安博维抗动脉粥样硬化作用ppt课件.ppt

SILVHIA研究是一项随机、双盲、平行试验。入选102例有轻中度高血压和左室肥厚患者，随机接受平均安博维? 251mg/天或阿替洛尔69mg/天，探索安博维?对患者颈总动脉内膜中层厚度(CCA-IMT)的作用。 研究结果显示：48周后，安博维?组平均降低颈总动脉内膜中层厚度达0.01mm，阿替洛尔组则平均增加0.03mm，两组具有统计学差异。 临床研究证实：安博维?可延缓颈动脉内膜中层厚度增厚。 * * SLIDE highlighting endothelial dysfunction * SLIDE 12 Inflammation Oxidative stress within the endothelium triggers a range of inflammatory responses: A range of adhesion molecules such as vascular cell adhesion molecule (VCAM-1), intracellular adhesion molecule (ICAM-1) and various selectins are expressed, causing adhesion of leukocytes to the endothelial surface.1 Leukocyte adhesion and invasion of the endothelium significantly exacerbates the inflammatory response.1,2 A battery of inflammatory molecules is released by the endothelial cells and invading monocytes and macrophages. These include inflammatory cytokines such as IL-6, chemokines such as monocyte chemoattractant protein (MCP) and inflammatory molecules such as superoxides.1-3 Matrix metalloproteinases (MMPs) are dysregulated, causing derangement of extracellular matrix deposition.1 Atherogenic inflammation is driven by a range of processes: Depletion of NO is one major contributory factor since this key endothelial regulator has anti-inflammatory effects.4 Systemic and local RAAS activation also drives vascular inflammation by a variety of mechanisms, including the induction of adhesive molecule expression on endothelial cells, leucocytes and platelets.1,2 Once the inflammatory process is initiated it becomes a self-sustaining process, with a range of cytokines driving the response and attracting further inflammatory cells to the site of injury. A large range of markers are available to assess endothelial inflammation. These include: Inflammatory cytokines such as IL-6 and TNF-alpha Anti-inflammatory cytokines such as IL-10 Inflammatory proteins such as high sensitivity C-reactive protein (hsCRP) Adhesive molecules such as VCAM-1 Monocyte binding assays MMP expression References 1. Strawn WB, F