Patient-Specific Computational Analysis of Hemodynamics and Wall Mechanics and Their Interactions in Pulmonary Arterial Hypertension

Abstract

Vascular wall stiffness and hemodynamic parameters are potential biomechanical markers for detecting pulmonary arterial hypertension (PAH). Previous computational analyses, however, have not considered the interaction between blood flow and wall deformation. Here, we applied an established computational framework that utilizes patient-specific measurements of hemodynamics and wall deformation to analyze the coupled fluid–vessel wall interaction in the proximal pulmonary arteries (PA) of six PAH patients and five control subjects. Specifically, we quantified the linearized stiffness (E), relative area change (RAC), diastolic diameter (D), regurgitant flow, and time-averaged wall shear stress (TAWSS) of the proximal PA, as well as the total arterial resistance (Rt) and compliance (Ct) at the distal pulmonary vasculature. Results found that the average proximal PA was stiffer [median: 297 kPa, interquartile range (IQR): 202 kPa vs. median: 75 kPa, IQR: 5 kPa; P = 0.007] with a larger diameter (median: 32 mm, IQR: 5.25 mm vs. median: 25 mm, IQR: 2 mm; P = 0.015) and a reduced RAC (median: 0.22, IQR: 0.10 vs. median: 0.42, IQR: 0.04; P = 0.004) in PAH compared to our control group. Also, higher total resistance (Rt; median: 6.89 mmHg × min/l, IQR: 2.16 mmHg × min/l vs. median: 3.99 mmHg × min/l, IQR: 1.15 mmHg × min/l; P = 0.002) and lower total compliance (Ct; median: 0.13 ml/mmHg, IQR: 0.15 ml/mmHg vs. median: 0.85 ml/mmHg, IQR: 0.51 ml/mmHg; P = 0.041) were observed in the PAH group. Furthermore, lower TAWSS values were seen at the main PA arteries (MPAs) of PAH patients (median: 0.81 Pa, IQR: 0.47 Pa vs. median: 1.56 Pa, IQR: 0.89 Pa; P = 0.026) compared to controls. Correlation analysis within the PAH group found that E was directly correlated to the PA regurgitant flow (r = 0.84, P = 0.018) and inversely related to TAWSS (r = −0.72, P = 0.051). Results suggest that the estimated elastic modulus E may be closely related to PAH hemodynamic changes in pulmonary arteries.

Patient-Specific Computational Analysis of Hemodynamics in Adult Pulmonary Hypertension

“…This limitation was resolved by coupling the hemodynamics with enclosing wall motion using fluid-structure interaction (FSI) simulations. 16,28,29,38,39 One FSI method involved a coupledmomentum model with the assumption of linearized stiffness for the arterial wall, 35,38,39 while Gutierrez et al 9 used small deformation theory. Su et al 28,29 employed idealized geometries.…”

“…A vast majority of modeling studies 5,10,11,16,21,38,39 have dealt with pulmonary arterial hypertension (PAH, WHO group I). However, left heart disease (WHO group II) and lung disease (WHO group III) are causative factors for PH in the majority of diagnosed cases.…”

A Computational Study of Blood Flow Dynamics in the Pulmonary Arteries

“…The PAH is a disease characterized by an elevated resistance in the distal branches of the pulmonary arteries (the microvasculature and the lungs compartment); this condition entails an increase in the working pressure of the right ventricle, possibly causing hypertrophy and failure [ 19 ]. It has been demonstrated that the hemodynamics parameters are significant indicators of PAH; in particular, changes in the right ventricle end-diastolic volume and a decrease of WSS at the proximal part of the pulmonary artery are suggested as a good indicator of PAH severity [ 45 ]. We model the PAH disease by increasing the resistance of microvascolature and lungs compartment: specifically, we quintuplicate the R O U T value with respect to the physiological case choosing .…”

“…11 , the right ventricle pressure-volume loop of both the scenarios. According to the literature the PAH case is characterized by an increase of pressures and volumes [ 19 , 42 , 45 ], corresponding to a decrease of the stroke volume.

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“…This is a restrictive choice because it leads to an overestimation of pressure, velocity and WSS, especially in the distal branches, as found in [ 23 ]; for a simulation including the 3D model of the microvasculature, the fluid-structure interaction approach becomes mandatory. Moreover, the pulmonary arterial stiffness seems to be one of the principal biomechanical markers for the identification of PAH disease [ 45 ], therefore an FSI simulation may give more accurate information about PAH.…”