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.
Highlights
Pulmonary arterial hypertension (PAH) is a complex cardiovascular disease characterized by a progressive remodeling of the pulmonary arteries
Linearized PA stiffness E was found to be significantly higher in the pulmonary arterial hypertension (PAH) group compared to the control group
The key findings are as follows: (1) the linearized elastic modulus E of the PA is significantly elevated in PAH patients compared to the control subjects, (2) E is directly correlated with the total regurgitant flow in the PA, (3) time-averaged wall shear stress (TAWSS) is inversely associated with the increase in the linearized elastic modulus E in PAH patients, and (4) distal resistances Rt and compliance Ct are, respectively, higher and lower with PAH
Summary
Pulmonary arterial hypertension (PAH) is a complex cardiovascular disease characterized by a progressive remodeling of the pulmonary arteries. This ongoing process, which is promoted by an increase in pulmonary arterial (PA) pressure, leads to right atrial dysfunction (Leng et al, 2019), right ventricular (RV) hypertrophy (Driessen et al, 2018), and impaired ventricular–vascular coupling (Zhao et al, 2019). The end stage of PAH is right heart failure (van der Bruggen et al, 2017), this is driven mainly by pathogenesis of the pulmonary vasculature. There is a pressing need to further understand the mechanisms leading to the progression of disease that can help identifying new biomechanical markers of PAH detection, especially at the earlier stages
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