Pulmonary artery compliance in different forms of pulmonary hypertension

Abstract

ObjectivePulmonary artery compliance (PAC), estimated as stroke volume (SV) divided by pulmonary artery pulse pressure (PP), may be a predictor of survival in pulmonary arterial hypertension (PAH). Resistance–compliance (RC) time, the product of PAC and pulmonary vascular resistance, is reported to be a physiological constant. We investigated if differences in PAC and RC time exist between pulmonary hypertension (PH) subgroups and examined whether PAC is an independent predictor of transplant-free survival in PAH.MethodsThis was a retrospective analysis of adult PAH (n=532) and chronic thromboembolic PH (CTEPH, n=84) patients enrolled in the US Pulmonary Hypertension Association Registry from 2015 to 2019. PAC and RC time were compared between PH subgroups (connective tissue disease-PAH (CTD-PAH), idiopathic/heritable-PAH (i/h-PAH), drug/toxin-PAH (d/t-PAH)). Cox proportional hazards models were constructed for transplant-free survival, adjusting for REVEAL 2.0 risk score.ResultsThere were no differences in estimated PAC between PAH subgroups, nor between PAH and CTEPH. RC time was shorter in CTEPH compared with PAH (median 0.55 (IQR 0.45–0.64) vs 0.62 (0.52–0.73) s, p<0.0001). RC time was shortest in CTD-PAH when compared with i/h-PAH and d/t-PAH ((0.59±0.18) vs (0.65±0.20) vs (0.73±0.25) s, p=0.0001). PAC was associated with transplant-free survival (HR 0.72, 95% CI 0.55 to 0.94, p=0.02) but was not an independent predictor of outcome after adjustment for REVEAL 2.0 score.ConclusionPAC was similar between PH groups and was not an independent predictor of transplant-free survival in PAH. RC time was different between PH subgroups, challenging RC time constancy.Trial registration numberNCT04071327

Relationship of TAPSE Normalized by Right Ventricular Area With Pulmonary Compliance, Exercise Capacity, and Clinical Outcomes

“…The median value of rest PCa of ≥3.0 mL/mm Hg was consistent with prior literature, as a cutoff for improved outcomes. 18 Similarly, the median value of peak VO 2 ≥50% predicted was also consistent with prior literature as a reliable cutoff for adverse outcomes. 27 Receiver operating characteristic curves with area under the curve values were used to compare the discriminative ability of the various parameters, and the optimal cut points were defined by the Youden index.…”

“…The current study is focused particularly on PCa, as this is a clinically available metric of pulsatile RV afterload and predictive of clinical outcomes in a wide spectrum of PH phenotypes, especially left heart disease. [16][17][18][19][31][32][33][34] While the PCa loses its prognostic ability as a singular metric in multivariate analyses in most studies, 18,19 it remains an important physiological metric and signifies the role of pulsatile pulmonary load, especially in postcapillary PH. As a metric of pulsatile load, PCa is possibly an oversimplified metric, while bioengineering metrics of pulmonary vascular impedance are more sophisticated and have been shown to correlate with RV dysfunction with better precision.…”

“…In this study, we hypothesized that TAPSE divided by RV end-systolic area (TAPSE/RVA-S) and RV enddiastolic area (TAPSE/RVA-D) are better markers of right heart function in PH than TAPSE alone. We assess the correlations of the TAPSE/RVA metrics with 3 different outcome variables: (1) pulmonary arterial compliance (PCa; pulmonary pulse pressure/stroke volume, normal value ≥3.0 mm Hg/mL) as a metric of pulsatile load impacting RV function and a unifying hemodynamic feature among different PH phenotypes, where a higher PCa protects the RV from pressure overload with exercise, while a lower PCa indicates vessel stiffness and is correlated with RV dysfunction 4,[16][17][18][19] ; (2) exercise capacity (as peak oxygen consumption, peak VO 2 as percentage predicted); and (3) adverse clinical outcomes (cardiovascular hospitalization and death) on 1-year follow-up.…”

Nebulisation of Paclitaxel, Sotatercept and Iloprost for pulmonary hypertension for lung cancer. From In vitro to In vivo

“…The main symptoms from increased PVR are: dyspnea, fatigue, orthopnea, dizziness, fainting, non-productive cough, peripheral edema angina pectoris, finally in severe cases leg swelling. [1] Pulmonary hypertension progressive and is considered a fatal condition in the final stages. Decreased exercise tolerance and heart failure is also observed.…”

Distensibility, an Early Disease Marker of Pulmonary Vascular Health: Ready for Clinical Application

“… 3 , 4 Pulmonary vascular health can be quantified by hemodynamic afterload faced by the right ventricle (RV afterload), which comprises steady and pulsatile components. 5 , 6 Although the steady load is captured by clinical metrics of pulmonary vascular resistance (PVR), the pulsatile load can be assessed with variable precision by different metrics: the simplified metric of pulmonary arterial compliance computed as stroke volume/pulmonary pulse pressure, 7 bioengineering metrics of pulmonary vascular impedance, 8 , 9 and pulmonary vascular distensibility with exercise 10 , 11 ( Figure ).…”