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Heart failure (HF) is an ongoing crisis reaching epidemic proportions worldwide. About 50% of HF patients have a preserved ejection fraction. Invasive hemodynamics have shown varied results in patients who have HF with preserved ejection fraction (HFpEF). This article attempts to summarize the importance of detecting pulmonary vascular remodeling in HFpEF using invasive hemodynamics. Incorporating newer invasive hemodynamic parameters such as diastolic pulmonary gradient, pulmonary arterial compliance, pulmonary vascular resistance, and pulmonary arterial pulsatility index may improve patient selection for studies used in defining advanced therapies and clinical outcomes. Profiling of patients using invasive hemodynamic parameters may lead to better patient selection for clinical research., Competing Interests: Disclosure Dr N. Nair has no disclosures with relevance to this work., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: An increase in the pulmonary capillary wedge pressure (PAWP) has been shown to impact on the inherent relationship between the pulmonary arterial compliance (PAC) and pulmonary vascular resistance (PVR), thus augmenting the pulsatile relative to the resistive load of the right ventricle. However, the PAWP comprises the integration of both the steady and the pulsatile pressure components. We sought to address the differential impact of the these distinct PAWP components on the PAC-PVR relationship in a cohort of patients with heart failure., Methods and Results: The study population consisted of 192 patients with hemodynamic findings diagnostic for heart failure. Off-line analysis was performed using the MATLAB software. The steady and pulsatile PAWP components were calculated as mid-A pressure and mean pressure during the V-wave oscillation, respectively. The PAC and PVR were hyperbolically and inversely associated and the subgroup of patients with PAWP above the median (>18 mm Hg) displayed a significant left and downward shift of the curve fit (P < .001). The shift in the PAC-PVR fit between patients with higher versus low steady PAWP was not significant (P = .43). In contrast, there was a significant downward and leftward shift of the PVR-PAC curve fit for the subgroup with a higher pulsatile PAWP (P < .001). Furthermore, only the pulsatile PAWP was significantly associated with the time-constant of the pulmonary circulation, assessed as the PAC × PVR product (P < .001)., Conclusions: In patients with heart failure, the pulsatile rather than the steady PAWP component stands for the previously documented shift of the PAC-PVR relationship occurring at an elevated PAWP., (Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.)

Background: The prognostic predictors of pulmonary hypertension (PH) due to advanced heart failure (HF) have yet to be explored., Objectives: To examine the prognostic value of hemodynamics and comorbidities in this patient group., Methods: We retrospectively enrolled consecutive patients with PH due to advanced HF diagnosed by echocardiography and right heart catheterization. Follow-up was performed every 6 months ± 2 weeks. Primary endpoints were all-cause mortality and heart or lung transplantation., Results: In total, 92 patients were included. The mean age was 46.82 years and mean left ventricular ejection fraction (LVEF) was 26.63%. During a median follow-up time of 9.72 months, 66 patients (71.7%) met primary endpoints. Pulmonary arterial compliance (PAC) was a significant predictor for primary endpoints and patients burdened with more than 3 comorbidities had worse prognoses (P = 0.0114)., Conclusions: In these patients, PAC can be a potential prognostic predictor and patients with a higher comorbidity burden have worse outcomes., Competing Interests: Declaration of Competing Interest The authors declare that there is no conflict of interest., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: Right ventricular (RV) adaptation to afterload is crucial for patients undergoing continuous-flow left ventricular assist device (cf-LVAD) implantation. We hypothesized that stratifying patients by RV pulsatile load, using pulmonary arterial compliance (PAC), and RV response to load, using the ratio of central venous to pulmonary capillary wedge pressure (CVP:PCWP), would identify patients at high risk for early right heart failure (RHF) and 6-month mortality after cf-LVAD., Methods: During the period from January 2008 to June 2014, we identified 151 patients at our center with complete hemodynamics prior to cf-LVAD. Pulsatile load was estimated using PAC indexed to body surface area (BSA), according to the formula: indexed PAC (PACi) = [SV / (PA systolic - PA diastolic )] / BSA, where SV is stroke volume and PA is pulmonary artery. Patients were divided into 4 hemodynamic groups by PACi and CVP:PCWP. RHF was defined as the need for unplanned RVAD, inotropic support ≥14 days or death due to RHF within 14 days. Risk factors for RHF and 6-month mortality were examined using logistic regression and Cox proportional hazards modeling., Results: Sixty-one patients (40.4%) developed RHF and 34 patients (22.5%) died within 6 months. Patients with RHF had lower PACi (0.92 vs 1.17 ml/mm Hg/m 2 , p = 0.008) and higher CVP:PCWP (0.48 vs 0.37, p = 0.001). Higher PACi was associated with reduced risk of RHF (adjusted odds ratio [adj-OR] 0.61, 95% confidence interval [CI] 0.39 to 0.94, p = 0.025) and low PACi with increased risk of 6-month mortality (adjusted hazard ratio [adj-HR] 3.18, 95% CI 1.40 to 7.25, p = 0.006). Compared to patients with low load (high PACi) and adequate right heart response to load (low CVP:PCWP), patients with low PACi and high CVP:PCWP had an increased risk of RHF (OR 4.74, 95% CI 1.23 to 18.24, p = 0.02) and 6-month mortality (HR 8.68, 95% CI 2.79 to 26.99, p < 0.001)., Conclusions: A hemodynamic profile combining RV pulsatile load and response to load identifies patients at high risk for RHF and 6-month mortality after cf-LVAD., (Copyright © 2016 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.)

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.

Awareness has grown in recent years that right ventricular (RV) function is equally important as left ventricular (LV) function in the setting of left-sided heart disease. RV dysfunction can be the consequence of an increased afterload imposed by the failing LV. The concept of "afterload" is physically most correctly described by vascular input impedance. However, for clinical purposes, afterload is most often modeled to consist of 3 components; pulmonary vascular resistance (PVR), pulmonary arterial compliance (PAC), and characteristic impedance. Whereas PVR is historically most described, PAC (which represents the distensibility of the vasculature) has rapidly gained recognition for its prognostic ability in both pulmonary arterial hypertension and left-sided heart disease. Owing to the specific anatomy of the pulmonary circulation, PVR and PAC have an inverse hyperbolic relationship, which position can be shifted by varying wedge pressures. Knowledge of the afterload components helps one to understand how elevated left-sided filling pressures increase pulsatile load on the RV. An increase in resistive load (known as "reactive" or "out-of-proportion" pulmonary hypertension) ultimately complements the increase in pulsatile load. Perturbations in nitric oxide metabolism are thought to be crucial in this evolution and have therefore been sought as a major therapeutic target., (Copyright © 2013 Elsevier Inc. All rights reserved.)