Estimation Of Pulmonary Artery Pressure Research Articles

Echocardiographic evaluation of systolic and mean pulmonary artery pressure in patients with pulmonary hypertension

We read with interest the recent article by Pyxaras et al .1 proposing corrected regression equations for improving the echocardiographic estimation of systolic pulmonary artery pressure (sPAP) and mean pulmonary artery pressure (mPAP) in patients with pulmonary hypertension (PH). The authors propose to slightly modify both the sPAP Bernouilli equation and the empirical mPAP equation (mPAP = 0.61 sPAP + 2 mmHg). Before accepting the authors' conclusion that their two corrected formulas may be more reliable than previous ones, we would like to make the …

Noninvasive Estimation of Diastolic Pulmonary Artery Pressure by Doppler Analysis of Tricuspid Regurgitation Velocity in Pediatric Patients

Diastolic pulmonary artery pressure (dPAP) is equal to right ventricular pressure at the time of pulmonary valve opening. We studied the accuracy of dPAP estimated from Doppler profile of tricuspid regurgitation (TR) jet in pediatric patients. Echocardiograms were prospectively performed on consecutive pediatric heart transplant recipients undergoing right-heart catheterization and endomyocardial biopsy. An estimate of dPAP was obtained by superimposing the pulmonary valve opening time, indexed to the electrocardiogram, onto the TR Doppler tracing. Echocardiographic estimates of dPAP from end-diastolic pulmonary regurgitation (PR) were obtained for comparison. Catheter-derived right atrial pressure was added to the Doppler gradient in both groups. Doppler estimates and catheter-derived measurements of dPAP were compared using Lin correlation and Bland-Altman analysis. Sixty-five catheterization studies were performed on 35 patients (20 males): median age at enrollment: 12.1 years (4 months to 18 years); median time: since transplant of 1.2 years (21 days to 16.1 years). Adequate TR signal was obtained in a significantly higher proportion of patients than an adequate PR signal (65% vs. 43%, respectively, P = .007). Median catheter-derived dPAP was 12 mm Hg (6-30 mm Hg) and right atrial pressure was 6 mm Hg (1-17 mm Hg). Median estimated dPAP from TR was 15 mm Hg (range: 7-29 mm Hg), with the Lin correlation coefficient of 0.74 (95% confidence interval [CI]: 0.6-0.87). Median estimate for dPAP from PR was 10 mm Hg (range: 2-25 mm Hg), with the Lin correlation coefficient of 0.74 (95% CI: 0.58-0.9). There was excellent interobserver agreement for dPAP from TR with the Lin correlation coefficient of 0.946 (95% CI: 0.803-0.986). Doppler estimation of dPAP from TR is a novel, reliable, noninvasive method and compares favorably with estimation from PR. Adequate TR signal for estimation of dPAP can be obtained more frequently in children than adequate PR signal, thereby increasing the proportion of patients in whom dPAP can be estimated noninvasively.

Inaccuracy of Doppler Echocardiographic Estimates of Pulmonary Artery Pressures in Patients With Pulmonary Hypertension: Implications for Clinical Practice

Recent studies suggest that Doppler echocardiography (DE)-based estimates of pulmonary artery systolic pressure (PASP) may not be as accurate as previously believed. We sought to determine the accuracy of PASP measurements using DE compared with right-sided heart catheterization (RHC) in patients with pulmonary hypertension (PH). We compared DE estimates of PASP to invasively measure PASP during RHC in 160 consecutive patients with PH (part one). To account for possible changes in hemodynamics between DE and RHC, we then prospectively determined PASP in an additional 23 consecutive patients undergoing simultaneous RHC and DE (part two). Bland-Altman analyses were performed to evaluate the agreement between RHC and DE measurements of PASP. Accuracy was predefined as 95% limits of agreement within ± 10 mm Hg for PASP estimates. In part one, there was moderate correlation between DE and RHC measurements of PASP (r = 0.68, P < .001). However, using Bland-Altman analysis, the bias for DE estimates of PASP was 2.2 mm Hg with 95% limits of agreement ranging from -34.2 to 38.6 mm Hg. DE estimates of PASP were determined to be inaccurate in 50.6% of patients. In part two, there was moderate correlation between DE and RHC measurements of PASP (r = 0.71, P < .01). However, despite simultaneous DE and RHC measurements, the bias for DE estimates of PASP was 8.0 mm Hg with 95% limits of agreement ranging from -28.4 to 44.4 mm Hg. DE estimates of PASP are inaccurate in patients with PH and should not be relied on to make the diagnosis of PH or to follow the efficacy of therapy.

Discerning Pulmonary Venous From Pulmonary Arterial Hypertension Without the Help of a Catheter

Pulmonary hypertension (PH) is an increasingly recognized cause of dyspnea and effort intolerance that may develop in response to 5 broad categories of disease.1 After excluding patients with hypoxic pulmonary disease, thromboembolism, and other systemic disorders, the differential diagnosis narrows to group I PH (or pulmonary arterial hypertension [PAH] due to abnormalities in the pulmonary arterial vasculature) and group II PH (due to pulmonary venous hypertension from left-sided heart disease). Group II PH is straightforward to diagnose noninvasively when obvious culprits such as left ventricular (LV) systolic dysfunction or valvular heart disease are identified by echocardiography.2 However, half of patients with left-sided heart failure have preserved ejection fraction (HFpEF),3 without significant valvular disease, and it can be challenging to distinguish this group of patients from those with PAH, who similarly have a normal EF, elevated pulmonary artery (PA) pressure estimates, and diastolic dysfunction on echocardiogram. The treatments and mechanisms underlying PAH and HFpEF are quite different, so distinction of one from the other is of obvious clinical importance. Article see p 257 In the absence of shunts, the pulmonary and systemic circulations receive approximately the same amount of blood flow per minute, but this is where the similarities end. Pulmonary vascular resistance (PVR) is >10-fold lower than resistance in the systemic circulation, and the pressure in the venous bed draining the pulmonary arteries (pulmonary veins, left atrium) accounts for a much greater percentage of total PA pressure (40% to 60%) than the corresponding downstream venous pressure in the systemic circuit (right atrium, accounting for only ≈5% of systemic pressure). Because PA pressure is so heavily influenced by left heart filling pressures, it is not surprising that group II PH is the most common form of PH.2 PH has traditionally been defined by mean PA pressure in …

Correlation of Atrial Natriuretic Factor and Renin-Aldosterone System With Chronic Pulmonary Hypertension Among Residents in a High Altitude

The study was performed to evaluate right ventricular contractility, plasma renin activity, and atrial natriuretic peptide in high altitude pulmonary arterial hypertension (HAPH). Sixty-eight patients with signs of pulmonary artery hypertension (PPA,syst > 25 mmHg, PPA > 15 mmHg) (Group II) and 40 with normal coronary angiograms and normal pulmonary artery pressures (Group I) were included in the study. Right heart catheterization with estimation of right ventricular and pulmonary artery pressures were performed in all the patients. The blood samples were taken from the pulmonary artery for measurement of mean oxygen saturatioýn (SaO2), atrial natriuretic factor (ANF) level, plasma renin activity (PRA), aldosterone level, and sodium and potassium concentrations. Statistical analysis was performed using unpaired Student's t test and linear regression analysis. The patients with HAPH had higher pulmonary artery pressures (PPA,syst, PPA, PPA,diast), total pulmonary resistance (Rpulm,tot), and right ventricular systolic pressure (PRv,syst). The significant correlation was found between ANF and PRA with right ventricular contractility indices and pulmonary vascular resistance.

Pulmonary Artery Acceleration Time Provides an Accurate Estimate of Systolic Pulmonary Arterial Pressure during Transthoracic Echocardiography

Transthoracic echocardiographic estimates of peak systolic pulmonary artery pressure are conventionally calculated from the maximal velocity of the tricuspid regurgitation (TR) jet. Unfortunately, there is insufficient TR to determine estimated peak systolic pulmonary artery pressure (EPSPAP) in a significant number of patients. To date, in the absence of TR, no noninvasive method of deriving EPSPAP has been developed. Five hundred clinically indicated transthoracic echocardiograms were reviewed over a period of 6 months. Patients with pulmonic stenosis were excluded. Pulsed-wave Doppler was used to measure pulmonary artery acceleration time (PAAT) and right ventricular ejection time. Continuous-wave Doppler was used to measure the peak velocity of TR (TR(Vmax)), and EPSPAP was calculated as 4 × TR(Vmax)(2)+ 10 mm Hg (to account for right atrial pressure). The relationship between PAAT and EPSPAP was then assessed. Adequate imaging to measure PAAT was available in 99.6% of patients (498 of 500), but 25.3% (126 of 498) had insufficient TR to determine EPSPAP, and 1 patient had significant pulmonic stenosis. Therefore, 371 were included in the final analysis. Interobserver variability for PAAT was 0.97. There were strong inverse correlations between PAAT and TR(Vmax) (r= -0.96), the right atrial/right ventricular pressure gradient (r= -0.95), and EPSPAP (r= -0.95). The regression equation describing the relationship between PAAT and EPSPAP was log(10)(EPSPAP)= -0.004 (PAAT)+ 2.1 (P < .001). PAAT is routinely obtainable and correlates strongly with both TR(Vmax) and EPSPAP in a large population of randomly selected patients undergoing transthoracic echocardiography. Characterization of the relationship between PAAT and EPSPAP permits PAAT to be used to estimate peak systolic pulmonary artery pressure independent of TR, thereby increasing the percentage of patients in whom transthoracic echocardiography can be used to quantify pulmonary artery pressure.

Diagnosis and Assessment of Pulmonary Vascular Disease by Doppler Echocardiography

Pulmonary hypertension (PH) is a relatively misunderstood disease, partly related to the fact that many perceive PH to be a singular diagnosis. An unintended consequence of this is the misapplication of the role of the Doppler-Echocardiographic (DE) examination, as well as an underappreciation for its ability to help discern PH pathophysiology prior to right heart catheterization. Since DE often serves as the “gatekeeper” to invasive right heart catheterization, misinterpretation of the DE can lead to missed or delayed diagnosis with devastating consequences. Too often, the primary or nearly exclusive focus of the DE examination is placed on the pulmonary artery pressure estimation. Two main issues with this approach are that Doppler pressure estimations can be inaccurate and even when accurate, without integration of additional 2-D and Doppler information, the clinician will often still not appreciate the pathophysiology of the PH nor its clinical significance. This review will focus on the 2-D and Doppler features necessary to assess pulmonary vascular disease (PVD), discern the salient differences between PVD and pulmonary venous hypertension (PVH), and how to integrate these key DE parameters such that PH pathophysiology can be determined noninvasively and early in the patient workup. Overreliance on any single DE metric, and especially PA pressure estimation, detracts from the overall diagnostic potential of the DE examination. Integrating the relative balance of right and left heart findings, along with proper Doppler interpretation provides a wealth of clinical and pathophysiologic insight prior to invasive hemodynamic assessment. The end results are heightened awareness and improved identification of which patients should be referred for further invasive testing, as well the use of the DE information to compliment the findings from invasive testing.

677 Estimation of Mean Pulmonary Artery Pressure in the Sickle Cell Population

Studies suggest a higher prevalence of pulmonary hypertension (PH) in sickle cell disease (SCD), however, these relied mainly on transthoracic echocardiography (TTE) to establish a diagnosis. PH prevalence confirmed by right heart catheterization (RHC) is not well reported. Tricuspid regurgitant velocity (TRV) as an estimate of right sided pressures in this population is not validated and subject to poor correlation with RHC. We hypothesize that a model incorporating hemoglobin (Hb) concentration and TRV will increase accuracy of PH diagnosis by TTE.

The role of echocardiography in the diagnosis and management of patients with pulmonary hypertension

Pulmonary hypertension (PH) is defined as an increased mean pulmonary artery pressure (P(pa)) >25 mmHg at rest as assessed by right heart catheterisation (RHC). However, this technique is invasive and noninvasive alternatives are desirable for early diagnosis of PH. Although estimation of systolic pulmonary arterial pressure is easily obtained using Doppler echocardiography, cases of under- and over-estimations are not rare and direct measurement of P(pa) is not possible using this method. Therefore, echocardiography should be considered as a tool for assessment of the likelihood rather than the definite presence or absence of PH. Transthoracic echocardiography may be useful for noninvasive screening of patients at risk of PH. On the basis of an echocardiographic assessment, patients showing signs suggestive of PH can be referred for a confirmatory RHC. A number of variables measured during echocardiography reflect the morphological and functional consequences of PH and have prognostic value. The presence of pericardial effusion, reduced tricuspid annular plane excursion and right atrial enlargement are associated with a poorer prognosis. Echocardiography is also an important procedure for monitoring the response of patients to therapy, and is recommended 3-4 months after initiation of, or a change in, therapy. Echocardiographic assessment as part of a goal-oriented approach to therapy is essential for the effective management of PH patients.

Spontaneous Closure of a Ventricular Septal Defect in a Horse

Spontaneous Closure of a Ventricular Septal Defect in a Horse

Echocardiography may help detect pulmonary vasculopathy in the early stages of pulmonary artery hypertension associated with systemic sclerosis.

BackgroundPulmonary arterial hypertension (PAH) in patients with systemic sclerosis is associated with a poor prognosis, but this can be improved by early disease detection. Abnormal pulmonary and cardiac function can be detected early by means of echocardiography, whereas right heart catheterization is usually performed later.ObjectivesThe purpose of this prospective study was to detect early the presence of pulmonary artery vasculopathy in patients with verified systemic sclerosis without significant pulmonary fibrosis, normal lung volumes and a mildly reduced lung diffusion capacity of carbon monoxide (DLCO).MethodsNineteen consecutive female NYHA class I-II patients with scleroderma and a PAPs of < 35 mm/Hg measured by echocardiography, were enrolled between September 2007 and September 2009. They had a mean age of 51 ± 13 years, body mass index of 25 ± 5 kg/m2). They all underwent complete Doppler echocardiography, CPET, a pulmonary ventilation test (carbon monoxide lung diffusion, DLCO), HRCT. To investigate PAH by means of complete resting Doppler echocardiography estimates of systolic pulmonary artery pressure (PAPs) derived from tr icuspid regurgitation, mean PAP derived from pulmonary regurgitation, pulmonary vessel resistance (PVR) derived from the acceleration time of the pulmonary outflow tract (ACTpo), and right ventricular function derived from tricuspid annular plane systolic excursion (TAPSE). Right heart catheterisation was conducted only, if pulmonary hypertension was suggested by echocardiography and an abnormal ventilator test.The data are given as mean values ± SD, unless otherwise stated. The correlations between the variables were analysed using Pearson's r coefficient, and the predictive value of the variables was calculated using linear regression analysis. A p value of > 0.05 was considered significant.ResultsRight heart catheterization detected PAH in 15/19 patients; mean PAP was 30.5 mm/Hg and RVP 3.6 UW. Coronary angiography of the patients aged more than 55 years showed some evidence of significant coronary artery disease. Echocardiography showed high systolic PAP values (46 ± 8 mmHg), whereas right ventricular function was normal (TAPSE 23 ± 3 mm), and in line with the NYHA class. ACTpo was reduced in the patients with a systolic PAP of < 46 mm/Hg (p > 0.001) and positively correlated with DLCO (p > 0.001) and the hemodynamic data.There was a good correlation between ACTpo and PVR (hemodynamic data) (r = -0615; p > 0.01).ConclusionsAlthough they need to be confirmed by studies of larger series of patients, our findings suggest that, in comparison with hemodynamic data, non-invasive echocardiographic measurements are an excellent means of identifying early-stage PAH.

Echocardiographic abnormalities and their correlation with bronchiectasis score in primary antibody deficiencies

Primary antibody deficiencies are characterized by defective antibody production and recurrent infections. Patients usually present with recurrent respiratory tract infections with consequent chronic pulmonary damage and bronchiectasis, which could potentially influence cardiac function. Our aim was to assess noninvasively the cardiac complications due to pulmonary disease in patients with primary antibody deficiency. A cross-sectional series of patients with primary antibody deficiency syndromes from our referral immunology center were recruited. Individuals undergoing high-resolution computed tomography (HRCT) and transthoracic echocardiography were reviewed. Thirty primary immunodeficient patients aged 5-55 years of age (21 males and 9 females) were enrolled in this study. Half of the patients (50%) were found to have bronchiectasis in HRCT imaging. In echocardiographic examination, 20 patients (67%) had at least one abnormality; among which pulmonary hypertension was the most common (33%). Patients with bronchiectasis had higher pulmonary artery pressures and HRCT bronchiectasis score was strongly correlated with pulmonary artery pressure (regression R = 0.59, P value = 0.001). Echocardiographic evaluation of right ventricular function and noninvasive estimation of pulmonary artery pressure could have an important diagnostic role in the follow-up and therapeutic management of patients with primary immune deficiency.

Estimation of pulmonary artery pressure by measuring the size of the right pulmonary artery with transesophageal ultrasonographic endoscopy

Estimation of pulmonary artery pressure by measuring the size of the right pulmonary artery with transesophageal ultrasonographic endoscopy

Functional Valve Assessment : The Emerging Role Of Cardiovascular Magnetic Resonance

The prevalence of valvular heart disease is increasing along with the life span of the population. In assessing individuals with valve disease, echocardiography is the primary imaging modality used by clinicians both for initial assessment and for longitudinal evaluation. Information regarding valve morphology and function, cardiac chamber size, wall thickness, ventricular function, and estimates of pulmonary artery pressures can be readily obtained and integrated to formulate an assessment of valve disease severity. In some instances, body habitus or the presence of coexisting lung disease may result in suboptimal acoustic windows on echocardiography, which may lead to technically difficult studies. Additionally, in some patients, information from clinical history and physical examination or other diagnostic tests may be discordant with echocardiographic findings. In these instances, there is a significant clinical role for cardiovascular magnetic resonance (CMR). The diagnostic capabilities of CMR have increased substantially over the past 20 years due to hardware and software advances. Today, CMR has a number of unique advantages over other imaging modalities - primarily, it provides a view of the entire heart without limitations from inadequate imaging windows or body habitus. Furthermore, CMR can obtain imaging data in any imaging plane prescribed by the scan operator, which makes it ideal for accurate investigation of all cardiac valves - aortic, mitral, pulmonic, and tricuspid. In addition, CMR for valve assessment is noninvasive, free of ionizing radiation, and in most instances does not require contrast administration. Since a comprehensive review of the role of CMR in all valve lesions is beyond the scope of this article, we will focus on the most common valvular indication for performance of clinical CMR techniques and an overview of selected validation and reproducibility studies. The objectives of a comprehensive CMR study for evaluating mitral insufficiency are threefold: 1) to provide insight into the mechanism of mitral insufficiency, and 3) to discern the consequences of the lesions including the effects on left ventricular (LV) volume, LV systolic function, and left atrial volumes. In most instances this information can be obtained without the need for intravenous contrast agents (gadolinium). Therefore, CMR can be performed even in patients with severe renal failure.

Acute Hemodynamic and Vascular Effects of Transfusion in Chronically Transfused Patients with Sickle Cell Anemia.

Abstract 1516Poster Board I-539 IntroductionPatients with sickle cell anemia (SCA) who are at risk for stroke or develop recurrent episodes of acute chest are often placed on chronic transfusion therapy. The acute hemodynamic and vascular consequences of transfusion are poorly characterized. In order to better characterize chronic changes in these patients, it is important to understand the acute changes involved with this intervention. MethodsWe enrolled SCA patients who are on chronic transfusion therapy in a prospective study to determine the cardiovascular effects of a single transfusion. The patients were older than 10 years of age, received chronic transfusions for greater than one year, and were crisis free for more than four weeks. All patients were studied immediately prior to transfusion and repeated within five days. Brachial artery relaxivity, laser doppler capillary blood flow monitoring, and near infrared spectroscopy of the hand was done in the setting of post occlusive reactive hyperemia. Studies included complete cardiac echocardiogram as well as laboratory markers of hemolysis, iron levels, blood count, viscosity and inflammation were obtained pre and post transfusion. Statistics utilized paired t-tests for paired data and for correlative data t-tests and chi square analysis was used. ResultsThere are 15 patients enrolled in the study with an average age of 18.7yrs. There are 8 females and 7 males with average ages of 20.6 and 16.4 yrs respectively. With transfusion, hemoglobin increased from 9.4 g/dl to 11.6 g/dl post (p<0.0001), reticulocyte count decreased from 12.4% to 7.8% (p=0.0019) and HbS% decreased from 38.2% to 31.5% (p=0.0001). Markers of hemolysis (LDH, Plasma Free Hemoglobin, Arg/Orn Ratio) do not differ significantly pre and post transfusion. Cardiac index decreased from 5.4L/min/m2 to 4.1 L/min/m2 (p=0.0012), resulting from decreased stroke volume (70.8ml to 58.9ml, p=0.0119) and lower heart rate (84 to 78bpm, p=0.0098). Systolic and diastolic function metrics were unchanged, as was estimates of pulmonary artery pressure. Blood pressure was unchanged, indicating that the change in cardiac output was matched by parallel changes in total vascular resistance. Endothelial function and regional vascular reactivity assessed using laser Doppler capillary flow analysis demonstrated no significant change in hyperemic response pre and post transfusion. Blood viscosity increased with transfusion in a shear-rate dependent manner, for low shear rates the viscosity increased an average of 62% using fully oxygenated samples and at higher shear rates the viscosity increased an average of 25% using fully oxygenated samples. DiscussionTransfusion therapy predictably increased oxygen carrying capacity, lowered reticulocyte count and %hemoglobin S. While these changes might improve tissue oxygen delivery, parallel changes in vascular resistance served to maintain relatively constant oxygen delivery. The rise in vascular resistance could result from increased blood viscosity or changes in vascular tone; we are currently conducting studies to try to separate these mechanisms. Despite the 24% reduction in cardiac index, no significant change was observed in microvascular perfusion or its response to forearm occlusion. The vascular system of SCA patients demonstrates chronic endothelial dysfunction but was not acutely influenced by transfusions, consistent with the lack of acute improvement in surrogates for hemolysis or nitric oxide metabolism. Further work is necessary to determine whether transfusion-mediated changes in tissue oxygen delivery vary among different organs and vascular beds. DisclosuresWood:Novartis: Research Funding.

Echocardiographic Evaluation of Diastolic Function Can Be Used to Guide Clinical Care

For normal cardiac performance, the left ventricle (LV) must be able to eject an adequate stroke volume at arterial pressure (systolic function) and fill without requiring an elevated left atrial (LA) pressure (diastolic function). These systolic and diastolic functions must be adequate to meet the needs of the body both at rest and during stress. Response by Tschope and Paulus on p 809 Systolic function is conveniently (although not always accurately) measured as the ejection fraction (EF), calculated as stroke volume divided by end-diastolic volume.1 The LV EF is easily interpreted. The lower limit of normal is ≈50%. The lower the EF is, the greater the reduction in systolic function. Diastolic function has been more difficult to evaluate.2 Traditionally, invasive measures of LV diastolic pressure-volume relations and the rate of LV pressure fall during isovolumetric relaxation have been used. However, these methods are not practical for routine clinical use and do not adequately evaluate all aspects of diastolic filling.3 Comprehensive echocardiographic evaluation of the dynamics of LV filling using blood pool and tissue Doppler has now progressed so that it provides clinically important information that can be used to direct patient care. We present data that support the use of echocardiographic evaluation of diastolic function to recognize cardiac dysfunction in patients with heart failure, especially those with preserved EF; to guide the management of patients by identifying those with and without elevated left filling pressures regardless of underlying EF; and to determine prognosis in a wide variety of patient populations. Although the LV end-diastolic pressure-volume relation describes the passive properties of the LV, LV filling is not a passive or slow process.3 In fact, the peak flow rate across the mitral valve is equal to or greater than the peak flow rate across the aortic valve. …

Bosentan Decreases Pulmonary Vascular Resistance and Improves Exercise Capacity in Acute Hypoxia

Altitude exposure is associated with mild pulmonary hypertension and decreased exercise capacity. We tested the hypothesis that pulmonary vascular resistance (PVR) contributes to decreased exercise capacity in hypoxic healthy subjects. An incremental cycle ergometer cardiopulmonary exercise test and echocardiographic estimation of pulmonary artery pressure (Ppa) and cardiac output to calculate total PVR were performed in 11 healthy volunteers in normoxia and after 1 h of hypoxic breathing (12% O(2)). The measurements were performed in a random order at 1-week intervals after the receiving either a placebo or bosentan, following a double-blind randomized crossover design. Bosentan was administered twice a day for 3 days, 62.5 mg on the first day and 125 mg on the next 2 days. Hypoxic breathing decreased the mean (+/- SE) pulse oximetric saturation (Spo(2)) from 99 +/- 1% to 3 +/- 1% and increased the mean PVR from 5.6 +/- 0.3 to 7.2 +/- 0.5 mm Hg/L/min/m(2), together with a decrease in mean maximum O(2) uptake (Vo(2)max) from 47 +/- 2 to 35 +/- 2 mL/kg/min. Bosentan had no effect on normoxic measurements and did not affect hypoxic Spo(2), but decreased PVR to 5.6 +/- 0.3 mm Hg/L/min/m(2) (p < 0.01) and increased Vo(2)max to 39 +/- 2 mL/kg/min (p < 0.01) in hypoxia. Bosentan therapy, on average, restored 30% of the hypoxia-induced decrease in Vo(2)max. Bosentan-induced changes in Ppa and Vo(2)max were correlated (p = 0.01). We conclude that hypoxic pulmonary hypertension partially limits exercise capacity in healthy subjects, and that bosentan therapy can prevent it.

Pulmonary venous wedge pressure provides a safe and accurate estimate of pulmonary arterial pressure in children with shunt-dependent pulmonary blood flow

To compare two methods of pulmonary arterial pressure measurement in children with shunt-dependent pulmonary blood flow. In children with shunt-dependent pulmonary blood flow, direct assessment of pulmonary arterial pressure requires passage of a catheter across the shunt. This can be technically difficult and dangerous. Use of the pulmonary venous wedge pressure offers an alternative but has not been validated in this patient population. We prospectively studied 18 children with shunt-dependent pulmonary blood flow. Pulmonary venous wedge pressure and directly measured pulmonary arterial pressures were independently assessed by two blinded cardiologists. Directly measured mean pulmonary arterial pressure and pulmonary venous wedge pressure are closely correlated (R2 = 0.80, P < 0.01). Agreement between the two measures is improved at lower mean pressures with greater differences at higher pressures. For 20 of 24 ipsilateral measurements, pulmonary venous wedge pressure was > or = directly measured pulmonary arterial pressure. Pulmonary venous wedge pressure never underestimated pulmonary arterial pressure by more than 3 mm Hg. Pulmonary venous wedge pressure provides a safe and accurate means of estimating pulmonary arterial pressure in children with shunt-dependent pulmonary blood flow. The slightly lower pressures seen on direct measurement compared with the reverse pulmonary vein may reflect impairment of flow across the shunt by the catheter.

Accuracy of Doppler Echocardiography in the Hemodynamic Assessment of Pulmonary Hypertension

Transthoracic Doppler echocardiography is recommended for screening for the presence of pulmonary hypertension (PH). However, some recent studies have suggested that Doppler echocardiographic pulmonary artery pressure estimates may frequently be inaccurate. Evaluate the accuracy of Doppler echocardiography for estimating pulmonary artery pressure and cardiac output. We conducted a prospective study on patients with various forms of PH who underwent comprehensive Doppler echocardiography within 1 hour of a clinically indicated right-heart catheterization to compare noninvasive hemodynamic estimates with invasively measured values. A total of 65 patients completed the study protocol. Using Bland-Altman analytic methods, the bias for the echocardiographic estimates of the pulmonary artery systolic pressure was -0.6 mm Hg with 95% limits of agreement ranging from +38.8 to -40.0 mm Hg. Doppler echocardiography was inaccurate (defined as being greater than +/-10 mm Hg of the invasive measurement) in 48% of cases. Overestimation and underestimation of pulmonary artery systolic pressure by Doppler echocardiography occurred with a similar frequency (16 vs. 15 instances, respectively). The magnitude of pressure underestimation was greater than overestimation (-30 +/- 16 vs. +19 +/- 11 mm Hg; P = 0.03); underestimates by Doppler also led more often to misclassification of the severity of the PH. For cardiac output measurement, the bias was -0.1 L/min with 95% limits of agreement ranging from +2.2 to -2.4 L/min. Doppler echocardiography may frequently be inaccurate in estimating pulmonary artery pressure and cardiac output in patients being evaluated for PH.

Noninvasive Estimation of Mean Pulmonary Arterial Pressure and Capacitance in Elderly Patients with Pulmonary Hypertension

Noninvasive Estimation of Mean Pulmonary Arterial Pressure and Capacitance in Elderly Patients with Pulmonary Hypertension