Function In Pulmonary Hypertension Research Articles

Treatment With Treprostinil and Metformin Normalizes Hyperglycemia and Improves Cardiac Function in Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction.

Pulmonary hypertension (PH) due to left heart disease (group 2), especially in the setting of heart failure with preserved ejection fraction (HFpEF), is the most common cause of PH worldwide; however, at present, there is no proven effective therapy available for its treatment. PH-HFpEF is associated with insulin resistance and features of metabolic syndrome. The stable prostacyclin analog, treprostinil, is an effective and widely used Food and Drug Administration-approved drug for the treatment of pulmonary arterial hypertension. While the effect of treprostinil on metabolic syndrome is unknown, a recent study suggests that the prostacyclin analog beraprost can improve glucose intolerance and insulin sensitivity. We sought to evaluate the effectiveness of treprostinil in the treatment of metabolic syndrome-associated PH-HFpEF. Approach and Results: Treprostinil treatment was given to mice with mild metabolic syndrome-associated PH-HFpEF induced by high-fat diet and to SU5416/obese ZSF1 rats, a model created by the treatment of rats with a more profound metabolic syndrome due to double leptin receptor defect (obese ZSF1) with a vascular endothelial growth factor receptor blocker SU5416. In high-fat diet-exposed mice, chronic treatment with treprostinil reduced hyperglycemia and pulmonary hypertension. In SU5416/Obese ZSF1 rats, treprostinil improved hyperglycemia with similar efficacy to that of metformin (a first-line drug for type 2 diabetes mellitus); the glucose-lowering effect of treprostinil was further potentiated by the combined treatment with metformin. Early treatment with treprostinil in SU5416/Obese ZSF1 rats lowered pulmonary pressures, and a late treatment with treprostinil together with metformin improved pulmonary artery acceleration time to ejection time ratio and tricuspid annular plane systolic excursion with AMPK (AMP-activated protein kinase) activation in skeletal muscle and the right ventricle. Our data suggest a potential use of treprostinil as an early treatment for mild metabolic syndrome-associated PH-HFpEF and that combined treatment with treprostinil and metformin may improve hyperglycemia and cardiac function in a more severe disease.

Clinical Significance of Right Ventricular Function in Pulmonary Hypertension.

Pulmonary hypertension (PH) is a progressive disease characterized by increased pulmonary vascular resistance that leads to right ventricular (RV) failure, a condition that determines its prognosis. This review focuses on the clinical value of the evaluation of RV function in PH. First, the pathophysiology of PH, including hemodynamics, RV function, and their interaction (known as ventriculoarterial coupling), are summarized. Next, non-invasive imaging modalities and the parameters of RV function, mainly assessed by echocardiography, are reviewed. Finally, the clinical impacts of RV function in PH are described. This review will compare the techniques that yield comprehensive information on RV function and their roles in the assessment of PH.

Assessing right atrial function in pulmonary hypertension: window to the soul of the right heart?

Assessing right atrial function in pulmonary hypertension: window to the soul of the right heart?

Right ventricular function correlates of right atrial strain in pulmonary hypertension: a combined cardiac magnetic resonance and conductance catheter study.

The functional relevance of right atrial (RA) function in pulmonary hypertension (PH) remains incompletely understood. The purpose of this study was to explore the correlation of cardiac magnetic resonance (CMR) feature tracking-derived RA phasic function with invasively measured pressure-volume (P-V) loop-derived right ventricular (RV) end-diastolic elastance (Eed) and RV-arterial coupling [ratio of end-systolic elastance to arterial elastance (Ees/Ea)]. In 54 patients with severe PH, CMR was performed within 24 h of diagnostic right heart catheterization and P-V measurements. RA phasic function was assessed by CMR imaging of RA reservoir, passive, and active strain. The association of RA phasic function with indexes of RV function was evaluated by Spearman's rank correlation and linear regression analyses. Median [interquartile range] RA reservoir strain, passive strain, and active strain were 19.5% [11.0-24.5], 7.0% [4.0-12.0], and 13.0% [7.0-18.5], respectively. Ees/Ea was 0.73 [0.48-1.08], and Eed was 0.14 mmHg/mL [0.05-0.22]. RV diastolic impairment [RV end-diastolic pressure (EDP) and Eed] was correlated with RA phasic function, but Ea and Ees were not. In addition, RA phasic function was correlated with inferior vena cava diameter. In multivariate linear regression analysis, adjusting for key P-V loop indexes, Eed and EDP remained significantly associated with RA phasic function. We conclude that RA phasic function is altered in relation to impaired diastolic function of the chronically overloaded right ventricle and contributes to backward venous flow and systemic congestion. These results call for more attention to RA function in the management of patients with PH.NEW & NOTEWORTHY There is growing awareness of the importance of the right atrial (RA)-right ventricular (RV) axis in pulmonary hypertension (PH). Our results uncover alterations in RA phasic function that are related to depressed RV lusitropic function and contribute to backward venous return and systemic congestion in chronic RV overload. Assessment of RA function should be part of the management and follow-up of patients with PH.

Cardiac Magnetic Resonance Imaging-Based Right Ventricular Strain Analysis for Assessment of Coupling and Diastolic Function in Pulmonary Hypertension

ObjectivesThis study sought to compare cardiac magnetic resonance (CMR) imaging-derived right ventricular (RV) strain and invasively measured pressure-volume loop-derived RV contractility, stiffness, and afterload and RV-arterial coupling in pulmonary hypertension (PH). BackgroundIn chronic RV pressure overload, RV-arterial uncoupling is considered the driving cause of RV maladaptation and eventual RV failure. The pathophysiological and clinical value of CMR-derived RV strain relative to that of invasive pressure-volume loop-derived measurements in PH remains incompletely understood. MethodsIn 38 patients with PH, global RV CMR strain was measured within 24 h of diagnostic right heart catheterization and conductance (pressure-volume) catheterization. Associations were evaluated by correlation, multivariate logistic binary regression, and receiver operating characteristic analyses. ResultsLong-axis RV longitudinal and radial strain and short-axis RV radial and circumferential strain were −18.0 ± 7.0%, 28.9% [interquartile range (IQR): 17.4% to 46.6%]; 15.6 ± 6.2%; and −9.8 ± 3.5%, respectively. RV-arterial coupling (end-systolic [Eds]/arterial elastance [Ea]) was 0.76 (IQR: 0.47 to 1.07). Peak RV strain correlated with Ees/Ea, afterload (Ea), RV diastolic dysfunction (Tau), and stiffness (end-diastolic elastance [Eed]) but not with contractility (Ees). In multivariate analysis, long-axis RV radial strain was associated with RV-arterial uncoupling (Ees/Ea: <0.805; odds ratio [OR]: 5.50; 95% confidence interval [CI]: 1.50 to 20.18), whereas long-axis RV longitudinal strain was associated with increased RV diastolic stiffness (Eed: ≥0.124 mm Hg/ml; OR: 1.23; 95% CI: 1.10 to 1.51). The long-axis RV longitudinal strain-to-RV end-diastolic volume/body surface area ratio strongly predicted RV diastolic stiffness (area under receiver operating characteristic curve: 0.908). ConclusionsIn chronic RV overload, CMR-determined RV strain is associated with RV-arterial uncoupling and RV end-diastolic stiffness and represents a promising noninvasive alternative to current invasive methods for assessment of RV-arterial coupling and end-diastolic stiffness in patients with PH. (Right Ventricular Haemodynamic Evaluation and Response to Treatment [Rightheart I]; NCT03403868)

What influences right ventricle function in pulmonary hypertension due to HFpEF?

Right ventricular (RV) function and pulmonary hypertension (PH) are increasingly recognized in heart failure with preserved ejection fraction (HFpEF), with high prevalence and poor outcome. Factors leading to worse RV function in PH-HFpEF patients are unknown. We thought to determine the parameters of RV dilation in HFpEF patients with PH. We analysed clinical, echocardiographic and hemodynamic characteristics of 112 PH-HFpEF patients (71 women) enrolled prospectively in our center. PH-HFpEF was defined by a resting mean pulmonary artery pressure (mPAP) ≥ 25 mmHg and pulmonary artery wedge pressure (PAWP) > 15 mmHg. RV dysfunction was defined as tricuspid annular plane systolic excursion (TAPSE) < 16 mm at echocardiography. Mean age (± SD) was 69 ± 11 years, mPAP was 40 ± 10 mmHg, PAWP was 21 ± 5 mmHg. Forty-seven PH-HFpEF patients (40%) had RV dysfunction. In univariate analysis, RV dysfunction was related to history of hypertension ( P = 0.04, OR = 1.01), atrial fibrillation ( P < 0.01; OR = 0.21), mPAP ( P = 0.06; OR = 0.97), and right atrial pressure (RAP) ( P = 0.02, OR = 0.92). In PH-HFpEF patients, we documented a significant relationship between RV dysfunction and Hypertension, atrial fibrillation, mPAP and RAP.

Clinical Utility and Prognostic Value of Right Atrial Function in Pulmonary Hypertension.

Background Although right atrial (RA) enlargement is an established marker for adverse outcomes, the prognostic importance of RA dysfunction independent of RA size in pulmonary arterial hypertension is not known. Methods and Results Study subjects with pulmonary arterial hypertension were prospectively enrolled from 2010 to 2014. RA function was measured using RA speckle-tracking longitudinal strain and strain rate (SR) during each phase of the cardiac cycle: (1) RA reservoir (peak longitudinal strain, peak systolic SR), (2) RA conduit (peak early diastolic SR), and (3) RA active contraction (peak active contraction strain, peak contraction SR). The primary outcome was a composite of time to hospitalization or death assessed on follow-up. A total of 63 subjects had complete echocardiographic data. Of these, 91% were females, and the mean age was 58±12 years. During the follow-up period (range: 1-58 months), 39 were hospitalized or had died. After multivariable adjustment for age, sex, and left atrial size, peak longitudinal strain, peak active contraction strain, and peak early diastolic SR were significantly associated with increased risk of the composite outcome ( P=0.0005, P=0.0167, and P=0.0054, respectively). Conclusions RA dysfunction independently predicts mortality and hospitalizations in patients with pulmonary arterial hypertension.

Vascular Adaptation of the Right Ventricle in Experimental Pulmonary Hypertension.

Optimal right ventricular (RV) function in pulmonary hypertension (PH) requires structural and functional coupling between the RV cardiomyocyte and its adjacent capillary network. Prior investigations have indicated that RV vascular rarefaction occurs in PH, which could contribute to RV failure by reduced delivery of oxygen or other metabolic substrates. However, it has not been determined if rarefaction results from relative underproliferation in the setting of tissue hypertrophy or from actual loss of vessels. It is also unknown if rarefaction results in inadequate substrate delivery to the RV tissue. In the present study, PH was induced in rats by SU5416-hypoxia-normoxia exposure. The vasculature in the RV free wall was assessed using stereology. Steady-state metabolomics of the RV tissue was performed by mass spectrometry. Complementary studies were performed in hypoxia-exposed mice and rats. Rats with severe PH had evidence of RV failure by decreased cardiac output and systemic hypotension. By stereology, there was significant RV hypertrophy and increased total vascular length in the RV free wall in close proportion, with evidence of vessel proliferation but no evidence of endothelial cell apoptosis. There was a modest increase in the radius of tissue served per vessel, with decreased arterial delivery of metabolic substrates. Metabolomics revealed major metabolic alterations and metabolic reprogramming; however, metabolic substrate delivery was functionally preserved, without evidence of either tissue hypoxia or depletion of key metabolic substrates. Hypoxia-treated rats and mice had similar but milder alterations. There is significant homeostatic vascular adaptation in the right ventricle of rodents with PH.

Tricuspid annular displacement measured by 2-dimensional speckle tracking echocardiography for predicting right ventricular function in pulmonary hypertension: A new approach to evaluating right ventricle dysfunction.

This study aimed to determine the ability of tricuspid annular displacement measured by 2-dimensional speckle tracking echocardiography (STE) to predict right ventricular (RV) dysfunction in pulmonary hypertension (PH) patients. Here, we present a new method for assessing RV function that also employs STE and is based on measurement of tricuspid annular displacement.A total of 225 patients were divided into 2 groups according to the pulmonary artery systolic blood pressure (PASP), estimated by echocardiographic measurement of tricuspid regurgitation: group I (PASP ≥50 mm Hg) and group II (36 mm Hg ≤ PASP <50 mm Hg). The tricuspid annular plane systolic excursion (TAPSE), RV index of myocardial performance (RIMP), RV fractional area change (RVFAC), tissue Doppler-derived tricuspid lateral annular systolic velocity (s'), and the tricuspid annular longitudinal displacement (TMAD) parameters were measured. Thirty patients underwent cardiac magnetic resonance (CMR) examination, and right ventricular ejection fraction (RVEF) was calculated.The conventional parameters as well as the TMAD parameters differed significantly between the 2 groups (all P < .01). Good correlation was observed between the TMAD parameters and CMR-derived RVEF (all P < .01). The TMAD parameters had moderate predictive value for predicting RV dysfunction in PH patients (all P < .01). From receiver operating characteristic curves, we determined the optimal cut-off values for TMAD parameters for detecting RV dysfunction with good sensitivity and specificity.The TMAD parameters can predict the decline of RV function in patients with PH and thus provide new diagnostic indices for clinical management of these patients.

Characteristics of Ventricular Function in Pulmonary Hypertension Patients with Different Shape of Interventricular Septum: Preliminary Study with Cardiac Magnetic Resonance Imaging

背景与目的通过心脏磁共振（cardiovascular magnetic resonance, CMR）分析室间隔（interventricular septum, IVS）有无形变的肺高血压（pulmonary hypertension, PH）患者心功能特点。方法经右心导管确诊为PH并接受CMR患者36例。根据IVS形态，分为无形变组（10例）和有形变组（26例）；并与22例健康志愿者比较，参数如下：右心室（right ventricle, RV）和左心室（left ventricle, LV）舒张末期容积指数（end-diastolic volume index, EDVI）、收缩末期容积指数（end-systolic volume index, ESVI）、每搏输出量指数（stroke volume index, SVI）、心指数（cardiac index, CI）、射血分数（ejection fraction, EF）、心肌质量指数（myocardial mass index, MMI）。结果ANOVA分析示，RVEDVI、RVESVI、RVSVI、RVCI、RVEF、RVMMI、LVEDVI、LVESVI、LVSVI及LVCI在三组间差别均有统计学意义。事后组间结果比较显示，PH患者IVS无形变组与对照组相比，RVSVI（P=0.017）、RVEF（P < 0.001）、LVEDVI（P=0.048）、LVSVI（P=0.015）均减低。IVS有形变组与IVS无形变组相比，RVEDVI（P < 0.001）、RVESVI（P < 0.001）、RVCI（P=0.002）、RVMMI（P=0.017）均升高；而RVEF（P=0.001）、LVEDVI（P=0.003）、LVSVI（P < 0.001）及LVCI（P=0.029）减低。IVS有形变组与对照组相比，RVEDVI（P < 0.001）、RVESVI（P < 0.001）、RVCI（P=0.004）、RVMMI（P=0.003）均升高；而RVEF（P < 0.001）、LVEDVI（P < 0.001）、LVESVI（P < 0.001）、LVSVI（P < 0.001）、LVCI（P < 0.001）均低于对照组。结论不同IVS形态的PH患者，心室功能各有特点，IVS的形变在一定程度上能够反映PH患者心室功能的变化。

Assessment of Right Ventricular Function in Pulmonary Hypertension with Multimodality Imaging.

Pulmonary hypertension (PH) is defined as resting mean pulmonary artery pressure ≥ 25 mmHg and is caused by multiple etiologies including heart, lung or other systemic diseases. Evaluation of right ventricular (RV) function in PH is very important to plan treatment and determine prognosis. However, quantification of volume and function of the RV remains difficult due to complicated RV geometry. A number of imaging tools has been utilized to diagnose PH and assess RV function. Each imaging technique including conventional echocardiography, three-dimensional echocardiography, strain echocardiography, computed tomography and cardiac magnetic resonance imaging has-advantages and limitations and can provide unique information. In this article, we provide a comprehensive review of the utility, advantages and shortcomings of the multimodality imaging used to evaluate patients with PH.

Helicity and Vorticity of Pulmonary Arterial Flow in Patients With Pulmonary Hypertension: Quantitative Analysis of Flow Formations.

BackgroundQualitative and quantitative flow hemodynamic indexes have been shown to reflect right ventricular (RV) afterload and function in pulmonary hypertension (PH). We aimed to quantify flow hemodynamic formations in pulmonary arteries using 4‐dimensional flow cardiac magnetic resonance imaging and the spatial velocity derivatives helicity and vorticity in a heterogeneous PH population.Methods and ResultsPatients with PH (n=35) and controls (n=10) underwent 4‐dimensional flow magnetic resonance imaging study for computation of helicity and vorticity in the main pulmonary artery (MPA), the right pulmonary artery, and the RV outflow tract. Helicity and vorticity were correlated with standard RV volumetric and functional indexes along with MPA stiffness assessed by measuring relative area change. Patients with PH had a significantly decreased helicity in the MPA (8 versus 32 m/s2; P<0.001), the right pulmonary artery (24 versus 50 m/s2; P<0.001), and the RV outflow tract–MPA unit (15 versus 42 m/s2; P<0.001). Vorticity was significantly decreased in patients with PH only in the right pulmonary artery (26 versus 45 1/s; P<0.001). Total helicity computed correlated with the cardiac magnetic resonance imaging–derived ventricular‐vascular coupling (−0.927; P<0.000), the RV ejection fraction (0.865; P<0.0001), cardiac output (0.581; P<0.0001), mean pulmonary arterial pressure (−0.581; P=0.0008), and relative area change measured at the MPA (0.789; P<0.0001).ConclusionsThe flow hemodynamic character in patients with PH assessed via quantitative analysis is considerably different when compared with healthy and normotensive controls. A strong association between helicity in pulmonary arteries and ventricular‐vascular coupling suggests a relationship between the mechanical and flow hemodynamic domains.

Non-invasive imaging of global and regional cardiac function in pulmonary hypertension.

Pulmonary hypertension (PH) is a progressive illness characterized by elevated pulmonary artery pressure; however, the main cause of mortality in PH patients is right ventricular (RV) failure. Historically, improving the hemodynamics of pulmonary circulation was the focus of treatment; however, it is now evident that cardiac response to a given level of pulmonary hemodynamic overload is variable but plays an important role in the subsequent prognosis. Non-invasive tests of RV function to determine prognosis and response to treatment in patients with PH is essential. Although the right ventricle is the focus of attention, it is clear that cardiac interaction can cause left ventricular dysfunction, thus biventricular assessment is paramount. There is also focus on the atrial chambers in their contribution to cardiac function in PH. Furthermore, there is evidence of regional dysfunction of the two ventricles in PH, so it would be useful to understand both global and regional components of dysfunction. In order to understand global and regional cardiac function in PH, the most obvious non-invasive imaging techniques are echocardiography and cardiac magnetic resonance imaging (CMRI). Both techniques have their advantages and disadvantages. Echocardiography is widely available, relatively inexpensive, provides information regarding RV function, and can be used to estimate RV pressures. CMRI, although expensive and less accessible, is the gold standard of biventricular functional measurements. The advent of 3D echocardiography and techniques including strain analysis and stress echocardiography have improved the usefulness of echocardiography while new CMRI technology allows the measurement of strain and measuring cardiac function during stress including exercise. In this review, we have analyzed the advantages and disadvantages of the two techniques and discuss pre-existing and novel forms of analysis where echocardiography and CMRI can be used to examine atrial, ventricular, and interventricular function in patients with PH at rest and under stress.

Three-dimensional echocardiography to evaluate right atrial volume and phasic function in pulmonary hypertension.

Pulmonary hypertension (PH) impairs right ventricular (RV) systolic and diastolic function, which in turn induces compensatory changes in right atrial (RA) function; the diverse effects on RA function are subject to much debate. We hypothesized that RA function plays a more important role in compensating RV dysfunction, than mere prevention of clinical failure in patients with PH. We studied 54 patients with PH and 23 healthy controls. RA volume, including maximum RA volume, minimum RA volume, and the volume before atrial systole, was evaluated by 3DE. RA maximum volume index (Vmax I), total emptying volume index (TotEVI), passive emptying volume index (PassEVI), and active ejection fraction (ActEF) were calculated. Receiver operating characteristic curve analysis was used to determine the sensitivity and specificity of various cutoff levels of the variables measured for predicting World Health Organization functional class (WHO-FC) IV in patients with PH. RAVmax I in patients with PH was higher than that in controls. In patients with PH, the TotEVI was significantly higher, while PassEVI was significantly lower as compared to that in controls. ActEF was increased in patients with WHO functional class (WHO-FC) III PH as compared to that in controls (P=.003) but was reduced in more advanced cases (WHO-FC IV). In addition, the area under the curve of 3D RA ActEF was larger than those of 2D RA ActEF, RA GLS, RA area, FAC, TAPSE, and RIMP (P<.01 for all) for predicting WHO-FC IV. We demonstrated that RA function plays a more important role in compensating RV dysfunction then mere prevention of clinical failure in PH.

Fatty acid synthase modulates proliferation, metabolic functions and angiogenesis in hypoxic pulmonary artery endothelial cells

Endothelial dysfunction plays an important role in structural remodeling occurring in the pulmonary vasculature during pulmonary hypertension (PH). Endothelial injury causes apoptosis and activation of endothelial cells. However, some endothelial cells show apoptosis-resistance and later proliferate extensively leading to vascular oculopathy and formation of plexiform lesions in PH. Studies have shown that rapidly proliferating cells exhibit increased expression of Fatty acid synthase (FAS), a regulatory enzyme responsible for the production of fatty acids. Our previous study has shown that FAS inhibition prevented smooth muscle cell proliferation, reversed pulmonary vascular remodeling and improved pulmonary vasoreactivity in monocrotaline induced PH model. However, the role of FAS in pulmonary artery endothelial cell proliferation and angiogenesis has not been explored. The present study was designed to explore the role of FAS in proliferation, metabolic dysfunctions, and angiogenesis in endothelial dysfunction associated with PH. The human pulmonary artery endothelial cells (HPAECs) were exposed to hypoxia and FAS siRNA (60nM) was used for the FAS inhibition. Increased expression and activity of FAS were observed in hypoxic HPAECs. Inhibition of FAS increased apoptosis and glucose oxidation, but decreased cellular proliferation, markers of autophagy and glycolysis in hypoxic HPAECs. FAS inhibition decreased the angiogenesis as evident by decreased tubule length and VEGF expression in hypoxic HPAECs. Inhibition of FAS also increased expression of endothelial NOS in hypoxic HPAECs, a marker of endothelial function. Our results proved, and further supported previous findings, that inhibition of FAS is beneficial for endothelial function in pulmonary hypertension.

Evaluation of the hemodynamics and right ventricular function in pulmonary hypertension by echocardiography compared with right-sided heart catheterization.

The present study aimed to evaluate hemodynamics and right ventricular function in patients with pulmonary hypertension (PH) using transthoracic echocardiography and to compare these results with measurements obtained using right-sided heart catheterization (RHC). A total of 75 patients with PH were examined using echocardiography and RHC. Patients were divided into the following two groups according to their difference between SPAPecho and SPAPRHC measurement: The overestimated group and underestimated group. The overestimated group included the subgroups groupover-A (difference <20 mmHg) and groupover-B (difference ≥20 mmHg), and the underestimated group included groupunder-A (absolute value of the difference <20 mmHg) and groupunder-B (absolute value of the difference ≥20 mmHg). SPAPecho measurements were revealed to be significantly positively correlated with SPAPRHC measurements (r=0.794; P<0.01). Among all echocardiographic measurements, only tricuspid annular plane systolic excursion (TAPSE) was significantly different between groups; it was increased in groupover-A and groupunder-A compared with groupover-B (P<0.01). Although SPAP measurements obtained using echocardiography were significantly positively correlated with those obtained using RHC, a high proportion of overestimation or underestimation of SPAP by echocardiography remained.

Right ventricular function in pulmonary hypertension due to left heart disease by two-dimensional speckle tracking and real time three-dimensional echocardiography.

Objective The aim of this study was to assess right ventricular (RV) function in pulmonary hypertension due to left heart disease (LHD-PH) by two-dimensional speckle tracking echocardiography (2D-S...

Use of β-Blockers in Pulmonary Hypertension.

Contrasting with the major attention that left heart failure has received, right heart failure remains understudied both at the preclinical and clinical levels. However, right ventricle failure is a major predictor of outcomes in patients with precapillary pulmonary hypertension because of pulmonary arterial hypertension, and in patients with postcapillary pulmonary hypertension because of left heart disease. In pulmonary hypertension, the status of the right ventricle is one of the most important predictors of both morbidity and mortality. Paradoxically, there are currently no approved therapies targeting the right ventricle in pulmonary hypertension. By analogy with the key role of β-blockers in the management of left heart failure, some authors have proposed to use these agents to support the right ventricle function in pulmonary hypertension. In this review, we summarize the current knowledge on the use of β-blockers in pulmonary hypertension.

(1107) - Comparison of Indirect Fick and Thermodilution Cardiac Output with Right Ventricular Function in Pulmonary Hypertension

(1107) - Comparison of Indirect Fick and Thermodilution Cardiac Output with Right Ventricular Function in Pulmonary Hypertension

Effects of Pulmonary Hypertension on Kidney Function

There is a scarcity of data defining hemodynamic correlates of renal function in pulmonary hypertension (PH). The aim of this study was to assess the correlation between standard and novel hemodynamic indices, including the pulmonary artery pulsatility index (PAPi) and the right atrial to pulmonary capillary wedge pressure (RA:PCWP) ratio, and renal function in PH. We conducted a retrospective study of adult patients with PH diagnosed by right-heart catheterization (RHC) between January 2007 and October 2012 at Einstein Medical Center, Philadelphia. Patients with end-stage renal disease were excluded. Pulmonary artery pulse pressure, RA:PCWP, PAPi (pulmonary artery pulse pressure/RA), as well as standard RHC variables were studied. The final cohort consisted of 171 patients. The median age was 59±13 years, 52% were men, and the mean pulmonary arterial pressure was 39±8.9 mm Hg. Sixty-eight patients had worsening creatinine from the time of admission to the time of RHC. Patients with a RA:PCWP of >0.86 had a significantly higher creatinine level at RHC (2.2±1.0 vs. 1.7±1.7 mg/dL, P=0.01) and worsening creatinine (+0.9±0.9 vs. +0.4±0.3 mg/dL, P=0.03). The major finding of this study is that in PH (all groups), worsening renal function from the time of admission to RHC correlated significantly with high RA:PCWP and low ejection fraction. High RA:PCWP was found to be a better predictor of worsening renal function than other novel and standard hemodynamic indices such as elevated right atrial pressure and PAPi.