Narayan Om, Parker Kim H, Davies Justin E, Hughes Alun D, Meredith Ian T, Cameron James D
aMonash Cardiovascular Research Centre, Monash University, Melbourne, Australia bDepartment of Bioengineering cInternational Centre for Circulatory Health, Imperial College dUCL Institute of Cardiovascular Science, University College, London, UK eMonashHeart, Monash Health, Victoria, Australia.
J Hypertens. 2017 Oct;35(10):2025-2033. doi: 10.1097/HJH.0000000000001424.
The development and propagation of the aortic blood pressure wave remains poorly understood, despite its clear relevance to major organ blood flow and potential association with cardiovascular outcomes. The reservoir pressure model provides a unified description of the dual conduit and reservoir functions of the aorta. Reservoir waveform analysis resolves the aortic pressure waveform into an excess (wave related) and reservoir (compliance related) pressure. The applicability of this model to the pressure waveform as it propagates along the aorta has not been investigated in humans.
We analysed invasively acquired high-fidelity aortic pressure waveforms from 40 patients undergoing clinically indicated coronary catheterization. Aortic waveforms were measured using a solid-state pressure catheter at five anatomical sites: the ascending aorta, the transverse aortic arch, the diaphragm, the level of the renal arteries, and at the aortic bifurcation. Ensemble average pressure waveforms were obtained for these sites for each patient and analysed to obtain the reservoir pressure [Pr(t)] and the excess pressure [Px(t)] at each aortic position.
Systolic blood pressure increased at a rate of 2.1 mmHg per site along the aorta, whereas diastolic blood pressure was effectively constant. Maximum Pr decreased only slightly along the aorta (changing by -0.7 mmHg per site), whereas the maximum of Px increased from the proximal to distal aorta (+4.1 mmHg per site; P < 0.001). The time, relative to the start of systolic upstroke, of the occurrence of the maximum excess pressure did not vary along the aorta. Of the parameters used to derive the reservoir pressure waveform the systolic and diastolic rate constants showed divergent changes with the systolic rate constant (ks) decreasing and the diastolic rate constant (kd) increasing along the aorta.
This analysis confirms the proposition that the magnitude of the calculated reservoir pressure waveform, despite known changes in aortic structure, is effectively constant throughout the aorta. A progressive increase of excess pressure accounts for the increase in pulse pressure from the proximal to distal aorta. The reservoir pressure rate constants seem to behave as arterial functional parameters. The accompanying decrease in ks and increase in kd are consistent with a progressive decrease in aortic compliance and increase in impedance. The reservoir pressure waveform therefore provides a model that might have utility in understanding the generation of central blood pressure and in specific cases might have clinical utility.
尽管主动脉血压波的发展和传播与主要器官的血流明显相关，且可能与心血管疾病的发生有关，但其机制仍未完全明确。血管弹性贮器压力模型对主动脉的双重管道和贮器功能进行了统一描述。贮器波形分析将主动脉压力波形分解为过剩（与波动相关）压力和贮器（与顺应性相关）压力。该模型在人体主动脉压力波形传播过程中的适用性尚未得到研究。
我们对40例因临床需要接受冠状动脉导管插入术患者的主动脉压力波形进行了有创分析。使用固态压力导管在五个解剖部位测量主动脉波形：升主动脉、主动脉弓横部、膈肌、肾动脉水平以及主动脉分叉处。对每位患者这些部位的总体平均压力波形进行分析，以获得每个主动脉位置的贮器压力[Pr(t)]和过剩压力[Px(t)]。
沿主动脉每个部位的收缩压以2.1 mmHg的速率升高，而舒张压基本保持恒定。最大贮器压力沿主动脉仅略有下降（每个部位下降0.7 mmHg），而过剩压力的最大值从主动脉近端向远端升高（每个部位升高4.1 mmHg；P<0.001）。相对于收缩期上升起始点，最大过剩压力出现的时间沿主动脉没有变化。在用于推导贮器压力波形的参数中，收缩期和舒张期速率常数呈现出不同的变化，收缩期速率常数(ks)沿主动脉下降，舒张期速率常数(kd)沿主动脉升高。
该分析证实了以下观点，即尽管已知主动脉结构存在变化，但计算得出的贮器压力波形大小在整个主动脉中实际上是恒定的。过剩压力的逐渐增加导致了从主动脉近端到远端脉压的增加。贮器压力速率常数似乎表现为动脉功能参数。伴随的ks下降和kd升高与主动脉顺应性逐渐降低和阻抗增加相一致。因此，贮器压力波形提供了一个可能有助于理解中心血压产生的模型，在特定情况下可能具有临床应用价值。
