目的:动脉粥样硬化性心血管疾病的发生和发展,这可能会导致严重的后果,比如心肌梗塞,中风,失去肢体,肾功能衰竭,和肠道梗塞,无论是通过由内而外还是由外而外的途径,都与动脉壁内膜成分的损伤密切相关。作为动脉粥样硬化起始途径的中膜损伤的作用是一个研究不足的领域。本文综述了血管壁损伤的潜在途径以及目前中老年人群的实验和临床研究。包括锻炼的作用,因为这与对中衣媒体的伤害有关。
方法:使用PubMed和GoogleScholar进行了数据库搜索,以查找1909年至2023年之间发表的研究文章,重点是动脉粥样硬化形成的途径和机械力对壁损伤的影响。搜索了以下关键词:墙伤,Tunica媒体,动脉粥样硬化,血管老化,和墙壁应变。研究进行了分析,并从每项研究中提取相关信息。
结果:发现了动脉壁中高机械应力与血管顺应性降低之间的联系。随着年龄的增长,动脉壁的硬化和钙化会引起高血压和脉压,从而引起高血压和心血管疾病。反过来,长时间的高机械应力,特别是壁应变,在剧烈运动中应用于动脉壁,导致中膜硬化和钙化,加速动脉老化,和心血管疾病事件。在这两种情况下,中膜是机械应力的主要目标,也是第一个响应血液动力学变化的目标。这些影响的周期性性质混淆了每种影响的结果,因为它们不是相互排斥的。
结论:压力在中膜中的作用似乎被忽视了,尽管它具有相关性,除了警告剧烈运动在老年人群中的作用外,还需要进一步研究新的初级预防疗法。
The occurrence and development of atherosclerotic cardiovascular disease, which can result in severe outcomes, such as myocardial infarction, stroke, loss of limb, renal failure, and infarction of the gut, are strongly associated with injury to the intimal component of the arterial wall whether via the inside-out or outside-in pathways. The role of injury to the tunica media as a pathway of atherosclerosis initiation is an underresearched area. This review focuses on potential pathways to vessel wall injury as well as current experimental and clinical research in the middle-aged and elderly populations, including the role of exercise, as it relates to injury to the tunica media.
A database search using PubMed and Google Scholar was conducted for research articles published between 1909 and 2023 that focused on pathways of atherogenesis and the impact of mechanical forces on wall injury. The following key words were searched: wall injury, tunica media, atherogenesis, vascular aging, and wall strain. Studies were analyzed, and the relevant information was extracted from each study.
A link between high mechanical stress in the arterial wall and reduced vascular compliance was found. The stiffening and calcification of the arterial wall with aging induce high blood pressure and pulse pressure, thereby causing incident hypertension and cardiovascular disease. In turn, prolonged high mechanical stress, particularly wall strain, applied to the arterial wall during vigorous exercise, results in stiffening and calcification of tunica media, accelerated arterial aging, and cardiovascular disease events. In both scenarios, the tunica media is the primary target of mechanical stress and the first to respond to hemodynamic changes. The cyclical nature of these impacts confounds the results of each because they are not mutually exclusive.
The role of stress in the tunica media appears to be overlooked despite its relevance, and further research into new primary preventive therapies is needed aside from cautioning the role of vigorous exercise in the elderly population.