0.029)和扣带回后部(β = -1.253,SE = 0.567,p = 0.028),而颈动脉钙化的增加会影响纺锤回(β = 1.660,SE = 0.498,p = 0.001)和丘脑(β = 1.505,SE = 0.571,p = 0.009)的代谢活动。我们观察到,动脉粥样硬化斑块的积聚,尤其是在颈动脉中的积聚,对支配认知、情绪、感官知觉和运动活动的脑区的代谢变化具有潜在的影响。我们的发现强调了早期干预的可能性,可用于预防或延缓与心血管疾病相关的认知功能衰退。
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Bilateral Carotid Calcification Correlates with Regional Cerebral Glucose Metabolism: Insights from PET/CT Imaging of Patients with Cardiovascular Risk Factors
Background: Cardiovascular disease is a leading cause of illness and death globally, primarily due to atherosclerosis. This disease reduces blood flow and oxygen delivery to organs, and when it affects the carotid arteries, it can lead to cognitive impairment and dementia. In a population of 104 individuals, comprising both healthy controls and individuals at elevated risk for developing cardiovascular diseases (CVD) due to identified risk factors, we used PET imaging with 18F-fluorodeoxyglucose (FDG) to assess cerebral glucose metabolism and 18F-sodium fluoride (NaF) to detect atherosclerotic calcification. Our statistical analysis revealed significant differences in metabolic activity between healthy and at-risk individuals in specific brain regions. 18F-FDG uptake in the brain varied inversely with respect to the clinical assessment of cardiovascular risk in regions such as the cuneus (β = −0.030, SE = 0.014, p = 0.035), middle occipital gyrus (β = −0.032, SE = 0.011, p = 0.005), and posterior cingulate gyrus (β = −0.032, SE = 0.015, p = 0.044). In contrast, areas including the basis pontis (β = 0.025, SE = 0.012, p = 0.038) and the pons (β = 0.034, SE = 0.013, p = 0.008) exhibited direct correlations. Notably, carotid 18F-NaF uptake had inverse associations with 18F-FDG uptake in the cerebellum (β = −0.825, SE = 0.354, p = 0.021), medulla (β = −0.888, SE = 0.405, p = 0.029), and posterior cingulate gyrus (β = −1.253, SE = 0.567, p = 0.028), while increased carotid calcification influenced metabolic activity in the fusiform gyrus (β = 1.660, SE = 0.498, p = 0.001) and globus pallidus (β = 1.505, SE = 0.571, p = 0.009). We observed that atherosclerotic plaque accumulation, especially in the carotid arteries, has potential implications for metabolic changes in brain regions governing cognition, emotion, sensory perception, and motor activities. Our findings underscore the possible early interventions that can be used to preempt or delay cognitive deterioration linked with cardiovascular ailments.
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