The isobaric pulmonary arterial compliance in pulmonary hypertension

Abstract

Pulmonary hypertension (PH) is associated with stiffening of pulmonary arteries which increases right ventricular pulsatile loading. High pulmonary artery wedge pressure (PAWP) in postcapillary PH (Pc-PH) further decreases PA compliance (PAC) at a given pulmonary vascular resistance (PVR) compared to precapillary PH, thus responsible for a higher total arterial load. In all other vascular beds, arterial compliance is considered as mainly determined by the distending pressure, due to non-linear stress-strain behaviour of arteries. We tested the applicability, advantages and drawbacks of two comparison methods of PAC depending on the level of mean PA pressure mPAP (isobaric PAC) or PVR.Right heart catheterisation data including PAC (stroke volume/pulse pressure) were obtained in 112Pc-PH (of whom 61 had combined postcapillary and precapillary PH) and 719 idiopathic pulmonary arterial hypertension (iPAH).PAC could be compared over the same mPAP range (25–66 mmHg) in 792/831 patients (95.3%) and over the same PVR range (3–10.7 WU) in only 520/831 patients (62.6%). The main assumption underlying comparisons at a given PVR was not verified as the PVR×PAC product (RC-time) was not constant but on the contrary more variable than mPAP. In the 788/831 (94.8%) patients studied over the same PAC range (0.62–6.5 mL·mmHg−1), PVR and thus total arterial load tended to be higher in iPAH.Our study favours comparing PAC at fixed mPAP level (isobaric PAC) rather than at fixed PVR. A reappraisal of the effects of PAWP on the pulsatile and total arterial load put on the right heart is needed, and this point deserves further studies.

Pulsatile pulmonary artery pressure in a large animal model of chronic thromboembolic pulmonary hypertension: Similarities and differences with human data

“…Some authors have suggested that the mPAP versus sPAP linear relationship reflects the constancy or near‐constancy of the time constant of the pulmonary Windkessel, as quantified by the pulmonary vascular resistance times PA compliance product 36,37 . This explanation has been recently ruled out because the value of the time constant of the pulmonary Windkessel is not constant but on the contrary more variable than mPAP in patients with either precapillary or postcapillary PH 38 . In other words, to continue to support the constancy or near‐constancy of the time constant of the pulmonary Windkessel would be as unrealistic as supporting that mPAP is constant or near‐constant in PH states 38 .…”

“… 36 , 37 This explanation has been recently ruled out because the value of the time constant of the pulmonary Windkessel is not constant but on the contrary more variable than mPAP in patients with either precapillary or postcapillary PH. 38 In other words, to continue to support the constancy or near‐constancy of the time constant of the pulmonary Windkessel would be as unrealistic as supporting that mPAP is constant or near‐constant in PH states. 38 One hypothesis may be that the redundancy between mPAP and sPAP is explained by the fact that changes in PA stiffness are primarily due to increases in mPAP under both experimental and clinical conditions.…”

“… 38 One hypothesis may be that the redundancy between mPAP and sPAP is explained by the fact that changes in PA stiffness are primarily due to increases in mPAP under both experimental and clinical conditions. 10 , 12 , 38 …”

“…38 In other words, to continue to support the constancy or near-constancy of the time constant of the pulmonary Windkessel would be as unrealistic as supporting that mPAP is constant or nearconstant in PH states. 38 One hypothesis may be that the redundancy between mPAP and sPAP is explained by the fact that changes in PA stiffness are primarily due to increases in mPAP under both experimental and clinical conditions. 10,12,38 Another species-independent finding was that there was a proportional relationship among sPAP, mPAP, and dPAP.…”

“…38 One hypothesis may be that the redundancy between mPAP and sPAP is explained by the fact that changes in PA stiffness are primarily due to increases in mPAP under both experimental and clinical conditions. 10,12,38 Another species-independent finding was that there was a proportional relationship among sPAP, mPAP, and dPAP.…”