Pulmonary Vascular Resistance In Patients Research Articles

A novel echocardiography formula for calculating predicted pulmonary vascular resistance in patients with mitral stenosis

Background: Pulmonary vascular resistance (PVR) plays an important role in the natural history, prognosis, and outcome after valve intervention in patients with mitral stenosis (MS). The existing formula to estimate PVR by means of echocardiography is not readily applicable in the MS patient subset because it does not specifically calculate the risk of PVR in MS. The aim of this study was to find a new echocardiography formula to estimate PVR in MS.Methods: This diagnostic study was conducted in 2 stages. In the first stage, 58 consecutive subjects with MS were studied to find some model formulas for estimating PVR by multiple regression. Eight echo parameters were analyzed to seek their correlation with the invasive PVR value as a gold standard. The formula that had the best correlation and was easiest to use would be selected. In the second stage, those model formulas were validated by applying them to a further 34 consecutive MS subjects.Results: Four formulas which gave a discriminator coefficient of r2 0.62–0.68 were derived. The best model formula was proposed for further application. The new selected formula PVR=-7.465+3.566 TRvmax –(0.23 TVs’)+6.799 (RV-MPI) showed good correlation (r=0.71, p<0.001) to the invasive PVR value, with good reliability. TRvmax is maximal velocity of tricuspid regurgitation, TVs’ is systolic velocity of tricuspid annulus, and RV-MPI is right ventricle index myocardial performance. ROC curve showed that the cut off point 7.2 has good sensitivity and specificity (90% and 88%, respectively) to predict PVR 7 WU.Conclusion: This study has shown that a novel echocardiography formula can estimate PVR with good correlation and reliability in subjects with mitral stenosis.

Sildenafil reduces pulmonary vascular resistance in single ventricular physiology

BackgroundHigh pulmonary vascular resistance (PVR) may be a risk factor for early and late mortality in both Glen shunt and Fontan operation patients. Furthermore, PVR may increase long after the Fontan operation. Whether pulmonary vasodilators such as phosphodiesterase 5 inhibitors can decrease PVR in patients with single ventricular physiology remains undetermined. Methods and resultsThis was a prospective, multicenter study. Patients with single ventricular physiology who have a PVR index higher than 2.5 Wood units·㎡ (WU) were enrolled. Cardiac catheterization was performed before and after administration of sildenafil in all patients. After the Fontan operation, a six minute walk test (6MWT) was also performed. A total of 42 patients were enrolled. PVR was significantly decreased in each stage of single ventricular physiology after sildenafil administration: from 4.3±1.5WU to 2.1±0.6WU (p<0.01) in patients before a Glenn shunt, from 3.2±0.5WU to 1.6±0.6WU (p<0.001) in patients after a Glenn shunt, and from 3.9±1.7WU to 2.3±0.8WU (p<0.001) in patients after Fontan. In patients after Fontan, the 6MWT increased from 416±74m to 485±72m (p<0.01), and NYHA functional class improved significantly (p<0.05) after sildenafil administration. No major side effects were observed in any patients. ConclusionsSildenafil reduced PVR in patients with single ventricle physiology. Sildenafil increased exercise capacity and improved NYHA functional class in patients after a Fontan operation. This implies that pulmonary vasodilation is a potential therapeutic target in selected patients with elevated PVR with single ventricle physiology. Long-term clinical significance warrants further study.

Left Ventricular Assist Devices or Inotropes for Decreasing Pulmonary Vascular Resistance in Patients with Pulmonary Hypertension Listed for Heart Transplantation

BackgroundFixed pulmonary hypertension is common in patients with advanced heart failure and is a contraindication for heart transplantation. Left ventricular assist devices (LVAD) and inotropes have been used to reduce pulmonary vascular resistance (PVR) and allow transplantation. However, little is known about the efficacy of this strategy. MethodsWe queried the United Network for Organ Sharing registry for all adult patients (age ≥18 years) listed for primary heart transplantation (2008–2014) with PVR of >5 wood units (WU) or transpulmonary gradient >16 mmHg who were treated with LVAD or IV inotropes as status 1a, 1b, or 7. We compared waitlist mortality/delisting and absolute changes in hemodynamics between listing and transplantation. ResultsOf 18,009 patients listed during the study period, 1016 were included in the analysis (393 LVAD, 623 inotropes), with a mean age of 52.9 ± 11.6 years, 74% male, and 38% had ischemic etiology. Mean PVR was 5.7 ± 2.4 WU and transpulmonary pressure gradient 19.3 ± 5.3 mmHg. Compared with the inotrope group, LVAD patients were more likely listed as status 1A (32.8% vs 18.1%, P < .001), had lower PVR (5.3 WU vs 5.9 WU, P = .001), and higher cardiac output (4.1 vs 3.6 L/min, P < .001). After a mean of 239 days, PVR decreased by 1.71 WU in the LVAD group vs 1.85 WU in the inotrope group (P = .52). PVR normalization (<2.5 WU) occurred at similar rates among those treated with inotropes and LVAD (30.7% vs 35.6%, P = .228). Waitlist mortality was similar between LVAD and inotropes (adjusted P = .837). Absolute PVR and transpulmonary pressure gradient reductions correlated with time on the waitlist (P < .001 for both comparisons). ConclusionOnly about one-third of patients with fixed pulmonary hypertension achieve normalization of PVR before transplant with either LVAD or inotropes. Similar waitlist mortality was observed among patients bridged with either strategy.

WCC 2016-119: Role of Speckle Tracking Echocardiography in Noninvasive Assessment of Pulmonary Vascular Resistance in Patients with Pulmonary Hypertension

WCC 2016-119: Role of Speckle Tracking Echocardiography in Noninvasive Assessment of Pulmonary Vascular Resistance in Patients with Pulmonary Hypertension

Assessment of Right Ventricular Afterload in COPD

Background: We aimed to study whether pulmonary hypertension (PH) and elevated pulmonary vascular resistance (PVR) could be predicted by conventional echo Doppler and novel tissue Doppler imaging (TDI) in a population of chronic obstructive pulmonary disease (COPD) free of LV disease and co-morbidities.Methods: Echocardiography and right heart catheterization was performed in 100 outpatients with COPD. By echocardiography the time-integral of the TDI index, right ventricular systolic velocity (RVSmVTI) and pulmonary acceleration-time (PAAcT) were measured and adjusted for heart rate. The COPD patients were randomly divided in a derivation (n = 50) and a validation cohort (n = 50). Results: PH (mean pulmonary artery pressure (mPAP) ≥ 25mmHg) and elevated PVR ≥ 2Wood unit (WU) were predicted by satisfactory area under the curve for RVSmVTI of 0.93 and 0.93 and for PAAcT of 0.96 and 0.96, respectively. Both echo indices were 100% feasible, contrasting 84% feasibility for parameters relying on contrast enhanced tricuspid-regurgitation. RVSmVTI and PAAcT showed best correlations to invasive measured mPAP, but less so to PVR. PAAcT was accurate in 90- and 78% and RVSmVTI in 90- and 84% in the calculation of mPAP and PVR, respectively. Conclusions: Heart rate adjusted-PAAcT and RVSmVTI are simple and reproducible methods that correlate well with pulmonary artery pressure and PVR and showed high accuracy in detecting PH and increased PVR in patients with COPD. Taken into account the high feasibility of these two echo indices, they should be considered in the echocardiographic assessment of COPD patients.

Pulmonary Vascular Resistance in Patients With Pulmonary Hypertension: Importance of the Quadratic Velocity-Pressure Relationship – Reply –

Pulmonary Vascular Resistance in Patients With Pulmonary Hypertension: Importance of the Quadratic Velocity-Pressure Relationship – Reply –

Three-Dimensional Echocardiography in the Evaluation of Right Ventricular Global and Regional Systolic Function in Patients with Atrial Septal Defect before and after Percutaneous Closure.

To evaluate right ventricular (RV) global and regional systolic function in patients with atrial septal defect (ASD) before and after percutaneous closure using real time three-dimensional echocardiography (RT3DE). RT3DE was performed in 81 patients with ASD within 24 hours before and after percutaneous closure to obtain RV global and regional ejection fraction (EF) in three compartments (inflow, body, and outflow). RV fractional area change (FAC), tricuspid annular plane systolic excursion (TAPSE), peak tricuspid systolic velocity (S), and pulmonary vascular resistance (PVR) were recorded. Forty matched normal adults were included as controls. When compared with controls, RV global and regional EF were decreased in preclosure patients (P < 0.001). FAC was lower while TAPSE and S were higher in preclosure patients than in controls (P < 0.05). After closure, RV systolic function parameters were all reduced (P < 0.001). Regional EF in the body compartment was the lowest among the three compartments in ASD patients (P < 0.05). Procedural percentage changes of RV global EF and regional EF in the inflow compartment were lower than those of two-dimensional systolic function parameters (P < 0.05). RV global and regional EF in the inflow compartment were negatively correlated with PVR in patients after closure (r = -0.601, -0.543, P < 0.001). RV global and regional systolic functions are impaired in open and closed ASD. RT3DE-derived systolic function parameters are negatively correlated with RV after load. RT3DE has potential value in the evaluation of RV systolic function in patients with ASD.

A feasible method for non-invasive measurement of pulmonary vascular resistance in pulmonary arterial hypertension: Combined use of transthoracic Doppler-echocardiography and cardiac magnetic resonance. Non-invasive estimation of pulmonary vascular resistance

BackgroundTransthoracic Doppler-echocardiography (TTE) can estimate mean pulmonary arterial pressure (MPAP) and pulmonary capillary wedge pressure (PCWP) reliably, and cardiac magnetic resonance (CMR) is the best modality for non-invasive measurement of cardiac output (CO). We speculated that the combined use of TTE and CMR could provide a feasible method for non-invasive measurement of pulmonary vascular resistance (PVR) in pulmonary arterial hypertension (PAH). Methods and resultsRight heart catheterization (RHC) was undertaken in 77 patients (17M/60F) with PAH, and simultaneous TTE was carried out to evaluate MPAP, PCWP and CO. Within 2days, CO was measured again with CMR in similar physiological status. Then, PVR was calculated with the integrated non-invasive method: TTE-derived (MPAP–PCWP)/CMR-derived CO and the isolated TTE method: TTE-derived (MPAP–PCWP)/TTE-derived CO, respectively. The PVR calculated with integrated non-invasive method correlated well with RHC-calculated PVR (r=0.931, 95% confidence interval 0.893 to 0.956). Between the integrated non-invasive PVR and RHC-calculated PVR, the Bland–Altman analysis showed the satisfactory limits of agreement (mean value: −0.89±2.59). In comparison, the limits of agreement were less satisfactory between TTE-calculated PVR and RHC-calculated PVR (mean value: −1.80±3.33). Furthermore, there were excellent intra- and inter-observer correlations for the measurements of TTE and CMR (P<0.001 for all). ConclusionsThe combined use of TTE and CMR provides a clinically reliable method to determine PVR non-invasively. In comparison with RHC, the integrated method shows good accuracy and repeatability, which suggests the potential for the evaluation and serial follow-up in patients with PAH. Translational perspectiveIn PAH, the non-invasive measurement of PVR is very important in clinical practice. Up to now, however, the widely accepted non-invasive method is still unavailable. Since TTE can estimate (MPAP–PCWP) reliably and CMR is the best image modality for the measurement of CO, the combined use of two modalities has the potential to determine PVR non-invasively. In this research, the integrated non-invasive method showed good diagnostic accuracy and repeatability compared with RHC. Therefore, it might be a feasible method for non-invasive measurement of PVR in patients with PAH.

Right Ventricular Outflow Tract Doppler Envelope Notching Predicts Pulmonary Vascular Resistance in Patients with Advanced Liver Disease

Portopulmonary hypertension (POPH) affects 6% of liver transplant (LT) candidates and is associated with poor outcomes. Screening for POPH with a transthoracic echocardiogram (TTE) is the standard of care, but diagnosis requires right heart catheterization (RHC) which carries risks in pts with advanced liver disease (ALD). Systolic deceleration or “notching” of the right ventricular outflow tract Doppler flow velocity envelope (FVERVOT) correlates with high pulmonary vascular resistance (PVR) in mixed pulmonary hypertension (PH) but has not been validated in pts with ALD. The ratio of peak tricuspid regurgitant velocity (TRV, m/s) and time-velocity integral of the RVOT (TVIRVOT) per the formula PVR=TRV/TVIRVOT x 10 has been shown to reliably estimate PVR. We investigated whether PVR can be predicted by the shape of FVERVOT or estimated by the TRV/TVIRVOT ratio in pts undergoing evaluation for LT. We included 100 pts who underwent RHC and TTE as part of LT evaluation from 01/10 to 03/15. Median time between the two tests was 5 days. We categorized the shape of FVERVOT as no (NN), late-systolic (LSN) or mid-systolic (MSN) notching. Unpaired t-tests were used to compare sample means for continuous variables and linear regression analysis to test the correlation between invasive and non-invasive PVR. The mean patient age was 57±8.5 years; 50% were male with diverse etiologies of ALD (35% HCV, 21% alcoholic, 10% cryptogenic, 6% NASH, 4% autoimmune, 24% other) and 79% were transplanted. The prevalence of POPH as defined by PVR≥3 on RHC was 12%. Elevated systolic pulmonary artery pressure (PAPs≥40mmHg) on TTE was present in 54% and mean PAP≥25mmHg on RHC in 24%. The shape of the FVERVOT Doppler exhibited NN in 81%, LSN in 10% and MSN in 9%. Pts with either LSN or MSN had higher mean PAP than those with NN (28±9 vs 35±11mmHg, p=0.007) and higher transpulmonary gradient (TPG), diastolic pulmonary gradient (DPG) and PVR; the difference between LSN and MSN was not significant. TAPSE was lower in pts with LSN or MSN compared to NN (Fig 1), and non invasively estimated PVR was higher (1.8±0.5 vs 1.4±0.5 WU, p=0.003). Poor correlation was observed between noninvasive and invasive PVR (R2=0.10, p=0.001). RVOT notching and non-invasive PVR were poor predictors of mortality. Elevated PAPs on TTE was a sensitive but not specific screening tool for PVR≥3 (Sn=82%, Sp=48%). RVOT Doppler flow velocity notching reliably predicts POPH in pts with ALD.

Noninvasive assessment of pulmonary vascular resistance by echocardiography in chronic thromboembolic pulmonary hypertension.

Pulmonary vascular resistance (PVR) is an important parameter in the management of patients with chronic thromboembolic pulmonary hypertension (CTEPH), and numerous noninvasive methods for PVR prediction have been proposed. However, a systematic evaluation of the methods that are specific for CTEPH has not been conducted. We compared a variety of echocardiography-derived prediction indices with direct right heart catheterization (RHC) to identify the most reliable noninvasive indicator of PVR in patients with CTEPH. Echocardiography and RHC were performed sequentially in 40 patients (mean age: 62.4±11.4 years; 30 females) with CTEPH. We measured the peak flow velocity of tricuspid regurgitation (TRV), tricuspid regurgitation pressure gradient (TRPG), right ventricular outflow tract (RVOT) time-velocity integral (TVIRVOT), left ventricular outflow tract (LVOT) time-velocity integral (TVILVOT), cardiac output at RVOT (CORVOT), and the LVOT (COLVOT) using echocardiography. The parameters TRV/TVIRVOT, TRV/TVILVOT, TRV/CORVOT, TRV/COLVOT, TRPG/TVIRVOT, TRPG/TVILVOT, TRPG/CORVOT, and TRPG/COLVOT were then calculated to predict the PVR. Finally, correlations between these echocardiographic predictors of PVR and the PVR data obtained from RHC (PVRRHC) were assessed. The mean pulmonary arterial pressure and PVRRHC were 32.1±11.4mmHg and 5.4±2.9 Wood units, respectively. TRV/TVIRVOT, TRV/TVILVOT, TRV/COLVOT, TRPG/TVIRVOT, TRPG/TVILVOT, TRPG/CORVOT, and TRPG/COLVOT were all significantly correlated with the PVRRHC, and TRPG/COLVOT was the most strongly correlated with the PVRRHC (r=0.807, p<0.001). Echocardiographic measurement of TRPG/COLVOT is a reliable noninvasive predictor of PVR in CTEPH patients.

(53) - Does Device Type Differentially Influence Pulmonary Vascular Resistance in Patients Bridged to Transplantation With a Continuous Flow Left Ventricular Assist Device?

(53) - Does Device Type Differentially Influence Pulmonary Vascular Resistance in Patients Bridged to Transplantation With a Continuous Flow Left Ventricular Assist Device?

REPEATED ORAL ADMINISTRATION OF THE SELECTIVE PROSTACYCLIN RECEPTOR AGONIST SELEXIPAG DOES NOT CAUSE TACHYPHYLAXIS IN SPONTANEOUSLY HYPERTENSIVE RATS

Selexipag, an orally available, selective prostacyclin (PGI2) receptor (IP receptor) agonist, significantly decreased pulmonary vascular resistance in patients with pulmonary arterial hypertension (PAH) in a phase 2 clinical trial. Selexipag is structurally different from PGI2. Reduced clinical

Upregulated expression of STIM2, TRPC6, and Orai2 contributes to the transition of pulmonary arterial smooth muscle cells from a contractile to proliferative phenotype.

Pulmonary arterial hypertension (PAH) is a progressive disease that, if left untreated, eventually leads to right heart failure and death. Elevated pulmonary arterial pressure (PAP) in patients with PAH is mainly caused by an increase in pulmonary vascular resistance (PVR). Sustained vasoconstriction and excessive pulmonary vascular remodeling are two major causes for elevated PVR in patients with PAH. Excessive pulmonary vascular remodeling is mediated by increased proliferation of pulmonary arterial smooth muscle cells (PASMC) due to PASMC dedifferentiation from a contractile or quiescent phenotype to a proliferative or synthetic phenotype. Increased cytosolic Ca(2+) concentration ([Ca(2+)]cyt) in PASMC is a key stimulus for cell proliferation and this phenotypic transition. Voltage-dependent Ca(2+) entry (VDCE) and store-operated Ca(2+) entry (SOCE) are important mechanisms for controlling [Ca(2+)]cyt. Stromal interacting molecule proteins (e.g., STIM2) and Orai2 both contribute to SOCE and we have previously shown that STIM2 and Orai2, specifically, are upregulated in PASMC from patients with idiopathic PAH and from animals with experimental pulmonary hypertension in comparison to normal controls. In this study, we show that STIM2 and Orai2 are upregulated in proliferating PASMC compared with contractile phenotype of PASMC. Additionally, a switch in Ca(2+) regulation is observed in correlation with a phenotypic transition from contractile PASMC to proliferative PASMC. PASMC in a contractile phenotype or state have increased VDCE, while in the proliferative phenotype or state PASMC have increased SOCE. The data from this study indicate that upregulation of STIM2 and Orai2 is involved in the phenotypic transition of PASMC from a contractile state to a proliferative state; the enhanced SOCE due to upregulation of STIM2 and Orai2 plays an important role in PASMC proliferation.

Stepwise Approach Using Combined Management in Patients with Congenital Heart Disease and Borderline Pulmonary Vascular Disease.

Background and ObjectivesDespite remarkable advances in pediatric cardiology, pulmonary arterial hypertension associated with congenital heart disease remains a major problem. In the past decade new vasodilators have been introduced and appear to be effective in reducing pulmonary vascular resistance (PVR).Subjects and MethodsFrom 2000 to 2011, we retrospectively reviewed the records of 22 patients who had congenital septal defects and borderline pulmonary vascular disease (PVD). The PVR in these patients was from 6 to 16 wood units · m2, and/or the systolic pulmonary arterial pressure was more than 2/3 of the systemic arterial pressure.ResultsThe median age was 16 years (range, 9 months-46 years). The median duration of follow-up was 7.4 years (range, 1.4-11.7 years). According to hemodynamic data and clinical symptoms, the initial management comprised targeted medical therapy in four (18%), complete closure in four (18%), and partial closure in 14 patients (63.6%). In the four patients who had a high PVR and negative vasoreactivity, the PVR decreased and vasoreactivity increased after targeted medical therapy; three of these patients underwent cardiac surgery later. Finally, 11 (50%) received targeted medical therapy and 21 patients (95.4%) underwent cardiac surgery. Complete closure resulted in six patients and partial closure in 17 patients. Mortality was observed in two patients. The other 19 patients (91%) had New York Heart Association functional class I.ConclusionTargeted medical therapy may be effective in reducing PVR in patients with congenital heart disease and borderline PVD. A stepwise approach may help to achieve improved outcomes in these patients.

Efficacy of pulmonary vasodilator therapy in patients with functionally single ventricle.

This study retrospectively evaluated the effectiveness of pulmonary vasodilator therapy with bosentan (n = 14) and/ or sildenafil (n = 23) in 34 patients with a functionally single ventricle. Vasodilator therapy was initiated before the Fontan procedure in 18 patients and after the procedure in 16 patients. The reasons for vasodilator treatment included high pulmonary artery pressure or pulmonary vascular resistance (n = 8), high central venous pressure after the Fontan or bidirectional Glenn procedure (n = 7), and ventilatory impairment (n = 8). In the 11 patients who underwent right heart catheterization before and after the initiation of therapy, the mean pulmonary artery pressure decreased significantly from 19.5 ± 5.5 mmHg to 14.3 ± 3.0 mmHg (P = 0.023) and the transpulmonary pressure gradient decreased significantly from 10.9 ± 4.6 mmHg to 7.2 ± 3.3 mmHg (P = 0.046). Of the 18 patients who started vasodilator therapy before the Fontan procedure, 10 survived surgery, 4 are awaiting surgery, 3 had not been evaluated for the Fontan procedure at the end of the study period, and 1 died of heart failure after discontinuing bosentan therapy. There were no deaths among the patients who started therapy after the Fontan procedure. Two of the 14 patients receiving bosentan discontinued treatment because of adverse effects (hepatic dysfunction and increased serum brain natriuretic peptide level). Bosentan or sildenafil therapy is usually safe and may contribute to reducing pulmonary vascular resistance in patients with a functionally single ventricle before and after a Fontan type operation.

Novel echocardiographic approach to the accurate measurement of pulmonary vascular resistance based on a theoretical formula in patients with left heart failure -- pilot study.

Several non-invasive methods for measuring pulmonary vascular resistance (PVR) have been proposed to date, but they remain empirical, lacking sufficient accuracy to be used in clinical practice. The aims of this study were to propose a novel echocardiographic measurement of PVR based on a theoretical formula and investigate the feasibilty and accuracy of this method in patients with heart failure. Echocardiography was performed in 27 patients before right heart catheterization. Peak tricuspid regurgitation pressure gradient (TRPG), pulmonary regurgitation pressure gradient in end-diastole (PRPGed), and cardiac output derived from the time-velocity integral and the diameter in the left ventricular outflow tract (COLVOT) were measured. PVR based on a theoretical formula (PVRtheo) was calculated as (TRPG-PRPGed)/3COLVOTin Wood units (WU). The results were compared with PVR obtained by right heart catheterization (PVRcath) using linear regression and Bland-Altman analysis. Mean PVRcathwas 2.4±1.4 WU. PVRtheocorrelated well with PVRcath(r=0.83, P<0.001). On Bland-Altman analysis the mean difference was 0.1±0.7 WU. The limits of agreements were smaller than for other non-invasive estimations previously reported. The new echocardiographic approach based on a theoretical formula provides a non-invasive and accurate assessment of PVR in patients with heart failure.

Abstract 17912: Importance of Acute Hemodynamic Effects of Inhaled Nitric Oxide in Optimization of Heart Failure Treatment in Patients with Pulmonary Hypertension due to Left Heart Disease

Background: Pulmonary hypertension (PH) due to left heart disease (LHD) is a major category of the disorder. We have recently reported that elevated pulmonary vascular resistance (PVR) in patients with post-capillary PH (pc-PH: defined as mean pulmonary arterial pressure (mPAP)≥25mmHg and pulmonary capillary wedge pressure (PCWP)&gt;15mmHg) is associated with poor prognosis compared with those with no PH or pc-PH without elevated PVR. Although new treatment is required for targeting pulmonary vascular disease (PVD), thereis a concern about raising PCWP. In this study, we thus examined acute hemodynamic effects of inhaled nitric oxide (iNO) in patients with PH due to LHD and whether optimal heart failure (HF) treatment ameliorates pc-PH. Methods: We examined 60 consecutive pc-PH patients with chronic heart failure (63±14[SD] years, M/F 38/22, NYHA≥2) who underwent acute vasoreactivity test by iNO (40 ppm for 10 min) under right heart catheterization at our hospital from June 2011 to May 2014. Among them, 25 had valvular heart disease (VHD) and 35 had non-VHD. PVD (defined as PVR&gt; 240dynes/s/cm -5 ) was noted in 18. We also evaluated right ventricular systolic pressure (RVSP) by echocardiography after optimization of HF treatment such as medications and valvular surgery. Results: iNO significantly decreased mPAP (-1.7±0.5 mmHg; P&lt;0.01) and PVR (-66 ±14dyne/s/cm -5 , P&lt;0.01) without altering cardiac output. iNO significantly increased PCWP (1.3±0.5 mmHg, P=0.01) only in non-VHD patients, while it significantly increased mean arterial pressure and systemic vascular resistance in VHD patients than in non-VHD patients (both P&lt;0.05). Pc-PH patients with PVD were re-classified as having pc-PH without PVD in 9 and no PH in 1. Eight patients remained pc-PH with PVD. After the optimal medical treatment for 7.6 months, RVSP was significantly decreased in both non-VHD and VHD patient (-8±3mmHg, P=0.04, -19±8mmHg, P=0.01, respectively). However, in non-VHD group, significant reduction in RVSP was noted only in pc-PH patients without PVD (-8±3mmHg, P=0.03). Conclusions: These results indicate that elevated PVR in patients with pc-PH and non-VHD could be a novel therapeutic indication for NO-related pulmonary vasodilators in the current practice of HF.

Noninvasive estimation of pulmonary vascular resistance in patients of pulmonary hypertension in unclassified congenital heart disease with unobstructed pulmonary flow

Noninvasive estimation of pulmonary vascular resistance in patients of pulmonary hypertension in unclassified congenital heart disease with unobstructed pulmonary flow

Pulmonary hypertension is related to peripheral endothelial dysfunction in heart failure with preserved ejection fraction.

Pulmonary hypertension (PH) and collagen metabolism abnormalities are prevalent in patients with heart failure with preserved ejection fraction (HFpEF). Peripheral endothelial dysfunction (PED) has been described in HF and in pulmonary arterial hypertension. Our aim is to determine whether PH is associated with PED and impaired collagen metabolism in patients with HFpEF.; Flow-mediated dilation of the brachial artery, matrix metalloproteinase-2 and matrix metalloproteinase-9, tissue metalloproteinase inhibitor 1, and C-terminal propeptide of type I procollagen were determined in 28 patients with HFpEF and 42 hypertensive controls. Patients with systolic pulmonary artery pressure >35 mm Hg on echocardiogram underwent a right heart catheterization. Patients with HFpEF had more severe PED than controls: flow-mediated dilation 1.95% (-0.81 to 4.92) versus 5.02% (3.90 to 10.12), P=0.002. Twenty patients with PH underwent right heart catheterization: mean pulmonary artery pressure 38 (27-52) mm Hg, wedge capillary pressure 18 (16-22) mm Hg, pulmonary vascular resistance 362 (235-603) dyn s cm(-5). There was a significant inverse correlation between flow-mediated dilation and pulmonary vascular resistance in patients with HFpEF and PH (r=-0.679; P=0.002). Patients with HFpEF showed higher matrix metalloproteinase-2 and C-terminal propeptide of type I procollagen values than hypertensive controls. Patients with HFpEF and higher C-terminal propeptide of type I procollagen values also had higher mean pulmonary artery pressure (r=0.553; P=0.014), transpulmonary gradient (r=0.560; P=0.013), and pulmonary vascular resistance (r=0.626; P=0.004). In patients with HFpEF, there is a significant correlation between PED and pulmonary vascular resistance. Collagen metabolism was more impaired in patients with HFpEF and PH. PED and collagen metabolism assessment could be useful tools to identify patients with HFpEF at risk of developing PH.

FRI0510 Good Detection of Early Pulmonary Hypertension Using Exercise Doppler Echocardiography in Patients with Connective Tissue Diseases and Its Comparison with Other Screening Tool

BackgroundExercise Doppler echocardiography helps to select patients who need right-sided heart catheterization (RHC) [1]. We introduced a formula for estimating mean pulmonary arterial pressure (mPAP) using it for connective tissue...