Claridge Martin, Hobbs Simon, Quick Clive, Day Nick, Bradbury Andrew, Wilmink Teun
Department of Vascular Surgery, University of Birmingham, Birmingham Heartlands Hospital, UK.
Vasc Health Risk Manag. 2005;1(2):149-53. doi: 10.2147/vhrm.1.2.149.64082.
Nonsteroidal antiinflammatory drugs (NSAIDS) have been shown to retard aneurysm growth in animal models. In vitro studies have shown an inhibitory effect of NSAIDS on matrix metalloproteinase-9, interleukin-1beta, and IL-6 mediated arterial wall elastolysis. The aim of this study was to investigate the effects of NSAIDs on arterial stiffness, a surrogate marker of elastolysis.
447 subjects enrolled in a community-based abdominal aortic aneurysm (AAA) screening program were assessed for age, blood pressure, smoking status, and drug history. Aortic diameter and stiffness were measured by M-Mode ultrasound. The concentration of the amino-terminal propeptide of type III procollagen was used as a proxy measurement of type III collagen turnover.
NSAID ingestion was significantly (p = 0.006) associated with increased aortic wall stiffness after adjusting for age, aortic diameter, blood pressure, and smoking status. No such effect was seen for beta-blockers, calcium channel antagonists, nitrates, angiotensin-converting enzyme inhibitors, diuretics, or antiplatelet agents.
These novel data show that NSAIDS are associated with increased aortic stiffness, possibly through the effects of cytokine mediated elastolysis. This in turn may prevent aortic expansion and the development of AAA.
在动物模型中，非甾体抗炎药（NSAIDs）已被证明可延缓动脉瘤生长。体外研究表明，NSAIDs对基质金属蛋白酶-9、白细胞介素-1β和IL-6介导的动脉壁弹性蛋白溶解具有抑制作用。本研究的目的是探讨NSAIDs对动脉僵硬度（弹性蛋白溶解的替代标志物）的影响。
对参与社区腹主动脉瘤（AAA）筛查项目的447名受试者进行年龄、血压、吸烟状况和用药史评估。通过M型超声测量主动脉直径和僵硬度。III型前胶原氨基端前肽浓度用作III型胶原周转的替代测量指标。
在调整年龄、主动脉直径、血压和吸烟状况后，NSAIDs摄入与主动脉壁僵硬度增加显著相关（p = 0.006）。β受体阻滞剂、钙通道拮抗剂、硝酸盐、血管紧张素转换酶抑制剂、利尿剂或抗血小板药物未观察到此类效果。
这些新数据表明，NSAIDs与主动脉僵硬度增加有关，可能是通过细胞因子介导的弹性蛋白溶解作用。这反过来可能会阻止主动脉扩张和AAA的发展。
