Simon F, Oberhuber A, Floros N, Düppers P, Schelzig H, Duran M
1Department of Vascular and Endovascular Surgery, Düsseldorf University, Moorenstr. 5, 40225 Düsseldorf, Germany.
Network for Fundamental Research in Vascular Medicine (Netzwerk Gefäßmedizinische Grundlagenforschung, NGG), Düsseldorf, Germany.
Gefasschirurgie. 2018;23(Suppl 1):13-18. doi: 10.1007/s00772-018-0380-1. Epub 2018 Apr 10.
Chronic ischemia of the lower extremities is an everyday problem in vascular surgery clinics. In Germany, approximately 3% of all hospitalizations are due to peripheral artery disease (PAD), with critical limb ischemia (CLI) in particular showing a rapid increase. The consequences of chronic undersupply range from reduced walking distance to loss of limbs. At the beginning there are stress factors, such as hyperlipidemia (LDL), free radicals, arterial hypertension, infections or subclinical inflammation that interfere with endothelial homeostasis and cause endothelial dysfunction with increased permeability. Cells of the immune system are attracted and migrate into the vascular wall, where they lead to the degradation of matrix components and destabilization of the plaque. By changing the phenotype of smooth muscle cells and macrophages towards osteoclast-like cells, bone-like hardening of the vessel wall takes place. Above a vessel wall thickness of approximately 100 µm, hypoxia-induced factor (HIF-1α) is intensified by the lack of oxygen, which leads to an increase in growth factors, such as vascular endothelial growth factor (VEGF). This promotes angiogenesis, but it is not sufficient to compensate for a stenosed artery. Arteriogenesis refers to the growth of existing collateral vessels. The driving forces are the pressure gradient before and after the stenosis and the shear forces acting on the vessel walls. In the case of progressive stenosis, the compensatory capacities can be overtaxed and a manifest hypoxia in the tissue with regression of the obtained vascular structures and tissue atrophy occurs.
下肢慢性缺血是血管外科诊所中常见的问题。在德国，所有住院病例中约3%是由外周动脉疾病（PAD）引起的，其中严重肢体缺血（CLI）尤其呈快速上升趋势。慢性供血不足的后果从行走距离缩短到肢体丧失不等。起初存在一些应激因素，如高脂血症（低密度脂蛋白）、自由基、动脉高血压、感染或亚临床炎症，这些因素会干扰内皮稳态，导致内皮功能障碍，通透性增加。免疫系统细胞被吸引并迁移到血管壁，在那里它们导致基质成分降解和斑块不稳定。通过将平滑肌细胞和巨噬细胞的表型转变为破骨细胞样细胞，血管壁会发生骨质样硬化。当血管壁厚度超过约100μm时，缺氧诱导因子（HIF-1α）会因缺氧而增强，这会导致血管内皮生长因子（VEGF）等生长因子增加。这促进了血管生成，但不足以补偿狭窄的动脉。动脉生成是指现有侧支血管的生长。驱动力是狭窄前后的压力梯度以及作用于血管壁的剪切力。在进行性狭窄的情况下，代偿能力可能会不堪重负，组织中会出现明显的缺氧，已形成的血管结构会退化，组织会萎缩。
