PS-C05-3: ESTIMATION OF PULMONARY PULSATILE ARTERIAL LOAD IN PATIENTS UNDERGOING INVESTIGATION FOR PULMONARY HYPERTENSION

Abstract

Objective: Diagnosis of pulmonary hypertension (PH) is typically confirmed by elevation of the pulmonary artery (PA) pressure and/or pulmonary vascular resistance (PVR). However, PVR may overlook the pulsatile component of RV hydraulic work which involves the dynamic interplay between PA resistance and compliance. PA vascular impedance (PVZ) offers a more comprehensive assessment of RV and PA load. This study aims to apply a method of PA pulsatile load as PVZ determination in a cohort of patients referred for PH evaluation. Design and Methods: Fifty-eight participants (71% females, mean 53 ± 18 years) were recruited, and underwent right heart catheterisation (RHC) to measure systolic (sPAP), diastolic (dPAP), mean (mPAP), and PA wedge pressures (PAWP), cardiac output (CO) and PVR; classified as precapillary PH (PrecPH), isolated postcapillary PH (IpcPH), combined PH (CpcPH) and control group. PA flows were recorded using 3T cardiac magnetic resonance (CMR); RV volume (V) were obtained by contouring endocardial and epicardial borders on the short axis at end diastolic (ED) and end systolic (ES) phases, and ejection fraction (RVEF) was calculated as (RVEDV - RVESV)/RVEDVx100. Volumetric flow was measured using phase-contrast velocity quantification using 3T cardiac magnetic resonance (CMR). PVZ was expressed as the relationship of pulsatile pressure to pulsatile flow in the frequency domain. Results: 76% of patients had evidence of PH on RHC (8 PrecPH, 17 IpcPH, 9 CpcPH). CpcPH and PrecPH patients tended to show poorer RV contractility compared with control and IpcPH groups, albeit not statistically significant. PVZ was highest in patients with PrecPH and CpcPH, while lowest in those with IpcPH. A correlation analysis was performed to seek association between mPAP, PVR and PVZ and other variables thought to be related to PH. In PrecPH, increased mPAP was found to be associated with raised PVR (p < 0.001; R = 0.94) and PVZ (p < 0.001; R = 0.78). However, there was no association between elevated mPAP and PVZ in IpcPH and CpcPH, despite a significant correlation with PVR (IpcPH P = 0.03, R = 0.55; CpcPH P = 0.01, R = 0.77). Conclusion: We describe a straightforward method to measure and compare pulsatile vascular load of the systemic and pulmonary circulations simultaneously, allowing further quantification of systemic/pulmonary vascular interactions. Further research is required to evaluate small-vessel contributions to the arterial circulation, especially in the pulmonary system.