Walter S. Speidl, MD Universitätsklinik für Innere Medizin II - klinische Abteilung für Kardiologie, Medizinische Universität Wien Währingergürtel 18-20, 1090 Wien, Austria, Tel. +43/1/404 00 46 14; Fax +43/1/404 00 42 16, E-mail:
Hamostaseologie. 2013;33(4):269-82. doi: 10.5482/HAMO-13-07-0039. Epub 2013 Sep 17.
Cardiovascular diseases remain to be the leading cause of death in Western societies. Despite major findings in vascular biology that lead to a better understanding of the pathomechanisms involved in atherosclerosis, treatment of the disease has only changed slightly within the last years. A big body of evidence suggests that atherosclerosis is a chronic inflammatory disease of the vessel wall. Accumulation and peroxidation of LDL-particles within the vessel wall trigger a strong inflammatory response, causing macrophage and T-cell accumulation within the vessel wall. Additionally, B-cells and specific antibodies against LDL-particles, as well as the complement system are implicated in atherogenesis. Besides data from clinical trials and autopsy studies it was the implementation of mouse models of atherosclerosis and the emerging field of direct gen-modification that lead to a thorough description of the pathophysiological mechanisms involved in the disease and created overwhelming evidence for a participation of the immune system. Recently, the cross-talk between coagulation and inflammation in atherogenesis has gained attention. Serious limitations and disparities in the pathophysiology of atherosclerosis in mice and men complicated the translation of experimental data into clinical practice. Despite these limitations, new anti-inflammatory medical therapies in cardiovascular disease are currently being tested in clinical trials.
心血管疾病仍然是西方社会的主要死亡原因。尽管血管生物学的重大发现使人们更好地了解了动脉粥样硬化相关的病理机制，但近年来该疾病的治疗方法仅略有改变。大量证据表明，动脉粥样硬化是血管壁的一种慢性炎症性疾病。LDL 颗粒在血管壁中的积累和过氧化会引发强烈的炎症反应，导致巨噬细胞和 T 细胞在血管壁中积聚。此外，B 细胞和针对 LDL 颗粒的特异性抗体以及补体系统也与动脉粥样硬化的发生有关。除了临床试验和尸检研究的数据外，动脉粥样硬化小鼠模型的实施和新兴的直接基因修饰领域也导致了对涉及该疾病的病理生理机制的全面描述，并为免疫系统的参与提供了压倒性的证据。最近，动脉粥样硬化发病机制中的凝血和炎症之间的相互作用引起了关注。小鼠和人类动脉粥样硬化的病理生理学存在严重的局限性和差异，这使得将实验数据转化为临床实践变得复杂。尽管存在这些局限性，但目前正在临床试验中测试心血管疾病的新型抗炎医学疗法。
