Department of Cardiology and Cardiovascular Surgery, Samara State Medical University, Samara, 443099, Russia.
Department of Histology and Embryology, Samara State Medical University, Samara, 443099, Russia.
Curr Cardiol Rev. 2023;19(2):e170822207573. doi: 10.2174/1573403X18666220817103105.
Due to the fact that atherosclerotic cardiovascular diseases (CVDs) dominate in the structure of morbidity, disability and mortality of the population, the study of the risk factors for the development of atherosclerotic CVDs, as well as the study of the underlying pathogenetic mechanisms thereof, is the most important area of scientific research in modern medicine. Understanding these aspects will allow improving the set of treatment and preventive measures and activities. One of the important risk factors for the development of atherosclerosis, which has been actively studied recently, is air pollution with fine particulate matter (PM 2.5). According to clinical and epidemiological data, the level of air pollution with PM 2.5 exceeds the normative indicators in most regions of the world and is associated with subclinical markers of atherosclerosis and mortality from atherosclerotic CVDs. The aim of this article is to systematize and discuss in detail the role of PM 2.5 in the development of atherosclerosis and myocardial damage with the consideration of epidemiological and pathogenetic aspects. Materials and Methods: This narrative review is based on the analysis of publications in the Medline, PubMed, and Embase databases. The terms "fine particles" and "PM 2.5" in combination with "pathophysiological mechanisms," "cardiovascular diseases", "atherosclerosis", "cardiac troponins", "myocardial damage" and "myocardial injury" were used to search publications. Conclusion: According to the conducted narrative review, PM 2.5 should be regarded as the significant risk factor for the development of atherosclerotic CVDs. The pro-atherogenic effect of fine particulate matter is based on several fundamental and closely interrelated pathophysiological mechanisms: endothelial dysfunction, impaired lipid metabolism, increased oxidative stress and inflammatory reactions, impaired functioning of the vegetative nervous system and increased activity of the hemostatic system. In addition, PM 2.5 causes subclinical damage to cardiac muscle cells by several mechanisms: apoptosis, oxidative stress, decreased oxygen delivery due to coronary atherosclerosis and ischemic damage of cardiomyocytes. Highly sensitive cardiac troponins are promising markers for detecting subclinical myocardial damage in people living in polluted regions.
由于动脉粥样硬化性心血管疾病（CVDs）在人群的发病率、残疾率和死亡率结构中占主导地位，因此研究动脉粥样硬化性 CVDs 的发展风险因素以及研究其潜在的发病机制是现代医学中最重要的科学研究领域。了解这些方面将有助于改善治疗和预防措施及活动。最近，作为动脉粥样硬化发展的一个重要危险因素，细颗粒物（PM 2.5）空气污染受到了积极研究。根据临床和流行病学数据，世界上大多数地区的 PM 2.5 空气污染水平超过了规范指标，与动脉粥样硬化的亚临床标志物和动脉粥样硬化性 CVDs 的死亡率有关。本文的目的是系统地讨论和详细探讨 PM 2.5 在动脉粥样硬化和心肌损伤发展中的作用，并考虑到流行病学和发病机制方面。
本叙述性综述基于对 Medline、PubMed 和 Embase 数据库中出版物的分析。使用了“细颗粒物”和“PM 2.5”这两个术语，并与“病理生理机制”、“心血管疾病”、“动脉粥样硬化”、“心肌钙蛋白”、“心肌损伤”和“心肌损伤”等词结合，来搜索出版物。
根据进行的叙述性综述，PM 2.5 应被视为动脉粥样硬化性 CVDs 发展的重要危险因素。细颗粒物的促动脉粥样硬化作用基于几个基本且密切相关的病理生理机制：内皮功能障碍、脂质代谢受损、氧化应激和炎症反应增加、自主神经功能障碍和止血系统活性增加。此外，PM 2.5 通过几种机制对心肌细胞造成亚临床损伤：细胞凋亡、氧化应激、由于冠状动脉粥样硬化导致的氧输送减少以及心肌细胞的缺血性损伤。高敏心肌钙蛋白是检测生活在污染地区人群亚临床心肌损伤的有前途的标志物。
