Key result
Elevated pulmonary impedance is linked to reduced RVSWI, RVEF, and CO, unlike PVR or mPAP.
Why the study?
Pulmonary hypertension effects on right ventricular afterload are commonly assessed by mPAP or PVR, but pulsatile components of flow captured by pulmonary impedance may provide additional prognostic information.
Does pulmonary impedance estimation using CMR/RHC better predict right ventricular dysfunction compared to mPAP or PVR in patients with pulmonary hypertension?
Observational (n=70)
Does pulmonary impedance estimation using CMR/RHC better predict right ventricular dysfunction compared to mPAP or PVR in patients with pulmonary hypertension?
Pulmonary impedance estimation using CMR and RHC is a stronger predictor of maladaptive right ventricular remodeling than standard measures like mPAP and PVR in patients with pulmonary hypertension.
Answers are grounded in this paper and cite their sources.
Pulmonary impedance may better flag RV dysfunction than mPAP or PVR in PH; leaves open prospective validation before clinical adoption.
Background The effect of pulmonary hypertension (PH) on right ventricular (RV) afterload is commonly defined by elevation of pulmonary artery (PA) pressure or pulmonary vascular resistance (PVR). In humans however, one-third to half of the hydraulic power in the PA is contained in pulsatile components of flow. Pulmonary impedance (Zc) expresses opposition of the PA to pulsatile blood flow. We evaluate pulmonary Zc relationships according to PH classification using a cardiac magnetic resonance (CMR)/right heart catheterization (RHC) method. Methods Prospective study of 70 clinically indicated patients referred for same-day CMR and RHC [60 ± 16 years; 77% females, 16 mPAP <25 mmHg (PVR <240 dynes.s.cm−5/mPCWP <15 mmHg), 24 pre-capillary (PrecPH), 15 isolated post-capillary (IpcPH), 15 combined pre-capillary/post-capillary (CpcPH)]. CMR provided assessment of PA flow, and RHC, central PA pressure. Pulmonary Zc was expressed as the relationship of PA pressure to flow in the frequency domain (dynes.s.cm−5). Results Baseline demographic characteristics were well matched. There was a significant difference in mPAP (P < 0.001), PVR (P = 0.001), and pulmonary Zc between mPAP<25 mmHg patients and those with PH (mPAP <25 mmHg: 47 ± 19 dynes.s.cm−5; PrecPH 86 ± 20 dynes.s.cm−5; IpcPH 66 ± 30 dynes.s.cm−5; CpcPH 86 ± 39 dynes.s.cm−5; P = 0.05). For all patients with PH, elevated mPAP was found to be associated with raised PVR (P < 0.001) but not with pulmonary Zc (P = 0.87), except for those with PrecPH (P < 0.001). Elevated pulmonary Zc was associated with reduced RVSWI, RVEF, and CO (all P < 0.05), whereas PVR and mPAP were not. Conclusions Raised pulmonary Zc was independent of elevated mPAP in patients with PH and more strongly predictive of maladaptive RV remodelling than PVR and mPAP. Use of this straightforward method to determine pulmonary Zc may help to better characterize pulsatile components of RV afterload in patients with PH than mPAP or PVR alone.
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Hungerford et al. (2023) conducted an observational in Pulmonary hypertension (n=70). Elevated pulmonary impedance (Zc) vs. Normal pulmonary impedance was evaluated on Right ventricular dysfunction (reduced RVSWI, RVEF, and CO) (p=<0.05). Elevated pulmonary impedance was associated with reduced right ventricular stroke work index, ejection fraction, and cardiac output (all P<0.05), whereas PVR and mPAP were not.
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