Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa1444
T. Oliveira, Luciana Tamie Kato-Morinaga, A. P. Assad, E. Oliveira, C. Jardim, J. Alves-Jr, R. Souza, C. Fernandes
{"title":"Platelets and chronic thromboembolic pulmonary hypertension","authors":"T. Oliveira, Luciana Tamie Kato-Morinaga, A. P. Assad, E. Oliveira, C. Jardim, J. Alves-Jr, R. Souza, C. Fernandes","doi":"10.1183/13993003.congress-2019.pa1444","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa1444","url":null,"abstract":"","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89400933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa1419
Zongye Cai, Claude van der Ley, M. Faassen, I. Kema, D. Duncker, D. Merkus
{"title":"Activation of de novo NAD synthesis in the lung of pulmonary hypertension","authors":"Zongye Cai, Claude van der Ley, M. Faassen, I. Kema, D. Duncker, D. Merkus","doi":"10.1183/13993003.congress-2019.pa1419","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa1419","url":null,"abstract":"","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91037978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa5048
B. Kinsella, E. Mulvaney, H. Reid
NTP42 is a novel antagonist of the thromboxane (TX)A2 receptor (TP), in development for treatment of pulmonary arterial hypertension (PAH). PAH is a devastating disease with multiple pathophysiological hallmarks including excessive pulmonary vasoconstriction, vascular remodelling, fibrosis, inflammation, thrombosis and right ventricular hypertrophy. Signalling through the TP, TXA2 is a potent vasoconstrictor, is a driver of platelet aggregation, a pro-mitogenic and a pro-inflammatory mediator. Mechanistically, TP antagonists should treat many of the hallmarks of PAH, including the excess vasoconstriction, remodelling, in situ thrombosis, fibrosis and inflammation. This study investigated the efficacy of NTP42 in a monocrotaline (MCT)-induced PAH rat model. PAH was induced by subcutaneous injection of 60 mg/kg MCT. Rats were assigned to the groups: 1) No MCT, 2) MCT Only, 3) MCT+NTP42, 4) MCT+Sildenafil and 5) MCT+Selexipag, where 28-day treatment was initiated 24hr post-MCT. From hemodynamic measurements, NTP42 reduced MCT-induced PAH including mean pulmonary arterial pressure (mPAP) and right systolic ventricular pressure (RSVP). Moreover, NTP42 was superior to standard-of-care (SoC) drugs Sildenafil or Selexipag in reducing vessel remodelling, inflammation and fibrosis. A multiparameter score of key disease indices, including mPAP, RVSP, Fulton’s index, vessel remodelling, inflammation and fibrosis, shows that NTP42 has significant treatment benefits and superior to the SoCs tested. These findings suggest that NTP42 and antagonism of TP signalling may alleviate PAH pathophysiology, representing a novel therapeutic target with marked benefits over existing therapies.
{"title":"NTP42, an antagonist of the thromboxane receptor, attenuates experimentally-induced pulmonary arterial hypertension","authors":"B. Kinsella, E. Mulvaney, H. Reid","doi":"10.1183/13993003.congress-2019.pa5048","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa5048","url":null,"abstract":"NTP42 is a novel antagonist of the thromboxane (TX)A2 receptor (TP), in development for treatment of pulmonary arterial hypertension (PAH). PAH is a devastating disease with multiple pathophysiological hallmarks including excessive pulmonary vasoconstriction, vascular remodelling, fibrosis, inflammation, thrombosis and right ventricular hypertrophy. Signalling through the TP, TXA2 is a potent vasoconstrictor, is a driver of platelet aggregation, a pro-mitogenic and a pro-inflammatory mediator. Mechanistically, TP antagonists should treat many of the hallmarks of PAH, including the excess vasoconstriction, remodelling, in situ thrombosis, fibrosis and inflammation. This study investigated the efficacy of NTP42 in a monocrotaline (MCT)-induced PAH rat model. PAH was induced by subcutaneous injection of 60 mg/kg MCT. Rats were assigned to the groups: 1) No MCT, 2) MCT Only, 3) MCT+NTP42, 4) MCT+Sildenafil and 5) MCT+Selexipag, where 28-day treatment was initiated 24hr post-MCT. From hemodynamic measurements, NTP42 reduced MCT-induced PAH including mean pulmonary arterial pressure (mPAP) and right systolic ventricular pressure (RSVP). Moreover, NTP42 was superior to standard-of-care (SoC) drugs Sildenafil or Selexipag in reducing vessel remodelling, inflammation and fibrosis. A multiparameter score of key disease indices, including mPAP, RVSP, Fulton’s index, vessel remodelling, inflammation and fibrosis, shows that NTP42 has significant treatment benefits and superior to the SoCs tested. These findings suggest that NTP42 and antagonism of TP signalling may alleviate PAH pathophysiology, representing a novel therapeutic target with marked benefits over existing therapies.","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74491053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa4752
Vicente Benavides, Melissa Silva-Medina Weil, S. Castaño, Mauricio Palacios
Metformin has been reported to have experimental effects that could be beneficial in the treatment of PH (pulmonary hypertension), though the specific mechanism of action is still under speculation. The current management of this condition is sildenafil, even in patients that requiere metformin as part of the treatment for other comorbilities. Both metformin and sildenafil effectively lower the systolic pressure in the right ventricle, however there are no reports comparing the hemodynamical effects of the two treatments. The goal of this study was to do so using a monocrotaline-induced PH rat model. The rats were divided in 5 groups, consisting of 3 treatment groups (metformin, sildenafil and combination therapy) and two control groups (positive and negative). They were followed for 60 days, at day 30 and 60 an echocardiogram was performed (ventricular ejection fraction was measured), and at day 60 cardiac catheterism was carried out, and Fulton index was estimated. No treatment scheme was effective using the right ventricle ejection fraction as a parameter. The three treatment groups had a positive response using the other outcome variables. The RVSP was improved compared to the positive (PH) controls, without reaching the negative control’s pressure regardless of the group. Fulton’s index remained pathological, but demonstrated a therapeutical effect of the pharmacological treatments. Metformin was not inferior to sildenafil in a PH rat model, interestingly combination treatment shows no hemodynamical synergy between these drugs. Safety evaluation of the kidney and liver showed no pathological or functional differences between the groups.
{"title":"Hemodynamical effects of metformin and sildenafil in the treatment of experimental pulmonary hypertension","authors":"Vicente Benavides, Melissa Silva-Medina Weil, S. Castaño, Mauricio Palacios","doi":"10.1183/13993003.congress-2019.pa4752","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa4752","url":null,"abstract":"Metformin has been reported to have experimental effects that could be beneficial in the treatment of PH (pulmonary hypertension), though the specific mechanism of action is still under speculation. The current management of this condition is sildenafil, even in patients that requiere metformin as part of the treatment for other comorbilities. Both metformin and sildenafil effectively lower the systolic pressure in the right ventricle, however there are no reports comparing the hemodynamical effects of the two treatments. The goal of this study was to do so using a monocrotaline-induced PH rat model. The rats were divided in 5 groups, consisting of 3 treatment groups (metformin, sildenafil and combination therapy) and two control groups (positive and negative). They were followed for 60 days, at day 30 and 60 an echocardiogram was performed (ventricular ejection fraction was measured), and at day 60 cardiac catheterism was carried out, and Fulton index was estimated. No treatment scheme was effective using the right ventricle ejection fraction as a parameter. The three treatment groups had a positive response using the other outcome variables. The RVSP was improved compared to the positive (PH) controls, without reaching the negative control’s pressure regardless of the group. Fulton’s index remained pathological, but demonstrated a therapeutical effect of the pharmacological treatments. Metformin was not inferior to sildenafil in a PH rat model, interestingly combination treatment shows no hemodynamical synergy between these drugs. Safety evaluation of the kidney and liver showed no pathological or functional differences between the groups.","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74016239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa5465
Layse N G Lima, F. Mendes, M. M. Moreira, D. Oliveira, M. C. Pereira
Background: Pulmonary arterial hypertension (PAH) reduces daily physical activity (DLPA) but the underlying mechanisms are not fully understood. The aim of this study was to evaluate DLPA and to determine its relationship to functional capacity and psychological factors in patients with PAH. Methods: This was a single-center prospective study of DLPA conducted in a Brazilian University hospital. Twenty stable PAH subjects mean age 44.3 ± 13.2 yrs, 80% Idiopathic PAH and 20% PAH associated to collagen disease, functional class (CF-NYHA I/II/III: N=7/10/3) completed a 7-day monitoring of daily walking steps by accelerometer and performed pulmonary function tests, 6-minute walk test (6MWT), 1-min sit-to-stand test (STST), and echocardiogram. They also answered 3 questionnaires (quality of life [SF-36], hospital anxiety and depression scale [HADS], and Manchester Respiratory Activities of Daily Living [MRADL]). Results: The mean number of daily steps was 4,280 ± 2,351, and the mean activity time was 41.6 ± 19.3minutes. The mean number of daily steps correlated positively (p Conclusion: DLPA is reduced in PAH and is associated to limitation of daily living activities, functional capacity and depression symptoms, but not with echo variables. These findings reinforce the multifactorial nature of exercise limitation in PAH. Also, they suggest that objective measurement of habitual activity might provide additive value in PAH assessment.
{"title":"Factors associated with daily physical activity in patients with Pulmonary arterial hypertension","authors":"Layse N G Lima, F. Mendes, M. M. Moreira, D. Oliveira, M. C. Pereira","doi":"10.1183/13993003.congress-2019.pa5465","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa5465","url":null,"abstract":"Background: Pulmonary arterial hypertension (PAH) reduces daily physical activity (DLPA) but the underlying mechanisms are not fully understood. The aim of this study was to evaluate DLPA and to determine its relationship to functional capacity and psychological factors in patients with PAH. Methods: This was a single-center prospective study of DLPA conducted in a Brazilian University hospital. Twenty stable PAH subjects mean age 44.3 ± 13.2 yrs, 80% Idiopathic PAH and 20% PAH associated to collagen disease, functional class (CF-NYHA I/II/III: N=7/10/3) completed a 7-day monitoring of daily walking steps by accelerometer and performed pulmonary function tests, 6-minute walk test (6MWT), 1-min sit-to-stand test (STST), and echocardiogram. They also answered 3 questionnaires (quality of life [SF-36], hospital anxiety and depression scale [HADS], and Manchester Respiratory Activities of Daily Living [MRADL]). Results: The mean number of daily steps was 4,280 ± 2,351, and the mean activity time was 41.6 ± 19.3minutes. The mean number of daily steps correlated positively (p Conclusion: DLPA is reduced in PAH and is associated to limitation of daily living activities, functional capacity and depression symptoms, but not with echo variables. These findings reinforce the multifactorial nature of exercise limitation in PAH. Also, they suggest that objective measurement of habitual activity might provide additive value in PAH assessment.","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74121513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa5455
P. Douschan, J. Horwath-winter, J. Hermann, M. Stradner, T. Sassmann, V. Foris, A. Avian, H. Olschewski, G. Kovacs
Background: Sjogren syndrome may be complicated by pulmonary hypertension (PH). However, there are no data available from prospective studies regarding its prevalence. Aims: We aimed to assess the prevalence of PVD including PH, borderline mPAP (20-24mmHg) and exercise PH (EPH) in patients with primary and secondary Sjogren syndrome. Methods: Consecutive patients with Sjogren syndrome underwent echocardiography at rest and during exercise. They were assigned to a low-, intermediate- or high-risk group according to their resting SPAP and their mPAP/CO slope during exercise. In high-risk patients (SPAP≥38mmHg, suspected PH) right heart catheterization (RHC) was suggested. Intermediate-risk patients (SPAP 30-37mmHg [suspected borderline mPAP] or exerciseSPAP≥46mmHg + TPR>3WU [suspected EPH]) RHC was advised in case of symptoms or significantly decreased peakVO2. Results: 86 patients were screened (female N=81, age 58±10yrs, primary Sjogren N=46). N=6 patients had a resting SPAP≥38mmHg, all of them meeting criteria for suspected EPH. N=9 and N=18 fulfilled criteria for suspected borderline mPAP and/or EPH, respectively. RHC was performed in 10 patients. EPH was diagnosed in N=8, borderline mPAP in N=1. No patient had PH. Patients with suspected EPH were older (64±10 vs 55±10, p Conclusions: In this first prospective study evaluating the prevalence of PVD in Sjogren syndrome, 0/86 patients had manifest PH, N=8 had EPH and N=1 had mild PAP elevation. These findings were associated with older age and diastolic LV-dysfunction.
{"title":"Pulmonary vascular disease (PVD) in patients with Sjögren syndrome - a prospective cross-sectional study","authors":"P. Douschan, J. Horwath-winter, J. Hermann, M. Stradner, T. Sassmann, V. Foris, A. Avian, H. Olschewski, G. Kovacs","doi":"10.1183/13993003.congress-2019.pa5455","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa5455","url":null,"abstract":"Background: Sjogren syndrome may be complicated by pulmonary hypertension (PH). However, there are no data available from prospective studies regarding its prevalence. Aims: We aimed to assess the prevalence of PVD including PH, borderline mPAP (20-24mmHg) and exercise PH (EPH) in patients with primary and secondary Sjogren syndrome. Methods: Consecutive patients with Sjogren syndrome underwent echocardiography at rest and during exercise. They were assigned to a low-, intermediate- or high-risk group according to their resting SPAP and their mPAP/CO slope during exercise. In high-risk patients (SPAP≥38mmHg, suspected PH) right heart catheterization (RHC) was suggested. Intermediate-risk patients (SPAP 30-37mmHg [suspected borderline mPAP] or exerciseSPAP≥46mmHg + TPR>3WU [suspected EPH]) RHC was advised in case of symptoms or significantly decreased peakVO2. Results: 86 patients were screened (female N=81, age 58±10yrs, primary Sjogren N=46). N=6 patients had a resting SPAP≥38mmHg, all of them meeting criteria for suspected EPH. N=9 and N=18 fulfilled criteria for suspected borderline mPAP and/or EPH, respectively. RHC was performed in 10 patients. EPH was diagnosed in N=8, borderline mPAP in N=1. No patient had PH. Patients with suspected EPH were older (64±10 vs 55±10, p Conclusions: In this first prospective study evaluating the prevalence of PVD in Sjogren syndrome, 0/86 patients had manifest PH, N=8 had EPH and N=1 had mild PAP elevation. These findings were associated with older age and diastolic LV-dysfunction.","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84917725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.oa5163
D. Ruigrok, P. Symersky, E. Nossent, A. Boonstra, A. Noordegraaf, L. Meijboom, H. Bogaard
Introduction: Although pulmonary endarterectomy (PEA) in chronic thromboembolic pulmonary hypertension (CTEPH) is a highly effective treatment with significant improvements in hemodynamics and right ventricular function, persistent exercise limitation is frequent with many unknowns regarding its mechanisms. Aims: In an observational analysis we aimed to analyze the changes in exercise parameters post-PEA and identify persistent exercise pathology typical for CTEPH. Methods: We analyzed 68 CTEPH patients with cardiopulmonary exercise testing 6 months post-PEA. Results: 6 months post-PEA max load and peakVO2 significantly improved compared to baseline; circulatory and gas exchange parameters (O2 pulse, PETCO2, VE/VCO2, SpO2) improved, while ventilatory parameters remained unchanged. 42/68 (62%) had persistent exercise limitation 6 months post-PEA (peakVO2 Conclusions: In 68 CTEPH patients exercise capacity significantly improved after PEA; improvements were mainly in the circulatory and gas exchange domain. Persistent exercise limitation was frequent and mainly due to cardiocirculatory pathology. Signs typical of pulmonary vascular limitation during exercise were frequent after PEA in CTEPH.
{"title":"An observational analysis of exercise capacity in CTEPH patients after pulmonary endarterectomy","authors":"D. Ruigrok, P. Symersky, E. Nossent, A. Boonstra, A. Noordegraaf, L. Meijboom, H. Bogaard","doi":"10.1183/13993003.congress-2019.oa5163","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.oa5163","url":null,"abstract":"Introduction: Although pulmonary endarterectomy (PEA) in chronic thromboembolic pulmonary hypertension (CTEPH) is a highly effective treatment with significant improvements in hemodynamics and right ventricular function, persistent exercise limitation is frequent with many unknowns regarding its mechanisms. Aims: In an observational analysis we aimed to analyze the changes in exercise parameters post-PEA and identify persistent exercise pathology typical for CTEPH. Methods: We analyzed 68 CTEPH patients with cardiopulmonary exercise testing 6 months post-PEA. Results: 6 months post-PEA max load and peakVO2 significantly improved compared to baseline; circulatory and gas exchange parameters (O2 pulse, PETCO2, VE/VCO2, SpO2) improved, while ventilatory parameters remained unchanged. 42/68 (62%) had persistent exercise limitation 6 months post-PEA (peakVO2 Conclusions: In 68 CTEPH patients exercise capacity significantly improved after PEA; improvements were mainly in the circulatory and gas exchange domain. Persistent exercise limitation was frequent and mainly due to cardiocirculatory pathology. Signs typical of pulmonary vascular limitation during exercise were frequent after PEA in CTEPH.","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86833190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa5040
J. Omura, K. Habbout, S. Martineau, S. Breuils-bonnet, V. Nadeau, F. Potus, Stephen L. Archer, R. Paulin, S. Provencher, O. Boucherat, S. Bonnet
Background: Right ventricular failure (RVF) is the major prognostic factor in pulmonary arterial hypertension (PAH). Recent Omics analyses have demonstrated the deregulation of several long non-coding RNAs (LncRNAs) in left heart failure, but their role in RVF remains unknown. The LncRNA H19 and its encoded miR-675 have been implicated in both cardiac hypertrophy and fibrosis (2 features of RVF) but never been studied in RVF. Methods and Results: By qRT-PCR, we showed in human RV biopsies obtained from control donors, compensated RV hypertrophy patients (CRVH, Cardiac index > 2.2) and decompensated RV hypertrophy patients (DRVH, PAH patients that died from RVF), that H19 and miR-675 were specifically up-regulated (p Conclusions: We demonstrated for the first time that H19 is implicated in the transition from CRVH to DRVH in human RVF. Circulating H19 represents a putative biomarker of RV function in PAH patients.
背景:右心室衰竭(RVF)是肺动脉高压(PAH)的主要预后因素。最近的组学分析表明，在左心衰过程中，一些长链非编码rna (LncRNAs)被解除管制，但它们在裂谷热中的作用尚不清楚。LncRNA H19及其编码的miR-675与心脏肥大和纤维化(裂谷热的两个特征)有关，但从未在裂谷热中进行过研究。方法和结果:通过qRT-PCR，我们发现从对照供体、代偿性右心室肥大患者(CRVH, Cardiac index > 2.2)和失代偿性右心室肥大患者(DRVH，死于RVF的PAH患者)获得的人类右心室活检中，H19和miR-675特异性上调(p结论:我们首次证明H19参与了人类RVF从CRVH向DRVH的转变。循环H19是PAH患者RV功能的推定生物标志物。
{"title":"Long Non-coding RNA H19 in Right Ventricular Failure associated with Pulmonary Arterial Hypertension","authors":"J. Omura, K. Habbout, S. Martineau, S. Breuils-bonnet, V. Nadeau, F. Potus, Stephen L. Archer, R. Paulin, S. Provencher, O. Boucherat, S. Bonnet","doi":"10.1183/13993003.congress-2019.pa5040","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa5040","url":null,"abstract":"Background: Right ventricular failure (RVF) is the major prognostic factor in pulmonary arterial hypertension (PAH). Recent Omics analyses have demonstrated the deregulation of several long non-coding RNAs (LncRNAs) in left heart failure, but their role in RVF remains unknown. The LncRNA H19 and its encoded miR-675 have been implicated in both cardiac hypertrophy and fibrosis (2 features of RVF) but never been studied in RVF. Methods and Results: By qRT-PCR, we showed in human RV biopsies obtained from control donors, compensated RV hypertrophy patients (CRVH, Cardiac index > 2.2) and decompensated RV hypertrophy patients (DRVH, PAH patients that died from RVF), that H19 and miR-675 were specifically up-regulated (p Conclusions: We demonstrated for the first time that H19 is implicated in the transition from CRVH to DRVH in human RVF. Circulating H19 represents a putative biomarker of RV function in PAH patients.","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76159728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.oa5162
Ayumi Sekine, X. Jais, Y. Taniguchi, M. Jevnikar, A. Boucly, L. Savale, D. Montani, O. Sitbon, N. Tanabe, M. Humbert, G. Simonneau
{"title":"The total cross-sectional area of bronchial arteries predicts the extent of persistent PH after endarterectomy","authors":"Ayumi Sekine, X. Jais, Y. Taniguchi, M. Jevnikar, A. Boucly, L. Savale, D. Montani, O. Sitbon, N. Tanabe, M. Humbert, G. Simonneau","doi":"10.1183/13993003.congress-2019.oa5162","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.oa5162","url":null,"abstract":"","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81445844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa1432
Kenichiro Atsumi, H. Hayashi, Shunichi Nishima, Toru Tanaka, Takeru Kashiwada, Yoshinobu Saito, M. Seike, A. Gemma, Y. Kubota, Y. Fukushima, H. Kimura
{"title":"Novel evaluation of pulmonary hypertension with chronic lung disease by perfusion SPECT/CT","authors":"Kenichiro Atsumi, H. Hayashi, Shunichi Nishima, Toru Tanaka, Takeru Kashiwada, Yoshinobu Saito, M. Seike, A. Gemma, Y. Kubota, Y. Fukushima, H. Kimura","doi":"10.1183/13993003.congress-2019.pa1432","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa1432","url":null,"abstract":"","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88503830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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