University of Birmingham Centre for Cardiovascular Sciences, Department of Medicine, City Hospital, Birmingham, England.
J Rheumatol. 2010 Apr;37(4):711-6. doi: 10.3899/jrheum.090699. Epub 2010 Feb 15.
To determine whether abnormalities in microvascular and macrovascular function in rheumatoid arthritis (RA) are associated with plasma markers [von Willebrand factor (VWF)] of endothelial dysfunction and inflammation [C-reactive protein (CRP)] and whether the abnormalities would be altered by treatment. Endothelial dysfunction and inflammation in RA may contribute to adverse cardiovascular events. Although endothelial dysfunction in RA has been demonstrated by altered plasma markers, the relationships with macrovascular and microvascular function are relatively unexplored.
We recruited 66 patients with chronic RA, 48 community controls (CC), and 25 patients with diabetes and hypertension as a disease control group (DC). Subjects had venous blood sampled for plasma markers, and underwent laser Doppler perfusion imaging of forearm skin (to assess microvascular circulation) following acetylcholine and sodium nitroprusside iontophoresis, to assess endothelium-dependent and endothelium-independent responses, respectively. Brachial artery flow-mediated dilatation assessed endothelial dysfunction in a macrovascular bed. A subgroup of 29 patients with RA were assessed pretherapy and after 2-4 weeks of antirheumatic therapy.
As expected, patients with RA had higher CRP, erythrocyte sedimentation rate (ESR), and VWF. Endothelium-independent vasoreactivity was abnormal in RA, and this correlated negatively with CRP. All aspects of microvascular function were abnormal in the DC compared to the CC. Macrovascular function was preserved in RA but was abnormal in the DC group. Four weeks of antiinflammatory therapy reduced CRP and ESR but had no effect on any vascular function index in the patients with RA.
Patients with RA have abnormal endothelium-independent microvascular function that correlates with inflammation but is not altered by short-term antiinflammatory therapy.
确定类风湿关节炎 (RA) 中小血管和大血管功能的异常是否与内皮功能障碍和炎症的血浆标志物 [血管性血友病因子 (VWF)] 和 [C 反应蛋白 (CRP)] 相关,以及这些异常是否会因治疗而改变。RA 中的内皮功能障碍和炎症可能导致不良心血管事件。尽管 RA 中的内皮功能障碍已通过改变的血浆标志物得到证实,但与大血管和微血管功能的关系尚未得到充分探讨。
我们招募了 66 名慢性 RA 患者、48 名社区对照者 (CC) 和 25 名糖尿病和高血压患者作为疾病对照组 (DC)。受试者抽取静脉血进行血浆标志物检测,并在乙酰胆碱和硝普钠离子电渗作用下进行前臂皮肤激光多普勒灌注成像,以分别评估微血管循环和内皮依赖性和非依赖性反应。肱动脉血流介导的扩张评估大血管内皮功能障碍。RA 患者的亚组在接受抗风湿治疗前和 2-4 周后进行评估。
正如预期的那样,RA 患者的 CRP、红细胞沉降率 (ESR) 和 VWF 较高。RA 患者的内皮非依赖性血管反应异常,与 CRP 呈负相关。与 CC 相比,DC 组的所有微血管功能方面均异常。RA 患者的大血管功能正常,但 DC 组异常。4 周的抗炎治疗降低了 CRP 和 ESR,但对 RA 患者的任何血管功能指标均无影响。
RA 患者存在异常的内皮非依赖性微血管功能,与炎症相关,但短期抗炎治疗不能改变这种功能。