a Department of Neurochemistry, Division of Basic and Applied Neurobiology , Serbsky Federal Medical Research Center of Psychiatry and Narcology , Moscow , Russia.
b Laboratory of Angiopathology , Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences , Moscow , Russia.
Ann Med. 2017 Dec;49(8):661-677. doi: 10.1080/07853890.2017.1366041. Epub 2017 Aug 22.
According to the current paradigm, chronic vascular inflammation plays a central role in the pathogenesis of atherosclerosis. The plaque progression is typically completed with rupture and subsequent acute cardiovascular complications. Previously, the role of adventitial vasa vasorum in atherogenesis was underestimated. However, investigators then revealed that vasa vasorum neovascularization can be observed when no clinical manifestation of atherosclerosis is present. Vasa vasorum is involved in various proatherogenic processes such as intimal accumulation of inflammatory leukocytes, intimal thickening, necrotic core formation, intraplaque haemorrhage, lesion rupture and atherothrombosis. Due to the destabilizing action of the intraplaque microenvironment, lesional vasa vasorum neovessels experience serious defects and abnormalities during development that leads to their immaturity, fragility and leakage. Indeed, intraplaque neovessels are a main cause of intraplaque haemorrhage. Visualization techniques showed that presence of neovascularization/haemorrhage can serve as a good indicator of lesion instability and higher risk of rupture. Vasa vasorum density is a strong predictor of acute cardiovascular events such as sudden death, myocardial infarction and stroke. At present, arterial vasa vasorum neovascularization is under intensive investigation along with development of therapeutic tools focused on the control of formation of vasa vasorum neovessels in order to prevent plaque haemorrhage/rupture and thromboembolism. KEY MESSAGE Neovascularization plays an important role in atherosclerosis, being involved in unstable plaque formation. Presence of neovascularization and haemorrhage indicates plaque instability and risk of rupture. Various imaging techniques are available to study neovascularization.
根据目前的模式，慢性血管炎症在动脉粥样硬化的发病机制中起着核心作用。斑块的进展通常伴随着破裂和随后的急性心血管并发症。以前，人们低估了外膜血管腔在动脉粥样硬化发生中的作用。然而，研究人员随后发现，当没有动脉粥样硬化的临床表现时，也可以观察到血管腔的新生血管化。血管腔参与各种促动脉粥样硬化过程，如炎症白细胞在内膜的堆积、内膜增厚、坏死核心形成、斑块内出血、斑块破裂和动脉血栓形成。由于斑块内微环境的不稳定作用，病变血管腔的新生血管在发育过程中经历严重的缺陷和异常，导致其不成熟、脆弱和渗漏。事实上，斑块内的新生血管是斑块内出血的主要原因之一。可视化技术表明，新生血管/出血的存在可以作为斑块不稳定和破裂风险较高的良好指标。血管腔密度是急性心血管事件（如猝死、心肌梗死和中风）的一个强有力的预测因子。目前，动脉血管腔的新生血管化正在得到深入研究，同时也在开发针对血管腔新生血管形成的治疗工具，以防止斑块出血/破裂和血栓栓塞。
新生血管化在动脉粥样硬化中起着重要作用，参与不稳定斑块的形成。新生血管和出血的存在表明斑块不稳定和破裂的风险。有多种成像技术可用于研究新生血管化。
