Abstract

Objective: Quantification of characteristic impedance (Zc) as an estimate of pulsatile load is now feasible using a hybrid non-invasive and invasive technique in any specific vascular bed. Vascular resistance (mean pressure ÷ mean flow) in a system may ignore the pulsatile component of ventricular hydraulic work incorporating the dynamic interaction between vascular resistance, compliance and wave reflection. This interaction is represented by vascular impedance which offers a comprehensive assessment of hydraulic load. This study aims to compare systemic (Ao-Zc) and pulmonary (PA-Zc) Zc in a cohort of patients with suspected pulmonary hypertension (PH) referred for routine right heart catheterisation (RHC) followed by cardiac magnetic resonance (CMR). Design and Methods: Thirty participants (77% females, mean 56 ± 18 years) were recruited, and had routine right heart catheterisation (RHC) to measure systolic (sPAP), diastolic (dPAP), mean (mPAP), and PA wedge pressures (PAWP), cardiac output (CO) and PVR. The remaining patients were assigned to the control group. Ao pressures were calibrated to brachial cuff pressures and derived from radial tonometric pressure acquisition (systolic, AoSP; diastolic, AoDP; mean, MP) before/ after CMR. Ao and PA volumetric flows were recorded using 3T cardiac magnetic resonance (CMR) using phase-contrast velocity quantification. Zc was expressed as the relationship of PA pulsatile pressure to PA pulsatile flow in the frequency domain. Results: 80% of patients had evidence of PH on RHC and classified as pre-capillary PH (n = 11, PrecPH), isolated post-capillary PH (n = 8, IpcPH) and combined PH (n = 5, CpcPH). In patients without PH, Ao-Zc was 83.0 ± 38.4 dynes.s.cm-5 and PA-Zc was 48.8 ± 13.7 dynes.s.cm-5, with PA-Zc being 33% lower than those with PH (72.9 ± 28.0 dynes.s.cm-5, p = 0.005) and Ao-Zc non-significantly lower (77.3 ± 29.6 dynes.s.cm-5, p = 0.575). In patients with PH, different hemodynamic relationships were observed. In those with PrecPH, PA-Zc was 9% higher than Ao-Zc (p = 0.74). An inverse relationship between PA-Zc and Ao-Zc was found in those with IpcPH (p = 0.11). This relationship approached 1:1 (p = 0.27) in patients with CpcPH. PA-Zc spectra in CpcPH subjects were qualitatively similar to Ao-Zc spectra, although the ratio of PVR to Zc was smaller. 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.

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