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Pulmonary hypertension (PH) is a common and prognostically important complication of mitral regurgitation (MR). Mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR) are traditionally used to diagnose PH, however these indices measure static rather than pulsatile load, leading to an incomplete representation of pulmonary vascular load on the right ventricle (RV). Pulmonary arterial compliance (PAC) is one method for quantifying pulsatile load, and is both a stronger predictor of prognosis in left heart failure, as well as a more sensitive measure of early pulmonary vascular dysfunction than PVR. With the expansion of transcatheter mitral and tricuspid valve therapies, there is renewed interest to more accurately define the load imposed by the pulmonary vasculature on the RV, especially in the early phase, prior to the onset of chronic PH. This review discusses the pathophysiology of pH in left heart failure and MR, the utility of PAC as a measure of RV afterload, and its calculation for clinical use and interpretation, underlining the utility of PAC as an adjunct for assessing pulmonary vascular haemodynamics.

Aims: A common feature of various forms of pulmonary hypertension (PH) is progressive decline of pulmonary arterial compliance (CPA), which correlates with reduced survival. In this acute study, we evaluated feasibility, safety and haemodynamic performance of the Aria pulmonary endovascular device in patients with PH associated with left heart disease (PH‐LHD) and chronic lung disease (PH‐CLD). Methods and results: Eight patients with PH‐LHD and 10 patients with PH‐CLD were included in this study. The device was placed in the main pulmonary artery via the right femoral vein and was connected by a catheter to a gas‐filled reservoir outside the body. During systole, gas shifts from the balloon to the reservoir, leading to deflation of the balloon. In diastole, the gas returns from the reservoir to the balloon, leading to balloon inflation and enhancing diastolic blood flow to the distal pulmonary capillary bed. Haemodynamics were assessed at baseline, and again with device off, device on and device off. The primary safety endpoint was the incidence of serious adverse events through 30 days after the procedure. No complications or investigational device‐related serious adverse events occurred. Device activation in PH‐LHD and PH‐CLD patients decreased pulmonary arterial pulse pressure by 5.6 ± 4.2 mmHg (−12%; p = 0.003) and 4.2 ± 2.2 mmHg (−11%; p < 0.001), increased CPA by 0.4 ± 0.2 ml/mmHg (+23%; p = 0.004) and 0.4 ± 0.3 ml/mmHg (+25%; p = 0.001), and increased right ventricular‐to‐pulmonary vascular (RV‐PV) coupling by 0.24 ± 0.18 (+40%; p = 0.012) and 0.11 ± 0.07 (+21%; p = 0.001), respectively. Conclusions: Temporary implantation of the Aria endovascular device was feasible and safe. Device activation resulted in acute improvement of CPA and RV‐PV coupling. [ABSTRACT FROM AUTHOR]

Background: Pulmonary arterial compliance (PAC) is a prognostic parameter in pulmonary arterial hypertension (PAH) reflecting the elasticity of the pulmonary vessels. Objectives: The objective of this post hoc analysis of a prospective randomized controlled trial (RCT) was to assess the effect of exercise training on PAC and stroke volume (SV) in patients with PAH and persistent/inoperable chronic thromboembolic pulmonary hypertension (CTEPH). Method: From the previous RCT, 43 out of 87 patients with severe PAH (n = 29) and CTEPH (n = 14) had complete haemodynamic examinations at baseline and after 15 weeks by right heart catheterization and were analysed (53% female, 79% World Health Organization functional class III/IV, 58% combination therapy, 42% on supplemental oxygen therapy, training group n = 24, and control group n = 19). Medication remained unchanged for all patients. Results: Low-dose exercise training at 4–7 days/week significantly improved PAC (training group 0.33 ± 0.65 mL/mm Hg vs. control group −0.06 ± 1.10 mL/mm Hg; mean difference 0.39 mL/mm Hg, 95% confidence interval [CI] 0.15–0.94 mL/mm Hg; p = 0.004) and SV (training group 9.9 ± 13.4 mL/min vs. control group −4.2 ± 11.0 mL/min; mean difference 14.2 mL, 95% CI 6.5–21.8 mL; p < 0.001) in the training versus control group. Furthermore, exercise training significantly improved cardiac output and pulmonary vascular resistance at rest, peak oxygen consumption, and oxygen pulse. Conclusions: Our findings suggest that supervised exercise training may improve right ventricular function and PAC at the same time. Further prospective studies are needed to evaluate these findings. [ABSTRACT FROM AUTHOR]

Abstract Aims Although pulmonary arterial remolding in pulmonary hypertension (PH) changes the mechanical properties of the pulmonary artery, most clinical studies have focused on static mechanical properties (resistance), and dynamic mechanical properties (compliance) have not attracted much attention. As arterial compliance plays a significant role in determining afterload of the right ventricle, we evaluated how PH changes the dynamic mechanical properties of the pulmonary artery using high-resolution, wideband input impedance (Z PA). We then examined how changes in Z PA account for arterial remodeling. Clarification of the relationship between arterial remodeling and Z PA could help evaluate arterial remodeling according to hemodynamics. Main methods PH was induced in Sprague–Dawley rats with an injection of Sugen5416 (20 mg/kg) and 3-week exposure to hypoxia (10% oxygen) (SuHx). Z PA was evaluated from pulmonary artery pressure and flow under irregular pacing. Pulmonary histology was examined at baseline and 1, 3, and 8 weeks (n = 7, each) after Sugen5416 injection. Key findings SuHx progressively increased pulmonary arterial pressure. Z PA findings indicated that SuHx progressively increased resistance (baseline: 9.3 ± 3.6, SuHx1W: 20.7 ± 7.9, SuHx3W: 48.8 ± 6.9, SuHx8W: 62.9 ± 17.8 mm Hg/mL/s, p < 0.01) and decreased compliance (baseline: 11.9 ± 2.1, SuHx1W: 5.3 ± 1.7, SuHx3W: 2.1 ± 0.7, SuHx8W: 1.9 ± 0.6 × 10−3 mL/mm Hg, p < 0.01). The time constant did not significantly change. The progressive reduction in compliance was closely associated with wall thickening of small pulmonary arteries. Significance The finding that changes in resistance were reciprocally associated with those in compliance indicates that resistant and compliant vessels are anatomically inseparable. The analysis of Z PA might help evaluate arterial remodeling in PH according to hemodynamics. Graphical abstract Unlabelled Image [ABSTRACT FROM AUTHOR]

Pulmonary hypertension associated with left heart disease is the most common form of pulmonary hypertension. Although its pathophysiology remains incompletely understood, it is now well recognized that the presence of pulmonary hypertension is associated with a worse prognosis. Right ventricular failure has independent and additive prognostic value over pulmonary hypertension for adverse outcomes in left heart disease. Recently, several new terminologies have been introduced to better define and characterize the nature and severity of pulmonary hypertension. Several new treatment options including the use of pulmonary arterial hypertension specific therapies are being considered, but there is lack of evidence. Here, we review the recent advances in this field and summarize the diagnostic and therapeutic modalities of use in the management of pulmonary hypertension associated with left heart disease. [ABSTRACT FROM AUTHOR]

Background Pulmonary hypertension (PH) is often found in cystic fibrosis (CF) patients affected by end-stage lung disease but its impact on outcome remains unclear. Pulmonary arterial compliance (PAC) is an important determinant of right ventricle (RV) workload and it is a strong predictor of survival in other forms of PH. The aim of this study is to investigate whether PAC is a predictor of long-term prognosis in a population of CF patients affected by advanced lung disease. Methods Between 2000 and 2014, 178 patients with CF have been evaluated for lung transplantation in our CF Center. Right heart catheterization (RHC) and follow up data were retrievable and analyzed in 141 of them. PAC was defined as the ratio between stroke volume (SV) and pulse pressure (PP) at heart catheterization. The association of PAC with survival was tested at 4 years and compared to other hemodynamic parameters. Results PH prevalence was 56.4%. Most patients had mild elevation of pulmonary artery pressure (PAP). No difference in mortality was observed in patients with PH compared to patients with normal PAP (HR 0.95: 95% CI 0.49–1.89, p = 0.89). At receiver operating characteristic curve (ROC) analysis, the optimal prognostic cut-off point of PAC was 1.95 ml/mmHg. An impaired PAC (≤ 1.95 ml/mmHg) was a strong independent predictor of long-term mortality (HR 3.44: 95% CI 1.51–7.85: p = 0.003). Conclusions Impaired PAC is associated with poor prognosis in CF patients awaiting lung transplantation. Other traditional hemodynamic parameters add no prognostic information. [ABSTRACT FROM AUTHOR]

The time constant of the pulmonary circulation, or product of pulmonary vascular resistance (PVR) and compliance (Ca), called the RC-time, has been reported to remain constant over a wide range of pressures, etiologies of pulmonary hypertension, and treatments. We wondered if increased wave reflection on proximal pulmonary vascular obstruction, like in operable chronic thromboembolic pulmonary hypertension, might also decrease the RC-time and thereby increase pulse pressure and right ventricular afterload. Pulmonary hypertension of variable severity was induced either by proximal obstruction (pulmonary arterial ensnarement) or distal obstruction (microembolism) eight anesthetized dogs. Pulmonary arterial pressures (Ppa) were measured with high-fidelity micromanometer-tipped catheters, and pulmonary flow with transonic technology. Pulmonary ensnarement increased mean Ppa, PVR, and characteristic impedance, decreased Ca and the RC-time (from 0.46 ± 0.07 to 0.30 ± 0.03 s), and increased the oscillatory component of hydraulic load (Wosc/Wtot) from 25 ± 2 to 29 ± 2%. Pulmonary microembolism increased mean Ppa and PVR, with no significant change in Ca and characteristic impedance, increased RC-time from 0.53 ± 0.09 to 0.74 ± 0.05 s, and decreased Wosc/Wtot from 26 ± 2 to 13 ± 2%. Pulse pressure increased more after pulmonary ensnarement than after microembolism. Concomitant measurements with fluid-filled catheters showed the same functional differences between the two types of pulmonary hypertension, with, however, an underestimation of Wosc. We conclude that pulmonary hypertension caused by proximal vs. distal obstruction is associated with a decreased RC-time and increased pulsatile component of right ventricular hydraulic load. [ABSTRACT FROM AUTHOR]

Previous studies have documented the normal values of pulmonary arterial compliance (Cp) in animals and adult humans. In the past, variations in Cp and its measurement in children with septal defects has been unknown. In the present study, we found the Windkessel model, which uses compliance and resistance as parameters, to be a useful tool in understanding Cp in pediatric patients. Calculations of Cp were based on the pulmonary arterial diastolic pressure waveform as an exponential function of time. First, Cp was estimated by studying pressure tracings of the main pulmonary artery (MPA) obtained from both routine cardiac catheterization and pressure measured by a catheter-tip manometer, which was performed during a catheterization study of seven children with various congenital heart diseases. Second, 124 children with atrial and ventricular septal defects aged between 45 days and 12 years were studied using the data obtained from routine catheterization. Hemodynamic data were used to calculate pulmonary vascular resistance (Rp), pulmonary arterial time constant (Tp) and Cp. A strong correlation ( r = 0.954) was found in the Cp value estimated by data obtained from routine catheterization and from the catheter-tip manometer study. The present study shows an estimated mean (SEM) Cp in normal children of 1.53 (0.17) ml/mmHg per m2. The estimated mean (SEM) Cp was 1.91 (0.10) and 1.70 (0.11) ml/mmHg per m2 in children with atrial septal defect (ASD) and ventricular septal defect (VSD), respectively. It was found that Cp was significantly ( P = 0.04) higher in female patients with a VSD. Also, a significantly low Cp (0.95 ± 0.06 ml/mmHg per m2) was observed in patients with a VSD and pulmonary hypertension (VSDPH). In conclusion, Cp was calculated by the exponential decay portion of the MPA diastolic pressure waveform. A normal Cp value was observed in ASD and VSD patients and a significantly low Cp was observed in children with a VSDPH. Cp was higher in female VSD patients than in male VSD patients. [ABSTRACT FROM AUTHOR]

Combined pulmonary fibrosis and emphysema (CPFE) is a common but under-recognized syndrome characterized with distinct profiles of both pulmonary fibrosis and emphysema. Pulmonary hypertension (PH) is particularly prone to develop as a common complication, leading to exercise limitation and worse prognosis of CPFE. Although the therapy of patients with PH from CPFE cannot be endorsed, an individual treatment may be considerable when accompanying severe PH. We report a case of a 71-year-old male with PH from CPFE, who improved pulmonary arterial compliance (PAC) and exercise capacity in response to pulmonary vasodilator. [ABSTRACT FROM AUTHOR]