scholarly journals Improving risk stratifcation of pulmonary hypertension patients

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
J P Dias Ferreira Reis ◽  
M Nogueira ◽  
L Branco ◽  
L Sousa ◽  
A Galrinho ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Prognostic Markers ◽  
Systolic Pressure ◽  
Right Atrial ◽  
Current Guideline ◽  
Group I ◽  
6Mwt Distance ◽  
Right Ventricular Strain

Abstract Background According to the 2016 ESC/ERS Guidelines on Pulmonary Hypertension (PH), the right atrial area (RAA) and the presence ofa pericardial effusion (PE) are the two main echocardiographic prognostic markers in PH patients (pts). Aim To assess the predictive ability of these two parameters. Methods Pts with PH were prospectively studied and several clinical/demographic/echocardiographic were retrieved as well as data from six-minute walk test (6MWT) and brain natriuretic peptide (BNP). All-cause mortality was analyzed by PE, RAA and other echocardiographic parameters for positive (PPV) and negative predictive value (NPV) to detect if the current guideline recommended cut-offs can precisely stratify risk in this setting. A survival analysis was performed to evaluate risk stratification (RS) provided by several different cut-offs. Results A total of 51 PH pts (mean age 54±46 years, 33.3% male, baseline BNP of 342.4±439.9pg/mL, mean 6MWT distance of 360.3±109.2 meters and baseline pulmonary artery systolic pressure of 78±26mmHg), of which 64.7% had Group I PH (GI) and 35.3% presented chronic thromboembolic pulmonary hypertension. There were no significant differences between these two groups, however pts in GI were significantly younger (p=0.001), achieved a lower 6MWT distance (p=0.038) and had worse values of right ventricular strain (p=0.040). 27 pts (52.9%) died during a mean follow-up of 52 months, with no differences between groups (p=0.756). The presence of a PE had a low NPV and PPV for the primary endpoint (45.0% and 45.5%, respectively), as well as the guideline recommended cut-offs for RAA (18cm2: NPV- 50.0% and PPV– 55.2%; 26cm2: NPV- 51.3% and PPV– 66.7%). A Pulsed Doppler Tei index (TIp) cut-off of 0.40 had a higher NPV (70.8%) and PPV (74.1%). By Kaplan-Meieran alysis, neither the presence of PE (log rank p=0.508) nor the recommended RAA cut-offs provided accurate risk discrimination (log rank p>0.05 for all). Pts below a TIp cut-off of 0.40 presented a significantly lower survival during follow-up (log rank p=0.002) Conclusion The currently recommended echocardiographic prognostic markers cannot precisely discriminate risk in PH pts. Markers of Right Ventricular Dysfunction may improve RS in this population. FUNDunding Acknowledgement Type of funding sources: None.

scholarly journals Right atrial strain by speckle-tracking echocardiography as a prognostic predictor in a pulmonary hypertension cohort

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
JP Dias Ferreira Reis ◽  
L Branco ◽  
M Nogueira ◽  
L Morais ◽  
L Sousa ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Primary Endpoint ◽  
Systolic Pressure ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Right Atrial ◽  
Pulmonary Artery Systolic Pressure ◽  
Improve Risk Stratification ◽  
Right Ventricular Strain ◽  
Significant Difference

Abstract Funding Acknowledgements Type of funding sources: None. Background Right atrial (RA) strain is as a promising technique for assessment of RA function and several studies have suggested it is a powerful prognostic marker in pulmonary hypertension (PH) patients (pts). Our aim was to assess the prognostic power of RA strain in Pulmonary Arterial Hypertension (PAH) and Chronic Thromboembolic Pulmonary Hypertension (CTEPH) pts. Methods Pts with PH were prospectively studied and several clinical/demographic/echocardiographic were retrieved as well as data from six-minute walk test (6MWT) and brain natriuretic peptide (BNP). Correlation between RA strain and other variables was tested with Pearson"s correlation analysis. Regression and survival analysis were performed to assess the combined endpoint of all-cause mortality or hospitalization in the first follow-up year (MH1). Results A total of 51 PH pts (mean age 54 ± 46 years, 33.3% male, baseline BNP of 342.4 ± 439.9pg/mL and baseline pulmonary artery systolic pressure – PASP - of 78 ± 26mmHg), of which 64.7% had PAH and 35.3% presented CTEPH. 19 ots (37.3%) met the primary endpoint. The mean RA strain was -21.9 ± -4.9%, with no significant difference between groups (-23.4% vs -17.8%, p = 0.150), however male pts had a significantly lower RA strain (-15.9% vs -25.1%, p = 0.014). There was a statistically significant (p < 0.05) correlation between RA strain and age (r = -0.287), indexed RA area (r = -0.539), index RA volume (r = -0.522) and right ventricular strain (r = -0.453). There was no correlation between RA strain and BNP value (p = 0.150), 6MWT distance (p = 0.145) or PASP (p = 0.072). RA strain was a predictor of MH1 (OR = 0.94, 95% CI: 0.894-0.998, p = 0.048). Pts who met the primary endpoint had a significantly worse RA strain (-17.0 vs -24.6%, p = 0.032). Those with a RA strain worse than -19% presented a significantly lower survival free of events during the first follow-up year (log rank p = 0.022). Conclusion RA strain is a powerful predictor of adverse events in a PH population and should be systematically assessed in order to improve risk stratification. Abstract Figure.

scholarly journals Prognostic relevance of the right ventricular myo-mechanical index (RV-MMI) in patients with precapillary pulmonary hypertension

Open Heart ◽  
2018 ◽  
Vol 5 (2) ◽  
pp. e000903
Author(s):  
Sebastian Greiner ◽  
Ferdinand Goppelt ◽  
Matthias Aurich ◽  
Hugo A Katus ◽  
Derliz Mereles
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Area Under The Curve ◽  
Strain Imaging ◽  
Right Atrial ◽  
Mechanical Index ◽  
Prognostic Information ◽  
Non Invasive ◽  
The Right

ObjectiveThe aim of the prospective New-RV study was to evaluate a parameter for non-invasive quantification of right ventricular (RV) dysfunction in patients with precapillary pulmonary hypertension (PH) that yields prognostic information and is applicable in daily clinical routine.MethodsSixty-five consecutive patients with precapillary PH under guideline conform therapy (43 women, 22 men) underwent clinical assessment, serological testing, as well as a comprehensive transthoracic echocardiography including strain imaging and a detailed assessment of RV haemodynamics.ResultsThe mean follow-up time was 844 days. Sixteen patients died during clinical follow-up. Right ventricular myo-mechanical index (RV-MMI) was calculated by right atrial size, mean RV pressure gradient and strain imaging of the RV free wall, and was measurable in all examinations. RV-MMI was tested for its diagnostic accuracy (sensitivity of 88% and specificity of 73% for an optimal cut-off value of ≤0.31 mm Hg*%; area under the curve=0.85), as well as its predictive value (HR=3.3, 95% CI 1.6 to 7.0, p<0.001), and was compared in detail with established parameters. RV-MMI and N-terminal pro-brain natriuretic peptide (NTproBNP)were independent predictors of survival (HR=2.9, 95% CI 1.4 to 6.2, p=0.006; and HR=2.6, 95% CI 1.5 to 4.6, p=0.001, respectively).ConclusionIn a cohort of patients with precapillary PH, the RV-MMI differentiates the outcome of patients better than other available non-invasive parameters of RV function by preload and afterload adjusted quantification.Trial registration numberNCT01230294.

Abstract 13077: Higher Occurrence of Right Ventricular Fibrosis in Right Ventricular Outflow Tract-dominant Than Diffuse Hypertrophic Types: A Pulmonary Hypertension Study Using Cardiac Computed Tomography

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Nobusada FUNABASHI ◽  
Koya Ozawa ◽  
Yoshio Kobayashi
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Wall Thickness ◽  
Cardiac Computed Tomography ◽  
Systolic Pressure ◽  
Right Ventricular Outflow Tract ◽  
Outflow Tract ◽  
Clinical Severity ◽  
Positive Correlations

Introduction: On cardiac CT of pulmonary hypertension (PH), two right ventricular (RV) hypertrophic (RVH) morphological types are seen, namely RV outflow tract-dominant and RV-diffuse. However, clinical significance of this difference is unclear. Hypothesis: These two morphological RVH types have different effects on myocardial characteristics, clinical severity and prognosis in PH patients. Methods: We retrospectively analyzed 43 PH patients (33 females, 55±15yrs, 31 chronic thromboembolic PH (CTEPH), 7 idiopathic pulmonary arterial (PA) hypertension). On CT, RV fibrosis was defined as contrast defects in early phase and abnormal enhancement in late phase. Cases were divided into 3 groups: RV outflow tract-dominant RVH (gp 1), RVH-diffuse (gp 2), and no RVH (gp 3). Mean follow up was 39.3±20.1, 58.3±17.7, 68.2±11.9 months, respectively. Results: There were 6, 26, 11 patients in gps 1, 2, 3, respectively. There were no significant differences in these percentages between CTEPH and idiopathic PA hypertension or between ages ≥60 and <60 yrs. There were no significant differences of R/S wave ratio on ECG V1 lead, maximum RV wall thickness on end-diastole (CT), plasma BNP and estimated PA systolic pressure (PASP) on TTE between gps 1 and 2. There were significant positive correlations between maximum RV wall thickness in end-diastole and plasma BNP in gp 1 (R=0.44) but no correlations in gp 2 (R=0.05). Similarly, there were significant positive correlations between maximum RV wall thickness in end-diastole and estimated PASP in gp 1 (R=0.38) but no correlations in gp 2 (R= -0.08). RV fibrosis was detected in 3 patients (50%) (gp1) and 1 patient (4%) (gp2) (P=0.003). Zero, 2, and 1 patients died due to PH during follow-up periods in gps 1, 2, 3 , respectively, and there were no significant differences in these percentages on Kaplan Meier analysis and log rank testing. Interobserver agreement between two observers was 91% in gp 1 and 77% in both gps 2 and 3. Conclusions: In PH patients, RV outflow tract-dominant RVH was relatively easy to diagnose and manifested with greater occurrence of RV fibrosis than diffuse-type. RV outflow tract-dominant RVH showed significant positive correlations of maximum RV wall thickness in end-diastole with plasma BNP and estimated PASP.

Serotonin transporter is not required for the development of severe pulmonary hypertension in the Sugen hypoxia rat model

2015 ◽  
Vol 309 (10) ◽  
pp. L1164-L1173 ◽  
Author(s):  
Michiel Alexander de Raaf ◽  
Yvet Kroeze ◽  
Anthonieke Middelman ◽  
Frances S. de Man ◽  
Helma de Jong ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Serotonin Transporter ◽  
Rat Model ◽  
Systolic Pressure ◽  
Serum Levels ◽  
Normal Function ◽  
Ventricular Systolic Pressure ◽  
Serotonin System ◽  
Pulmonary Arterial

Increased serotonin serum levels have been proposed to play a key role in pulmonary arterial hypertension (PAH) by regulating vessel tone and vascular smooth muscle cell proliferation. An intact serotonin system, which critically depends on a normal function of the serotonin transporter (SERT), is required for the development of experimental pulmonary hypertension in rodents exposed to hypoxia or monocrotaline. While these animal models resemble human PAH only with respect to vascular media remodeling, we hypothesized that SERT is likewise required for the presence of lumen-obliterating intima remodeling, a hallmark of human PAH reproduced in the Sugen hypoxia (SuHx) rat model of severe angioproliferative pulmonary hypertension. Therefore, SERT wild-type (WT) and knockout (KO) rats were exposed to the SuHx protocol. SERT KO rats, while completely lacking SERT, were hemodynamically indistinguishable from WT rats. After exposure to SuHx, similar degrees of severe angioproliferative pulmonary hypertension and right ventricular hypertrophy developed in WT and KO rats (right ventricular systolic pressure 60 vs. 55 mmHg, intima thickness 38 vs. 30%, respectively). In conclusion, despite its implicated importance in PAH, SERT does not play an essential role in the pathogenesis of severe angioobliterative pulmonary hypertension in rats exposed to SuHx.

Abstract 15388: Persistent Pulmonary Hypertension After Transcatheter Aortic Valve Implantation: Impact on Mortality

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Maria Drakopoulou ◽  
Konstantinos Stathogiannis ◽  
Konstantinos Toutouzas ◽  
George Latsios ◽  
Andreas Synetos ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Aortic Stenosis ◽  
Pulmonary Artery ◽  
Severe Aortic Stenosis ◽  
Systolic Pressure ◽  
Right Atrial ◽  
Pulmonary Artery Systolic Pressure ◽  
End Point ◽  
The Right ◽  
The Impact

Objective: Severe aortic stenosis leads to increased pulmonary arterial systolic pressure. A controversy still remains regarding the impact of persistent pulmonary hypertension (PHT) on prognosis of patients undergoing transcatheter aortic valve implantation (TAVI). We sought to investigate the impact of persistent PHT on 2-year all-cause mortality of patients with severe aortic stenosis following TAVI. Methods: Patients with severe and symptomatic aortic stenosis (effective orifice area [EOA]≤1 cm 2 ) who were scheduled for TAVI with a self-expanding valve at our institution were prospectively enrolled. Prospectively collected echocardiographic data before and after TAVI were retrospectively analyzed in all patients. Pulmonary artery systolic pressure was estimated as the sum of the right ventricular to the right atrial gradient during systole and the right atrial pressure. PHT following TAVI was classified as absent if <35 mmHg and persistent if ≥35 mmHg. Primary clinical end-point was 2-year all-cause mortality defined according to the criteria proposed by the Valve Academic Research Consortium-2. Results: Hundred and forty patients (mean age: 82±9 years) were included in the study. The primary clinical end point occurred in 17 patients (12%) during a median follow-up period of 2 years. Mean pulmonary artery systolic pressure was reduced in all patients following TAVI (45±9 versus 41±6 mmHg, p<0.01). Mortality rate was higher in patients with persistent PHT compared to patients with normal pulmonary artery systolic pressure following TAVI (26% versus 14 %, p<0.01). Patients that reached the primary clinical end point had a higher post procedural mean systolic pulmonary pressure (43±9 versus 39±6 mmHg, p=0.02). In multivariate regression analysis, persistence of PHT (OR: 2.51, 95% CI: 1.109-7.224, p=0.01) was an independent predictor of long-term mortality. Conclusions: The persistence of pulmonary hypertension after TAVI is associated with long term mortality. Identifying the population that will clearly benefit from TAVI is still need to be validated by larger trials.

Anti-monocyte chemoattractant protein-1 gene therapy attenuates pulmonary hypertension in rats

2002 ◽  
Vol 283 (5) ◽  
pp. H2021-H2028 ◽  
Author(s):  
Yasuhiro Ikeda ◽  
Yoshikazu Yonemitsu ◽  
Chu Kataoka ◽  
Shiro Kitamoto ◽  
Terutoshi Yamaoka ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Mononuclear Cells ◽  
Systolic Pressure ◽  
Signal Pathway ◽  
Dominant Negative ◽  
Monocyte Chemoattractant Protein 1 ◽  
Ventricular Systolic Pressure

Monocyte/macrophage chemoattractant protein-1 (MCP-1), a potent chemoattractant chemokine and an activator for mononuclear cells, may play a role in the initiation and/or progression of pulmonary hypertension (PH). To determine whether blockade of a systemic MCP-1 signal pathway in vivo may prevent PH, we intramuscularly transduced a naked plasmid encoding a 7-NH2terminus-deleted dominant negative inhibitor of the MCP-1 (7ND MCP-1) gene in monocrotaline-induced PH. We also simultaneously gave a duplicate transfection at 2-wk intervals or skeletal muscle-directed in vivo electroporation (EP) to evaluate whether a longer or higher expression might be more effective. The intramuscular reporter gene expression was enhanced 10 times over that by EP than by simple injection, and a significant 7ND MCP-1 protein in plasma was detected only in the EP group. 7ND MCP-1 gene transfer significantly inhibited the progression of MCT-induced PH as evaluated by right ventricular systolic pressure, right ventricular hypertrophy, medial hypertrophy of pulumonary arterioles, and mononuclear cell infiltration into the lung. Differential effects of longer or higher transgene expression were not apparent. Although the in vivo kinetics of 7ND MCP-1 gene therapy should be studied further, these encouraging results suggest that an anti-inflammatory strategy via blockade of the MCP-1 signal pathway may be an alternative approach to treat subjects with PH.

scholarly journals A stepwise composite echocardiographic score predicts severe pulmonary hypertension in patients with interstitial lung disease

2018 ◽  
Vol 4 (2) ◽  
pp. 00124-2017 ◽  
Author(s):  
Simon Bax ◽  
Charlene Bredy ◽  
Aleksander Kempny ◽  
Konstantinos Dimopoulos ◽  
Anand Devaraj ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Predictive Value ◽  
Validation Cohort ◽  
Systolic Pressure ◽  
Right Atrial ◽  
Receiver Operating Curve ◽  
Severe Pulmonary Hypertension ◽  
Right Heart Catheterisation

European Respiratory Society (ERS) guidelines recommend the assessment of patients with interstitial lung disease (ILD) and severe pulmonary hypertension (PH), as defined by a mean pulmonary artery pressure (mPAP) ≥35 mmHg at right heart catheterisation (RHC). We developed and validated a stepwise echocardiographic score to detect severe PH using the tricuspid regurgitant velocity and right atrial pressure (right ventricular systolic pressure (RVSP)) and additional echocardiographic signs.Consecutive ILD patients with suspected PH underwent RHC between 2005 and 2015. Receiver operating curve analysis tested the ability of components of the score to predict mPAP ≥35 mmHg, and a score devised using a stepwise approach. The score was tested in a contemporaneous validation cohort. The score used “additional PH signs” where RVSP was unavailable, using a bootstrapping technique.Within the derivation cohort (n=210), a score ≥7 predicted severe PH with 89% sensitivity, 71% specificity, positive predictive value 68% and negative predictive value 90%, with similar performance in the validation cohort (n=61) (area under the curve (AUC) 84.8% versus 83.1%, p=0.8). Although RVSP could be estimated in 92% of studies, reducing this to 60% maintained a fair accuracy (AUC 74.4%).This simple stepwise echocardiographic PH score can predict severe PH in patients with ILD.

scholarly journals Chronic Hypoxia Decreases Endothelial Connexin 40, Attenuates Endothelium‐Dependent Hyperpolarization–Mediated Relaxation in Small Distal Pulmonary Arteries, and Leads to Pulmonary Hypertension

2020 ◽  
Vol 9 (24) ◽  
Author(s):  
Rui Si ◽  
Qian Zhang ◽  
Jody Tori O. Cabrera ◽  
Qiuyu Zheng ◽  
Atsumi Tsuji‐Hosokawa ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Knockout Mice ◽  
Chronic Hypoxia ◽  
Systolic Pressure ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Pulmonary Endothelial Cells ◽  
Endothelium Dependent Relaxation

Background Abnormal endothelial function in the lungs is implicated in the development of pulmonary hypertension; however, there is little information about the difference of endothelial function between small distal pulmonary artery (PA) and large proximal PA and their contribution to the development of pulmonary hypertension. Herein, we investigate endothelium‐dependent relaxation in different orders of PAs and examine the molecular mechanisms by which chronic hypoxia attenuates endothelium‐dependent pulmonary vasodilation, leading to pulmonary hypertension. Methods and Results Endothelium‐dependent relaxation in large proximal PAs (second order) was primarily caused by releasing NO from the endothelium, whereas endothelium‐dependent hyperpolarization (EDH)–mediated vasodilation was prominent in small distal PAs (fourth–fifth order). Chronic hypoxia abolished EDH‐mediated relaxation in small distal PAs without affecting smooth muscle–dependent relaxation. RNA‐sequencing data revealed that, among genes related to EDH, the levels of Cx37 , Cx40 , Cx43 , and IK were altered in mouse pulmonary endothelial cells isolated from chronically hypoxic mice in comparison to mouse pulmonary endothelial cells from normoxic control mice. The protein levels were significantly lower for connexin 40 (Cx40) and higher for connexin 37 in mouse pulmonary endothelial cells from hypoxic mice than normoxic mice. Cx40 knockout mice exhibited significant attenuation of EDH‐mediated relaxation and marked increase in right ventricular systolic pressure. Interestingly, chronic hypoxia led to a further increase in right ventricular systolic pressure in Cx40 knockout mice without altering EDH‐mediated relaxation. Furthermore, overexpression of Cx40 significantly decreased right ventricular systolic pressure in chronically hypoxic mice. Conclusions These data suggest that chronic hypoxia‐induced downregulation of endothelial Cx40 results in impaired EDH‐mediated relaxation in small distal PAs and contributes to the development of pulmonary hypertension.

scholarly journals Retrospective single center cohort study: effect of intensive home hemodialysis on right ventricular systolic pressure and clinical outcomes

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Michael Girsberger ◽  
Christopher T. Chan
Keyword(s):  
Cohort Study ◽  
Right Ventricular ◽  
Clinical Outcomes ◽  
Systolic Pressure ◽  
Composite Endpoint ◽  
Single Center ◽  
Right Ventricular Systolic Pressure ◽  
Home Hemodialysis ◽  
Ventricular Systolic Pressure

Abstract Background Increased right ventricular systolic pressure (RVSP), a surrogate marker for pulmonary hypertension, is common in patients with end-stage kidney disease. Limited data suggest improvement of RVSP with intensive dialysis, but it is unknown whether these improvements translate to better clinical outcomes. Methods We conducted a retrospective single center cohort study at the Toronto General Hospital. All patients who performed intensive home hemodialysis (IHHD) for at least a year between 1999 and 2017, and who had a baseline as well as a follow-up echocardiogram more than a year after IHHD, were included. Patients were categorized into two groups based on the RVSP at follow-up: elevated (≥ 35 mmHg) and normal RVSP. Multivariate and cox regression analyses were done to identify risk factors for elevated RVSP at follow-up and reaching the composite endpoint (death, cardiovascular hospitalization, treatment failure), respectively. Results One hundred eight patients were included in the study. At baseline, 63% (68/108) of patients had normal RVSP and 37% (40/108) having elevated RVSP. After a follow-up of 4 years, 70% (76/108) patient had normal RVSP while 30% (32/108) had elevated RVSP. 8 (10%) out of the 76 patients with normal RVSP and 15 (47%) out of the 32 patients with elevated RVSP reached the composite endpoint of death, cardiovascular hospitalization or technique failure. In a multivariate analysis, age, diabetes and smoking were not associated with elevated RVSP at follow-up. Elevated RVSP at baseline was not associated with a higher likelihood in reaching the composite endpoint or mortality. Conclusion Mean RVSP did not increase in patients on IHHD over time, and maintenance of normal RVSP was associated with better clinical outcomes.

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