Influence of distal resistance and proximal stiffness on hemodynamics and RV afterload in progression and treatments of pulmonary hypertension: a computational study with validation using animal models.

Influence of distal resistance and proximal stiffness on hemodynamics and RV afterload in progression and treatments of pulmonary hypertension: a computational study with validation using animal models.
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DOI:
10.1155/2013/618326
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发表时间:
2013
影响因子:
--
通讯作者:
Hunter KS
Hunter KS
中科院分区:
工程技术4区
文献类型:
--
作者:
Su Z;Tan W;Shandas R;Hunter KS

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我们开发了一个简单的计算模型的基础上,从缺氧的新生小牛模型肺动脉高压(PH)的测量,以探讨血管和心室的措施之间的相互作用,在设置渐进的PH。模型参数直接从体内和体外测量新生小牛。17组模型预测的阻抗和平均肺动脉压(mPAP)显示出良好的协议与动物测量,从而验证模型。接下来,我们考虑了一个预测模型,其中三个参数,PVR,弹性模量(EM)和动脉厚度,从一个模拟到下一个单独变化,以研究它们在PH进展中的各自作用。最后,我们使用该模型来预测临床(血管舒张)和理论(顺应性增加)PH治疗对改善肺血流动力学的个体影响。我们的模型(1)显示了与测量的整体肺参数的良好的患者特异性一致性:(2)PVR与平均压力和PVS与脉压之间的定量关系,以及研究右心室(RV)后负荷,其可以通过肺动脉压力和流量波的频谱分析计算的液压负荷来测量;(3)定性证实了进行性PH中血管壁剪切应力的紊乱;(4)确定通过逆转近端血管重塑的理论治疗降低近端血管刚度可降低RV后负荷。
We develop a simple computational model based on measurements from a hypoxic neonatal calf model of pulmonary hypertension (PH) to investigate the interplay between vascular and ventricular measures in the setting of progressive PH. Model parameters were obtained directly from in vivo and ex vivo measurements of neonatal calves. Seventeen sets of model-predicted impedance and mean pulmonary arterial pressure (mPAP) show good agreement with the animal measurements, thereby validating the model. Next, we considered a predictive model in which three parameters, PVR, elastic modulus (EM), and arterial thickness, were varied singly from one simulation to the next to study their individual roles in PH progression. Finally, we used the model to predict the individual impacts of clinical (vasodilatory) and theoretical (compliance increasing) PH treatments on improving pulmonary hemodynamics. Our model (1) displayed excellent patient-specific agreement with measured global pulmonary parameters; (2) quantified relationships between PVR and mean pressure and PVS and pulse pressure, as well as studiying the right ventricular (RV) afterload, which could be measured as a hydraulic load calculated from spectral analysis of pulmonary artery pressure and flow waves; (3) qualitatively confirmed the derangement of vascular wall shear stress in progressive PH; and (4) established that decreasing proximal vascular stiffness through a theoretical treatment of reversing proximal vascular remodeling could decrease RV afterload.
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