内侧钙化对动脉力学和血流动力学的影响。

IF 4.7 2区 医学 Q1 NEUROSCIENCES
Pak-Wing Fok, Kun Gou, Brandon Myers, Peter Lanzer
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引用次数: 0

摘要

内侧动脉钙化(MAC)常发生在老化的动脉中,由糖尿病和慢性肾脏疾病促进。晚期MAC是慢性肢体威胁性缺血和肢体截肢的常见原因。通过一维血流动力学模拟,我们研究了随着MAC的发展,钙化动脉组织的力学特性和外周循环中的水力阻力如何共同影响血流动力学。我们发现:(i)与健康动脉相比,钙化动脉的收缩压下降幅度更大,但如果左心室功能完好,这种下降可以被更大的外周阻力抵消;(ii)钙化和外周阻力增强都会导致血流速率降低、外周灌注减少和外周组织低氧血症;(iii)受压的钙化动脉存在比健康动脉更小的管腔区域。即使它们在不加压的时候更大。我们还探讨了正性重塑和血压升高的影响。我们发现,整体管腔扩张降低了钙化动脉的收缩压降和平均压降,同时增加了平均流出率,从而使钙化动脉在流体动力学上表现得更像健康动脉。增加钙化动脉的总压力进一步增强了收缩压和平均压的下降,同时增加了平均流出率。我们的模拟表明,钙化动脉的阻抗增加是由于体内管腔区域变小所致。这可以降低流出率,但由于小动脉闭合、血管几何形状和整体压力的影响,效果变得复杂。这些发现证实了先前报道的钙化动脉血流减少的观察结果。重点:内侧动脉钙化(MAC)常发生在老化的动脉中,由糖尿病和慢性肾脏疾病促进。晚期钙化患者可能因灌注不良而发展为危及肢体的缺血。通过理论建模和模拟,我们发现钙化动脉的流速降低,因为与健康动脉相比,钙化动脉的管腔面积更小。钙化动脉的收缩压降低,而健康动脉的收缩压通常升高。这些发现对MAC的局部检测具有广泛的意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Impact of medial calcification on arterial mechanics and haemodynamics.

Medial arterial calcification (MAC) often occurs in ageing arteries, promoted by diabetes mellitus and chronic kidney disease. Advanced MAC represents a frequent cause of chronic limb-threatening ischaemia and limb amputation. Through a 1D haemodynamics simulation, we study how the mechanical properties of calcified arterial tissue and hydraulic resistance in the peripheral circulation jointly impact haemodynamics as MAC develops. We find that (i) there is a greater drop in systolic pressure across calcified arteries compared to healthy arteries, but this drop can be offset by greater peripheral resistance, provided left ventricular function is intact, (ii) both calcification and enhanced peripheral resistance lead to reduced flow rates, reduced peripheral perfusion and peripheral tissue hypoxaemia, and (iii) pressurized calcified arteries present lumen areas that are smaller than healthy arteries, even though they are larger when unpressurized. We also explore the effects of positive remodelling and elevated blood pressure. We find that a global luminal enlargement reduces the systolic and mean pressure drop across a calcified artery while increasing the mean outflow rate, thereby making a calcified artery behave more like a healthy one, hydrodynamically. Increasing the global pressure in a calcified artery further enhances the drop in systolic and mean pressure while increasing the mean outflow rate. Our simulations suggest that the increased impedance in calcified arteries results from smaller in vivo lumen areas. This can reduce the outflow rate, but the effect is complicated by arteriole closures, vessel geometry and global pressure. These findings confirm previously reported observations of flow reduction in calcified arteries. KEY POINTS: Medial arterial calcification (MAC) often occurs in ageing arteries, promoted by diabetes mellitus and chronic kidney disease. Patients with advanced calcification may develop limb-threatening ischaemia due to malperfusion. Through theoretical modelling and simulation, we find that calcified arteries experience a reduced flow rate because they present smaller lumen areas compared to healthy arteries. Systolic pressure decreases across calcified arteries, whereas in healthy arteries it usually increases. These findings have broad implications for localized detection of MAC.

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来源期刊
Journal of Physiology-London
Journal of Physiology-London 医学-神经科学
CiteScore
9.70
自引率
7.30%
发文量
817
审稿时长
2 months
期刊介绍: The Journal of Physiology publishes full-length original Research Papers and Techniques for Physiology, which are short papers aimed at disseminating new techniques for physiological research. Articles solicited by the Editorial Board include Perspectives, Symposium Reports and Topical Reviews, which highlight areas of special physiological interest. CrossTalk articles are short editorial-style invited articles framing a debate between experts in the field on controversial topics. Letters to the Editor and Journal Club articles are also published. All categories of papers are subjected to peer reivew. The Journal of Physiology welcomes submitted research papers in all areas of physiology. Authors should present original work that illustrates new physiological principles or mechanisms. Papers on work at the molecular level, at the level of the cell membrane, single cells, tissues or organs and on systems physiology are all acceptable. Theoretical papers and papers that use computational models to further our understanding of physiological processes will be considered if based on experimentally derived data and if the hypothesis advanced is directly amenable to experimental testing. While emphasis is on human and mammalian physiology, work on lower vertebrate or invertebrate preparations may be suitable if it furthers the understanding of the functioning of other organisms including mammals.
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