Laboratory of Hemodynamics and Cardiovascular Technology, Ecole Polytechnique Fédérale de Lausanne, EPFL STI IBI-STI LHTC, BM 5128, Station 17, 1015 Lausanne, Switzerland.
Ann Biomed Eng. 2012 Mar;40(3):742-9. doi: 10.1007/s10439-011-0443-x. Epub 2011 Oct 21.
Decrease in arterial compliance leads to an increased pulse pressure, as explained by the Windkessel effect. Pressure waveform is the sum of a forward running and a backward running or reflected pressure wave. When the arterial system stiffens, as a result of aging or disease, both the forward and reflected waves are altered and contribute to a greater or lesser degree to the increase in aortic pulse pressure. Two mechanisms have been proposed in the literature to explain systolic hypertension upon arterial stiffening. The most popular one is based on the augmentation and earlier arrival of reflected waves. The second mechanism is based on the augmentation of the forward wave, as a result of an increase of the characteristic impedance of the proximal aorta. The aim of this study is to analyze the two aforementioned mechanisms using a 1-D model of the entire systemic arterial tree. A validated 1-D model of the systemic circulation, representative of a young healthy adult was used to simulate arterial pressure and flow under control conditions and in presence of arterial stiffening. To help elucidate the differences in the two mechanisms contributing to systolic hypertension, the arterial tree was stiffened either locally with compliance being reduced only in the region of the aortic arch, or globally, with a uniform decrease in compliance in all arterial segments. The pulse pressure increased by 58% when proximal aorta was stiffened and the compliance decreased by 43%. Same pulse pressure increase was achieved when compliance of the globally stiffened arterial tree decreased by 47%. In presence of local stiffening in the aortic arch, characteristic impedance increased to 0.10 mmHg s/mL vs. 0.034 mmHg s/mL in control and this led to a substantial increase (91%) in the amplitude of the forward wave, which attained 42 mmHg vs. 22 mmHg in control. Under global stiffening, the pulse pressure of the forward wave increased by 41% and the amplitude of the reflected wave by 83%. Reflected waves arrived earlier in systole, enhancing their contribution to systolic pressure. The effects of local vs. global loss of compliance of the arterial tree have been studied with the use of a 1-D model. Local stiffening in the proximal aorta increases systolic pressure mainly through the augmentation of the forward pressure wave, whereas global stiffening augments systolic pressure principally though the increase in wave reflections. The relative contribution of the two mechanisms depends on the topology of arterial stiffening and geometrical alterations taking place in aging or in disease.
动脉顺应性下降会导致脉搏压升高，这可以用风箱效应来解释。压力波是正向运行压力波和反向运行或反射压力波的总和。当动脉系统因衰老或疾病而变硬时，正向波和反射波都会发生变化，并在一定程度上导致主动脉脉搏压升高。文献中提出了两种机制来解释动脉僵硬导致的收缩期高血压。最流行的一种机制基于反射波的增强和更早到达。第二种机制是由于近端主动脉特征阻抗增加，导致正向波增强。本研究旨在使用整个系统动脉树的一维模型分析上述两种机制。使用代表年轻健康成年人的系统循环的经过验证的一维模型，在控制条件下和存在动脉僵硬的情况下模拟动脉压力和流量。为了帮助阐明导致收缩期高血压的两种机制的差异，通过仅在主动脉弓区域减小顺应性或通过在所有动脉段均匀减小顺应性来局部或全局地使动脉树变硬。当近端主动脉变硬且顺应性降低 43%时，脉搏压增加 58%。当全局变硬的动脉树的顺应性降低 47%时，达到相同的脉搏压增加。在主动脉弓局部变硬的情况下，特征阻抗增加到 0.10mmHg s/mL，而对照为 0.034mmHg s/mL，这导致正向波的幅度大幅增加（91%），达到 42mmHg，而对照为 22mmHg。在全局变硬的情况下，正向波的脉搏压增加 41%，反射波的幅度增加 83%。反射波在收缩期更早到达，增加了它们对收缩压的贡献。使用一维模型研究了动脉树局部和全局顺应性丧失的影响。近端主动脉的局部僵硬主要通过正向压力波的增强来增加收缩压，而全局僵硬则主要通过波反射的增加来增加收缩压。这两种机制的相对贡献取决于动脉僵硬的拓扑结构和衰老或疾病中发生的几何变化。
