Key result
Patients with pulmonary arterial hypertension had significantly stiffer proximal pulmonary arteries compared to healthy controls (median 297 kPa vs 75 kPa, P=0.007).
Why the study?
Previous computational analyses of vascular wall stiffness and hemodynamic parameters in PAH had not considered the interaction between blood flow and wall deformation.
Does patient-specific computational fluid-structure interaction modeling identify differences in pulmonary artery biomechanics in patients with PAH compared to healthy controls?
Observational (n=11)
No
Does patient-specific computational fluid-structure interaction modeling identify differences in pulmonary artery biomechanics in patients with PAH compared to healthy controls?
Absolute Event Rate: 297% vs 75%
p-value: p=0.007
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 ( R t ) and compliance ( C t ) 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 ( R t ; 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 ( C t ; 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.
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Zambrano et al. (2021) conducted an observational in Pulmonary Arterial Hypertension (n=11). Pulmonary Arterial Hypertension vs. Healthy controls was evaluated on Linearized stiffness (E) of the proximal pulmonary artery (p=0.007). Patients with pulmonary arterial hypertension had significantly stiffer proximal pulmonary arteries compared to healthy controls (median 297 kPa vs 75 kPa, P=0.007).
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