Neelakantan Sunder, Mendiola Emilio A, Zambrano Byron, Vang Alexander, Myers Kyle J, Zhang Peng, Choudhary Gaurav, Avazmohammadi Reza
Department of Biomedical Engineering Texas A&M University College Station Texas USA.
J. Mike Walker'66 Department of Mechanical Engineering Texas A&M University College Station Texas USA.
Bioeng Transl Med. 2025 Jun 26;10(4):e70035. doi: 10.1002/btm2.70035. eCollection 2025 Jul.
Pulmonary hypertension (PH) is defined as an elevation in the right ventricular (RV) afterload, characterized by increased hemodynamic pressure in the main pulmonary artery (PA). Elevations in RV afterload increase RV wall stress, resulting in RV remodeling and potentially RV failure. From a biomechanical standpoint, the primary drivers for RV afterload elevations include increases in pulmonary vascular resistance (PVR) in the distal vasculature and decreases in vessel compliance in the proximal arteries. However, the individual contributions of the various vascular remodeling events toward the progression of PA pressure elevations and altered vascular hemodynamics remain elusive. In this study, we used a subject-specific one-dimensional (1D) fluid-structure interaction (FSI) model to investigate the alteration of pulmonary hemodynamics in PH and to quantify the contributions of decreased compliance and increased resistance toward increased main pulmonary artery (MPA) pressure. We used a combination of subject-specific hemodynamic measurements, ex-vivo mechanical testing and histological analysis of arterial tissue specimens, and ex-vivo x-ray micro-tomography imaging to develop the 1D FSI model and dissect the contribution of PA remodeling events toward alterations in the MPA pressure waveform. Both the amplitude and pulsatility of the MPA pressure waveform were analyzed. Our results indicated that increased distal resistance has the greatest effect on the increase in maximum MPA pressure, while decreased vessel compliance caused significant elevations in the characteristic impedance. The method presented in this study will serve as an essential step toward understanding the complex interplay between PA remodeling events that lead to the most adverse effect on RV function.
肺动脉高压（PH）被定义为右心室（RV）后负荷升高，其特征是主肺动脉（PA）血流动力学压力增加。RV后负荷升高会增加RV壁应力，导致RV重塑，并可能引发RV衰竭。从生物力学角度来看，RV后负荷升高的主要驱动因素包括远端血管系统中肺血管阻力（PVR）增加以及近端动脉血管顺应性降低。然而，各种血管重塑事件对PA压力升高和血管血流动力学改变进展的具体贡献仍不明确。在本研究中，我们使用特定个体的一维（1D）流固耦合（FSI）模型来研究PH患者肺血流动力学的改变，并量化顺应性降低和阻力增加对主肺动脉（MPA）压力升高的贡献。我们结合特定个体的血流动力学测量、动脉组织标本的体外力学测试和组织学分析以及体外X射线显微断层扫描成像来建立1D FSI模型，并剖析PA重塑事件对MPA压力波形改变的贡献。同时分析了MPA压力波形的幅度和搏动性。我们的结果表明，远端阻力增加对MPA最大压力升高的影响最大，而血管顺应性降低导致特征阻抗显著升高。本研究中提出的方法将是理解导致对RV功能产生最不利影响的PA重塑事件之间复杂相互作用的重要一步。
