Karsch K R
Medizinische Klinik, Universität Tübingen.
Herz. 1992 Oct;17(5):309-19.
Aim of this review is, to analyse the current knowledge of the pathogenesis of atherosclerosis from the viewpoint of a clinical cardiologists. All the current ideas about the pathogenesis of atherosclerosis have been derived from the theories of three pathologists. The first was Rokitanski 1852, his theory was somewhat modified by Virchow 1856 and revitalised and modified again by Ross in 1986. All current theories however are based on the term response to injury leading to accelerated atherosclerosis. Following the classification of Stary et al. and the suggestions of the report of the Committee on Vascular Lesions of the Council of Arteriosclerosis the early lesions (Stary class I and II) should be renamed as normal vascular adaptation to physical or chemical causes. These causes include not only shears stress or turbulences due to increased blood pressure but also hypercholesterolemia and certain changes of plasma protein content. The classification of Fuster et al. is mainly dependent on a mechanical injury to the arterial wall induced by the interventional cardiologist. Thus far, it seems questionable, if such a response to injury is indeed the leading mechanism ultimately resulting in advanced arteriosclerosis. In view of the multifactorial processes involved in the pathogenesis of either adaptation or then accelerated arteriosclerosis we have to admit, that our insight is still limited. Thus far, the only lesson to be learned for practising clinicians is that we have to accept that the process of normal adaptation of the vascular arterial wall to the abnormal development of a clinical significant lesion is dynamic and is not well characterized by the response-to-injury theory. We do know that even in the stage of acute coronary syndromes lesion changes are unpredictable. This coincides with the finding from the experimental laboratory that lesion growth is episodic and a result of different stages of activity of the involved cell types and growth factors. Thus, we should avoid looking only for certain stages but rather accept that this is 1. a normal adaptative alteration of the arterial wall which might 2. result in accelerated atherosclerosis due to genetic determination of smooth muscle cells and accumulation of a variety of growth factors.
本综述的目的是从临床心脏病学家的角度分析动脉粥样硬化发病机制的现有知识。目前所有关于动脉粥样硬化发病机制的观点均源自三位病理学家的理论。第一位是罗基坦斯基（1852年），他的理论在1856年被魏尔啸稍加修改，并于1986年由罗斯再次使其复兴并修改。然而，目前所有理论均基于对损伤的反应这一术语，该反应会导致动脉粥样硬化加速。按照斯塔里等人的分类以及动脉硬化理事会血管病变委员会报告的建议，早期病变（斯塔里I级和II级）应重新命名为血管对物理或化学因素的正常适应。这些因素不仅包括因血压升高引起的剪切应力或湍流，还包括高胆固醇血症和血浆蛋白含量的某些变化。福斯特等人的分类主要取决于介入心脏病学家对动脉壁造成的机械损伤。到目前为止，如果这种对损伤的反应确实是最终导致晚期动脉硬化的主要机制，这似乎值得怀疑。鉴于在适应或加速动脉硬化发病机制中涉及多因素过程，我们不得不承认，我们的认识仍然有限。到目前为止，临床医生唯一能学到的教训是，我们必须接受血管动脉壁对具有临床意义的病变异常发展的正常适应过程是动态的，并且损伤反应理论并不能很好地描述这一过程。我们确实知道，即使在急性冠状动脉综合征阶段，病变变化也是不可预测的。这与实验实验室的发现一致，即病变生长是间歇性的，是所涉及细胞类型和生长因子不同活动阶段的结果。因此，我们应避免只关注某些阶段，而应接受这是1. 动脉壁的正常适应性改变，其可能2. 由于平滑肌细胞的基因决定和多种生长因子的积累而导致动脉粥样硬化加速。
