Department of Medicine, Maastricht University Medical Centre, The Netherlands.
J Hypertens. 2012 Apr;30(4):744-52. doi: 10.1097/HJH.0b013e328350a487.
Biomarkers of low-grade inflammation and endothelial dysfunction are associated with cardiovascular disease. Arterial stiffening may be a mechanism through which low-grade inflammation and (or) endothelial dysfunction lead to cardiovascular disease. Therefore, we investigated whether low-grade inflammation and endothelial dysfunction were associated with greater carotid stiffness in a population-based cohort of elderly individuals.
We determined biomarkers of low-grade inflammation (C-reactive protein, serum amyloid A, interleukin 6, interleukin 8, tumour necrosis factor α and soluble intercellular adhesion molecule 1), and of endothelial dysfunction (von Willebrand factor, soluble vascular cell adhesion molecule 1, soluble endothelial selectin, soluble thrombomodulin, soluble intercellular adhesion molecule 1 and flow-mediated dilation), and combined these into mean z-scores (n = 572; women = 286; age 67.5 ± 6.6 years). Additionally, we determined by ultrasonography carotid diameter, distension, pulse pressure and intima-media thickness. Carotid stiffness indices were determined by calculation of the distensibility and compliance coefficient, Young's elastic modulus and β stiffness index.
The study population was characterized by a high prevalence of cardiovascular disease (46%), hypertension (66%) and the use of lipid-lowering (16%) and antihypertensive (34%) medication. After adjustment for the above in addition to sex, age, glucose tolerance status and current smoking, the low-grade inflammation z-score was positively associated with Young's elastic modulus [β (95% confidence interval) 0.080 (0.021-0.139), P = 0.008]. This association was primarily driven through greater diameter. After adjustment for the variables above, the endothelial dysfunction z-score was not associated with carotid stiffness.
These data suggest that low-grade inflammation, in the elderly, plays an important role in carotid artery remodelling and stiffening.
低度炎症和内皮功能障碍的生物标志物与心血管疾病相关。动脉僵硬度可能是低度炎症和（或）内皮功能障碍导致心血管疾病的机制之一。因此，我们研究了在一个基于人群的老年个体队列中，低度炎症和内皮功能障碍是否与颈动脉僵硬度增加相关。
我们测定了低度炎症的生物标志物（C 反应蛋白、血清淀粉样蛋白 A、白细胞介素 6、白细胞介素 8、肿瘤坏死因子 α 和可溶性细胞间黏附分子 1）和内皮功能障碍的生物标志物（血管性血友病因子、可溶性血管细胞黏附分子 1、可溶性内皮选择素、可溶性血栓调节蛋白、可溶性细胞间黏附分子 1 和血流介导的扩张），并将这些生物标志物组合成平均 z 分数（n=572；女性=286；年龄 67.5±6.6 岁）。此外，我们通过超声检查测定颈动脉直径、扩张度、脉搏压和内膜-中层厚度。通过计算顺应性系数、杨氏弹性模量和 β 僵硬度指数来确定颈动脉僵硬度指数。
研究人群的心血管疾病（46%）、高血压（66%）和降脂（16%）及降压（34%）药物的使用率都很高。在校正上述因素以及性别、年龄、葡萄糖耐量状态和当前吸烟状况后，低度炎症 z 分数与杨氏弹性模量呈正相关[β（95%置信区间）0.080（0.021-0.139），P=0.008]。这种相关性主要是通过更大的直径驱动的。在校正上述变量后，内皮功能障碍 z 分数与颈动脉僵硬度无关。
这些数据表明，在老年人中，低度炎症在颈动脉重塑和僵硬中起着重要作用。
