心力衰竭的左心室重构(第一部分):目前对病理机制和相关心肌功能障碍的理解

T. Chursina, A. Kravchenko, K. Mikhaliev
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引用次数: 1

摘要

目的:对心力衰竭(HF)患者左室重构的各种病理机制及其在心肌功能障碍发生发展中的作用进行文献综述。本文是文献综述的第一部分,对心衰患者左室重构的病理生理研究现状进行了综述。材料和方法。在过去十年中发表的专题科学论文构成了研究材料。研究方法包括文献语义学方法和结构逻辑分析方法。结果和讨论。左室重构是分子、细胞和组织水平复杂变化的结果,影响心肌质量、几何形状和性能,最终导致心衰的发生和进展。左室收缩功能障碍的发生机制多种多样,包括肌节功能缺陷、兴奋-收缩偶联异常和钙稳态异常、离子通道功能障碍、线粒体和代谢异常、心肌细胞生存信号抑制、氧化还原病理生物学、炎症和血管生成不足。术语“左室舒张功能障碍”涵盖左室舒张性、充盈或舒张的改变,无论左室(整体)收缩功能是否正常或异常,也无论患者是否有心衰的临床表现。最新的心衰合并左室舒张功能障碍和左室(整体)收缩功能保留的病理生理学范式认为,全身炎症是心肌结构和功能改变的关键病理机制,由各种心血管和心外条件促进。反过来,全身性炎症促进内皮功能障碍,导致多个终末器官损伤。结论。加深对心衰患者左室重构及相关心肌功能障碍的各种病理机制的认识,是为进一步的基础研究找到新的视角,以及更加合理地设计未来的临床试验的重要前提。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
LEFT VENTRICULAR REMODELING IN HEART FAILURE (PART I): CURRENT UNDERSTANDING OF PATHOMECHANISMS AND RELATED MYOCARDIAL DYSFUNCTION
Aim: to provide a literature review of the current data on various pathomechanisms of left ventricular (LV) remodeling in heart failure (HF) patients and their role in the development and progression of myocardial dysfunction. This paper is a first part of the review, devoted to the current state of pathophysiology of LV remodeling in HF. Material and methods. The thematic scientific papers, published during the last decade, constituted the study material. The research methodology involved bibliosemantic method and structural and logical analysis. Results and discussion. LV remodeling is the result of complex changes at the molecular, cellular and tissue levels, affecting the myocardial mass, geometry and performance, and ultimately leading to HF development and progression. LV systolic dysfunction occurs through the numerous mechanisms, including the defects in sarcomere function, abnormal excitation-contraction coupling and calcium homeostasis, ion channel dysfunction, mitochondrial and metabolic abnormalities, depressed cardiomyocytes survival signaling, redox pathobiology, inflammation and inadequate vasculogenesis. The term «LV diastolic dysfunction» covers the alterations in diastolic distensibility, filling or relaxation of the LV, regardless of whether LV (global) systolic function is normal or abnormal, and regardless of whether the patient has clinical manifestations of HF. The up-to-date pathophysiological paradigm of the development and progression of HF with LV diastolic dysfunction and preserved LV (global) systolic function considers systemic inflammation as a key pathomechanism of structural and functional changes of the myocardium, promoted by various cardiovascular and extracardiac conditions. In its turn, the systemic inflammation promotes endothelial dysfunction, contributing to multiple end-organ damage. Conclusion. The deepening one`s knowledge of various pathomechanisms of LV remodeling and related myocardial dysfunction in HF patients is an important prerequisite for identifying new perspectives on further fundamental research аnd more rational designing of future clinical trials.
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34
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