Increased Pulmonary Vascular Impedance in Patients with Severe Pulmonary Arterial Hypertension
Authors: Ravellette Keeley , Kubba Saad , Airhart Sophia , Yuan Jason X.J , Rischard Franz P. , Vanderpool Rebecca 
Published: June 2021

Introduction

Pulmonary arterial hypertension (PAH) is characterized by increased pulmonary artery (PA) pressure and resistance due to pulmonary vascular remodeling. The functional effect of this vascular remodeling on the pulsatile pulmonary hemodynamics has not been well studied. Pulmonary vascular impedance (PVZ) represents the relationship between pulsatile pressure and flow in the pulmonary artery (PA) and provides a more comprehensive view of pulmonary arterial function. We hypothesized that decreased pulmonary vascular compliance and increased pulmonary vascular resistance (PVR) would significantly alter the pulsatile pulmonary hemodynamics in severe PAH.

Methods

Group 1 PAH patients (mean pulmonary arterial pressure (mPAP) ≥ 25 mmHg, pulmonary capillary wedge pressure ≤ 15 mmHg) and control patients (without pulmonary hypertension (PH), mPAP < 25 mmHg) with both an echocardiogram including right ventricular outflow tract (RVOT) images and a right heart catheterization (RHC) within three months were identified from the University of Arizona PH registry. The PAH patients were divided into those with mild PH (PVR < 7 mmHg*min/L) and severe PH (PVR ≥ 7 mmHg*min/L). RVOT Doppler flow velocity profiles were first traced using a custom MATLAB program. Flow velocity profiles were multiplied by the average PA diameter (ratio of thermodilution cardiac output and mean RVOT flow velocity) to determine PA flow profiles. PVZ was calculated in the frequency domain using RHC measured PA pressure and PA flow profiles. Characteristic Impedance (ZC) was calculated as the mean of Z2–4. Data is presented as mean ± standard error or median [interquartile range].

Results

Fourteen subjects were identified (Control: n = 2, 2 female, 70 ± 3 yrs; Mild PAH: n = 6, 2 female, 63 ± 11 yrs; and Severe PAH: n = 6, 4 female, 45 ± 13 yrs, p = 0.05). The median time between the RHC and echo was 8 [1 − 15] days. Severe PAH patients have increased mPAP (60 ± 19 vs 38 ± 17 mmHg, p = 0.04) and end‐diastolic elastance (1.05 ± 0.43 vs 0.39 ± 0.3 mmHg/mL, p = 0.2), decreased stroke volume (61 ± 7 vs 91 ± 20 mL, p = 0.01) and no change in cardiac output (5.16 ± 0.81 vs 6.23 ± 1.3 L/min) compared to controls. Severe PAH showed increased 0 Hz impedance (Z0, 966 ± 138 dynes/sec/cm−5) compared to controls (288 ± 34 dynes/sec/cm−5, p = 0.02) and mild PAH (538 ± 64 dynes/sec/cm−5, p = 0.03, Figure 1). ZC in severe PAH had a non‐significant increase compared to controls (139 ± 23 vs 69 ± 19 dynes/sec/cm−5, respectively). Z1 was significantly increased in severe PAH compared to controls (52 ± 91 vs 5 ± 43 dynes/sec/cm−5, p = 0.02) but not compared to mild PAH (52 ± 91 vs 64 ± 54 dynes/sec/cm−5, p = 0.09).

Conclusion

Pulmonary vascular impedance analysis in a small PAH cohort demonstrated that vascular resistance (Z0) and global vascular stiffness (Z1) are increased in severe PAH patients and that there is a non‐significant increase in proximal vascular stiffness (ZC).

Support or Funding Information

This work was supported in part by grants from the Arizona Biomedical Research Commission (ABRC NIA ADHS18‐198871 (RRV))

This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.