Mazzolai Lucia, Hayoz Daniel
Service of Vascular Medicien, Department of Internal Medicine, CHUV (Hôpital Nestlé), Av. Pierre Decker 5, 1011 Lausanne, Switzerland.
Curr Hypertens Rep. 2006 Apr;8(1):47-53. doi: 10.1007/s11906-006-0040-9.
Atherosclerosis is an insidious and complex disease of large- and medium-sized arteries. The primum movens of the disease is characterized by co-localization of lipids, inflammatory cells, and fibrous elements within the intima of vessels. Starting as a "fatty streak," the disease evolves over decades into complex lesions that can progress toward a stable or a vulnerable plaque. During the past decade, we have become familiar with the features of the vulnerable plaque; however, the mechanisms that cause a stable plaque to change into a vulnerable lesion with its dramatic clinical outcome still remain largely unknown. There is good evidence from epidemiologic, experimental, and clinical studies that the renin-angiotensin system, via its active peptide angiotensin II, may contribute to atherosclerosis development and progression, not only by increasing blood pressure but also through multiple direct effects. Moreover, recent studies have shown a potential role for angiotensin II as a mediator of plaque vulnerability.
动脉粥样硬化是一种隐匿且复杂的大中型动脉疾病。该疾病的首要动因表现为脂质、炎症细胞和纤维成分在血管内膜中共存。疾病起始于“脂纹”，历经数十年发展为复杂病变，可进展为稳定或易损斑块。在过去十年中，我们已熟知易损斑块的特征；然而，导致稳定斑块转变为具有显著临床后果的易损病变的机制在很大程度上仍不为人知。来自流行病学、实验和临床研究的充分证据表明，肾素-血管紧张素系统通过其活性肽血管紧张素II，不仅可通过升高血压，还可通过多种直接作用，促进动脉粥样硬化的发生和发展。此外，近期研究表明血管紧张素II作为斑块易损性的介质具有潜在作用。
