Assessment of Pulmonary Vascular Impedance in Patients With Severe Pulmonary Arterial Hypertension

Introduction Pulmonary arterial hypertension (PAH) is characterized by progressive pulmonary vascular remodeling. Pulmonary vascular impedance (PVZ) provides a comprehensive view of pulmonary arterial function. We hypothesized that functional vascular remodeling significantly alters pulsatile pulmonary hemodynamics and PVZ in severe PAH. Methods Participants with a right heart catheterization (RHC) and an echocardiogram including right ventricular outflow tract (RVOT) images (delay: 24 [5–76] days) were identified from the University of Arizona PH registry. Participants were split using the World Symposium PH classifications and PVR (mild: < 3.9WU, Moderate: 3.9–8.5WU and Severe: > 8.5WU). PVZ was calculated in the frequency domain using pulmonary artery (PA) pressure and RVOT‐PA flow profiles. Impedance measures of resistance ( Z 0 ), global stiffness ( Z 1 ) and proximal stiffness ( Z C , average Z 2‐4Hz ) were derived. To evaluate proximal arterial mechanics, we used the Z c‐mPAP relationship to distinguish pressure‐dependent from stiffness‐related changes on Z C . Data were presented as median [interquartile range]. Results Forty‐eight subjects were identified (Control (mPAP < 25 mmHg): n = 8 and WSPH1: n = 40). Z 0 and Z C were significantly increased in WSPH1 compared to Control ( p < 0.05). Z 0 , Z 1 , and Z C were increased in WSPH1‐severe compared WSPH1‐mild and WSPH1‐moderate ( p < 0.05). All impedance parameters correlated with end‐systolic elastance (Ees) and arterial elastance (Ea, p < 0.05) but only Z 0 correlated with Ees/Ea ( p < 0.05). Z C ‐mPAP relationships were modeled for Control and WSPH groups using estimated unstressed diameters (16.7–27.0 mm) and wall thickness/elastic modulus pairs. Conclusion PVZ analysis demonstrates increased resistance ( Z 0 ), global stiffness ( Z 1 ), and proximal stiffness ( Z C ) in severe PAH. The Z C ‐mPAP relationship suggests proximal vascular stiffening.