G Simonneau

Hôpital Bicêtre (Hôpitaux Universitaires Paris-Sud), Lutetia Parisorum, Île-de-France, France

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Publications (688)4339.72 Total impact

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    ABSTRACT: BACKGROUND: The mean pulmonary artery pressure (mPAP) replaces mean systolic ejection pressure (msePAP) in the classic formula of right ventricular stroke work (RVSW) = (mPAP - RAP) × stroke volume, where RAP is mean right atrial pressure. Only the steady work is thus taken into account, not the pulsatile work, whereas pulmonary circulation is highly pulsatile. Our retrospective, high-fidelity pressure study tested the hypothesis that msePAP was proportional to mPAP, and looked at the implications for RVSW. METHODS: Eleven patients with severe, precapillary pulmonary hypertension (PH) (six patients with idiopathic pulmonary arterial hypertension and five with chronic thromboembolic PH; mPAP = 57 ± 10 mm Hg) were studied at rest and during mild to moderate exercise. Eight non-PH control subjects were also studied at rest (mPAP = 16 ± 2 mm Hg). The msePAP was averaged from end diastole to dicrotic notch. RESULTS: In the full data set (53 pressure-flow points), mPAP ranged from 14 to 99.5 mm Hg, cardiac output from 2.38 to 11.1 L/min, and heart rate from 53 to 163 beats/min. There was a linear relationship between msePAP and mPAP (r2 = 0.99). The msePAP matched 1.25 mPAP (bias, -0.5 ± 2.6 mm Hg). Results were similar in the resting non-PH group and in resting and the exercising PH group. This implies that the classic formula markedly underestimates RVSW and that the pulsatile work may be a variable 20% to 55% fraction of RVSW, depending on RAP and mPAP. At rest, RVSW in patients with PH was twice as high as that of the non-PH group (P < .05), but pulsatile work fraction was similar between the two groups (26 ± 4% vs 24 ± 1%) because of the counterbalancing effects of high RAP (11 ± 5 mm Hg vs 4 ± 2 mm Hg), which increases the fraction, and high mPAP, which decreases the fraction. CONCLUSIONS: Our study favored the use of an improved formula that takes into account the variable pulsatile work fraction: RVSW = (1.25 mPAP - RAP) × stroke volume. Increased RAP and increased mPAP have opposite effects on the pulsatile work fraction.
    Chest 05/2013; 143(5):1343-1350. DOI:10.1378/chest.12-1880 · 7.13 Impact Factor
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    ABSTRACT: The performance of the right ventricle is considered as a cornerstone of the patients’ outcome in pulmonary arterial hypertension (PAH). We evaluated the prognostic value of right ventricle ejection fraction (RVEF) assessed by planar equilibrium radionuclide angiography at baseline, and of its change after initiating PAH specific therapy.Methods and MaterialsAmong 222 newly diagnosed patients with idiopathic, heritable or drug-induced PAH (1995-2011), 101 patients had a RVEF measurement at diagnosis before treatment as part of routine evaluation, 78 with a follow-up measurement 3-6 months after initiation of therapy [endothelin receptor antagonists (47%), sildenafil (27%), prostacyclin (9%), and calcium channel blockers (2%)].ResultsAfter a median follow-up of 2.6 years (range: 0.11-15.2 years), 31 deaths occurred, including 25 from a cardiovascular cause. Patients with RVEF ≥25% had a better survival than those with RVEF<25% using Kaplan Meier analysis (p<0.001). The baseline RVEF at diagnosis was associated with all-cause (hazard ratio [HR]: 0.93; p=0.002) and cardiovascular mortality (HR: 0.93; p=0.003) by univariate Cox regression. RVEF was the only independent predictor of all-cause mortality using multivariate adjusted Cox regression (HR: 0.94; p=0.024). Patients with stable or increased RVEF at 3-6 months had less cardiovascular mortality (p=0.012) by Kaplan Meier analysis than those in whom RVEF decreased despite therapy. In 75% of patients, PVR decreased after medical therapy. Seventy nine percent of those patients with decreased PVR showed a stable or increase of RV function. Conversely 53% of patients with increased PVR showed a decrease of RV function (p=0.017). In univariate analysis, RVEF was directly correlated with TAPSE, TAPSV, cardiac index and mixed venous blood saturation. Moreover, RVEF was inversely correlated with NT-pro-BNP and PVR.ConclusionsRVEF assessed with conventional planar radionuclide angiography at baseline and after initiation of PAH therapy predicts outcomes in patients with PAH.
    The Journal of Heart and Lung Transplantation 04/2013; 32(4):S105. DOI:10.1016/j.healun.2013.01.1030 · 5.61 Impact Factor
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    ABSTRACT: Pulmonary arterial hypertension (PAH) is a rare, severe disease resulting from progressive obliteration of small-caliber pulmonary arteries by proliferating vascular cells. PAH can occur without recognized etiology (idiopathic PAH), be associated with a systemic disease or occur as a heritable form, with BMPR2 mutated in approximately 80% of familial and 15% of idiopathic PAH cases. We conducted a genome-wide association study (GWAS) based on 2 independent case-control studies for idiopathic and familial PAH (without BMPR2 mutations), including a total of 625 cases and 1,525 healthy individuals. We detected a significant association at the CBLN2 locus mapping to 18q22.3, with the risk allele conferring an odds ratio for PAH of 1.97 (1.59-2.45; P = 7.47 × 10(-10)). CBLN2 is expressed in the lung, and its expression is higher in explanted lungs from individuals with PAH and in endothelial cells cultured from explanted PAH lungs.
    Nature Genetics 03/2013; 45(5). DOI:10.1038/ng.2581 · 29.65 Impact Factor
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    ABSTRACT: Les récentes études hémodynamiques estiment entre 6 et 10 % la prévalence de l’hypertension pulmonaire associée à la drépanocytose de l’adulte dont plus de la moitié correspondent en réalité à des hypertensions pulmonaires postcapillaires. L’hypertension artérielle pulmonaire (HTAP) précapillaire est une complication relativement peu fréquente de cette maladie (de l’ordre de 3 à 4 % des patients). Elle se caractérise par un profil hémodynamique différent de l’HTAP idiopathique avec des niveaux de pressions pulmonaires et de résistances vasculaires pulmonaires beaucoup plus basses. Néanmoins, ce type d’atteinte vasculaire pulmonaire semble avoir un impact important sur le statut fonctionnel et le pronostic vital des patients drépanocytaires. La valeur prédictive de l’échographie cardiaque pour dépister l’hypertension pulmonaire dans cette population est basse (25 à 32 %) lorsque le seuil de vitesse d’insuffisance tricuspidienne de 2,5 m/s est utilisé. À l’heure actuelle, aucun des traitements spécifiques de l’hypertension artérielle pulmonaire n’est approuvé pour le traitement de l’HTAP associée à la drépanocytose du fait du manque de données dans cette population spécifique.
    La Presse Médicale 03/2013; 42(3):338–346. DOI:10.1016/j.lpm.2012.04.021 · 1.17 Impact Factor
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    ABSTRACT: BACKGROUND: By its inhibitory effect on platelet-derived growth factor signaling, imatinib could be efficacious in treating patients with pulmonary arterial hypertension (PAH). METHODS AND RESULTS: IMPRES, a randomized, double-blind, placebo-controlled 24-week trial evaluated imatinib in patients with pulmonary vascular resistance (PVR) ≥800 dynes•sec•cm(-5) symptomatic on ≥2 PAH therapies. The primary outcome was change in 6-minute walk distance (6MWD). Secondary outcomes included changes in hemodynamics, functional class, serum levels of N-terminal brain natriuretic peptide (NT-proBNP), and time to clinical worsening (TTCW). After completion of the core study, patients could enter an open-label long-term extension study. Of 202 patients enrolled, 41% patients received 3 PAH therapies with the remainder on 2 therapies. After 24 weeks, the mean placebo-corrected treatment-effect on 6MWD was 32 m (95% confidence interval [CI], 12, 52; P=0.002), an effect maintained in the extension study in patients remaining on imatinib. PVR decreased by 379 dynes•sec•cm(-5) (95% CI: -502, -255; P<0.001; between-group difference). Functional class, TTCW and mortality did not differ between treatments. Serious adverse events and discontinuations were more frequent with imatinib than placebo (44% versus 30%, 33% versus 18% respectively). Subdural hematoma occurred in 8 patients (2 in the core study, 6 in the extension) receiving imatinib and anticoagulation. CONCLUSIONS: Imatinib improved exercise capacity and hemodynamics in patients with advanced PAH but serious adverse events and study drug discontinuations were common. Further studies are needed to investigate the long-term safety and efficacy of imatinib in patients with PAH. CLINICAL TRIAL REGISTRATION INFORMATION: URL: http://www.clinicaltrials.gov. Identifier: NCT00902174 (core study); NCT01392495 (extension).
    Circulation 02/2013; 127(10). DOI:10.1161/CIRCULATIONAHA.112.000765 · 14.95 Impact Factor
  • Joanna Pepke-Zaba · Pavel Jansa · Nick H Kim · Robert Naejie · Gerald Simonneau
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    ABSTRACT: Chronic thromboembolic pulmonary hypertension (CTEPH) is a progressive disease with poor prognosis if not treated. The treatment of choice is surgery with pulmonary endarterectomy. However, a significant percentage of patients are deemed non-operable due to distal distribution of the disease and arteriopathy in the non-occluded areas that is indistinguishable from pulmonary arterial hypertension (PAH). The overlap in clinical presentation, pathological features and pathogenesis between PAH and CTEPH provides a compelling rationale for exploring the efficacy of PAH-targeted therapies in CTEPH. These therapies are often considered for non-operable patients and are also used in operable patients as a bridge to surgery or as post-PEA therapy for persistent pulmonary hypertension, despite the fact they are not licensed for CTEPH.Two randomised clinical trials (RCTs) have been performed in non-operable CTEPH patients. The BENEFiT study, with the endothelin receptor antagonist bosentan, did not show improvement in walking distance. Recently, the CHEST-1 trial, with the soluble guanylate cyclase stimulator riociguat, met study endpoint and demonstrated significant improvement in walking distance in patients with non-operable CTEPH.There is an urgent need for more RCTs designed to clarify whether administration of PAH-targeted therapies improves clinically meaningful endpoints in various CTEPH populations.
    European Respiratory Journal 02/2013; 41(4). DOI:10.1183/09031936.00201612 · 7.13 Impact Factor
  • Revue des Maladies Respiratoires 01/2013; 30:A132. DOI:10.1016/j.rmr.2012.10.438 · 0.49 Impact Factor
  • Revue des Maladies Respiratoires 01/2013; 30:A15. DOI:10.1016/j.rmr.2012.10.053 · 0.49 Impact Factor
  • Revue des Maladies Respiratoires 01/2013; 30:A15. DOI:10.1016/j.rmr.2012.10.054 · 0.49 Impact Factor
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    Marc Humbert · David Montani · Oleg V Evgenov · Gérald Simonneau
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    ABSTRACT: Pulmonary hypertension is defined as an increase of mean pulmonary arterial pressure ≥25 mmHg at rest as assessed by right heart catheterization. According to different combinations of values of pulmonary wedge pressure, pulmonary vascular resistance and cardiac output, a hemodynamic classification of pulmonary hypertension has been proposed. Of major importance is the pulmonary wedge pressure which allows to distinguish pre-capillary (pulmonary wedge pressure ≤15 mmHg) and post-capillary (pulmonary wedge pressure >15 mmHg) pulmonary hypertension. Pre-capillary pulmonary hypertension includes the clinical groups 1 (pulmonary arterial hypertension), 3 (pulmonary hypertension due to lung diseases and/or hypoxia), 4 (chronic thrombo-embolic pulmonary hypertension) and 5 (pulmonary hypertension with unclear and/or multifactorial mechanisms). Post-capillary pulmonary hypertension corresponds to the clinical group 2 (pulmonary hypertension due to left heart diseases).
    Handbook of experimental pharmacology 01/2013; 218:3-29. DOI:10.1007/978-3-642-38664-0_1
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    ABSTRACT: Rational: Pulmonary arterial hypertension (PAH) and pulmonary veno-occlusive disease (PVOD) both display occlusive remodeling of the pulmonary vasculature responsible for increased pulmonary vascular resistances. Cytotoxic T-(CTL), Natural Killer-(NK) and Natural Killer T-(NKT) cells play a critical role in vascular remodeling in different physiological and pathological conditions. Granulysin (GNLY) represents a powerful effector protein for all these subpopulations. OBJECTIVES: To analyze the cytolytic compartment of inflammatory cells in PAH and PVOD patients. METHODS: The overall functional status of the cytolytic compartment was studied through epigenetic analysis of the GNLY gene in explanted lungs and in PBMC. Flow cytometry technology allowed analysis of specific circulating cytolytic cells and GNLY contents. A GNLY-specific ELISA allowed measurement of GNLY serum concentrations. MEASUREMENTS AND MAIN RESULTS: A decrease in GNLY demethylation in the gDNA extracted from PBMC and explanted lungs was found specifically in PVOD but not in PAH. This was associated with a decrease in populations and subpopulations of CTL and NKT, and an increase of NK populations. Despite the reduced granulysin-containing cells in PVOD patients, GNLY serum levels were higher, suggesting these cells were wasting their content. Furthermore, the increase of GNLY concentration in the serum of PVOD was significantly higher than in PAH patients. CONCLUSIONS: PVOD is characterized by alterations of circulating cytotoxic cell-subpopulations and by epigenetic dysregulation within the GNLY gene. Our findings may be helpful in the quest to develop needed diagnostic tools, including flow cytometry analyses, in order to screen for suspected PVOD in patients with pulmonary hypertension.
    American Journal of Respiratory and Critical Care Medicine 12/2012; 187(2). DOI:10.1164/rccm.201208-1364OC · 11.99 Impact Factor
  • European Respiratory Review 12/2012; 21(126):267-70. DOI:10.1183/09059180.00005312
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    ABSTRACT: Objective To assess the survival and prognostic factors in patients with newly diagnosed incident systemic sclerosis (SSc)–associated pulmonary arterial hypertension (PAH) in the modern management era. Methods Prospectively enrolled SSc patients in the French PAH Network between January 2006 and November 2009, with newly diagnosed PAH and no interstitial lung disease, were analysed (85 patients, mean age 64.9±12.2 years). Median follow-up after PAH diagnosis was 2.32 years. Results A majority of patients were in NYHA functional class III–IV (79%). Overall survival was 90% (95% CI 81% to 95%), 78% (95% CI 67% to 86%) and 56% (95% CI 42% to 68%) at 1, 2 and 3 years from PAH diagnosis, respectively. Age (HR: 1.05, 95% CI 1.01 to 1.09, p=0.012) and cardiac index (HR: 0.49, 95% CI 0.27 to 0.89, p=0.019) were significant predictors in the univariate analysis. We also observed strong trends for gender, SSc subtypes, New York Heart Association functional class, pulmonary vascular resistance and capacitance to be significant predictors in the univariate analysis. Conversely, six-min walk distance, mean pulmonary arterial and right atrial pressures were not significant predictors. In the multivariate model, gender was the only independent factor associated with survival (HR: 4.76, 95% CI 1.35 to 16.66, p=0.015 for male gender). Conclusions Incident SSc-associated PAH remains a devastating disease even in the modern management era. Age, male gender and cardiac index were the main prognosis factors in this cohort of patients. Early detection of less severe patients should be a priority.
    Annals of the rheumatic diseases 11/2012; 72(12). DOI:10.1136/annrheumdis-2012-202489 · 10.38 Impact Factor
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    Dataset: Final
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    ABSTRACT: SESSION TYPE: Late-Breaking AbstractsPRESENTED ON: Tuesday, October 23, 2012 at 04:30 PM - 05:45 PMPURPOSE: Riociguat is the first member of a novel class of compounds, the soluble guanylate cyclase (sGC) stimulators. With a dual mode of action, it synergizes with endogenous nitric oxide (NO) and also directly stimulates sGC independent of NO availability. Riociguat restores the NO-sGC-cGMP pathway resulting in a significant improvement in pulmonary vascular hemodynamics and an increase in exercise ability. Here, we present results from the Phase III, multicenter, randomized, double-blind, placebo-controlled CHEST-1 study, which investigated the efficacy and safety of riociguat in patients with inoperable chronic thromboembolic pulmonary hypertension (CTEPH).METHODS: Patients with inoperable CTEPH (as assessed by an independent adjudication committee) or with persisting or recurrent pulmonary hypertension (PH) after pulmonary endarterectomy (PEA), and a mean pulmonary vascular resistance (PVR) >480 dyn·s/cm5 were enrolled in the trial. Treatment with supportive PH therapies was permitted but patients were treatment naïve with regards to pulmonary arterial hypertension-specific therapies. Patients were randomized to either placebo or oral riociguat, which was titrated from a starting dose of 1 mg three times daily (t.i.d.) according to systolic blood pressure (range 0.5-2.5 mg t.i.d.). The primary outcome measure was the change from baseline in 6-minute walking distance after 16 weeks of treatment. Secondary endpoints included change from baseline in PVR, functional class, time to clinical worsening, and safety and tolerability.RESULTS: The study has enrolled a total of 263 patients. Results will be available and presented at the time of the congress.CONCLUSIONS: The CHEST-1 study is the largest placebo-controlled trial to date in CTEPH and will assess the therapeutic benefit of the sGC stimulator riociguat.CLINICAL IMPLICATIONS: At present, no approved pharmacologic therapy exists for CTEPH and as a result there is an urgent unmet need in patients who are not eligible for PEA, or who have persistent or recurrent PH after PEA.DISCLOSURE: Hossein Ghofrani: Grant monies (from sources other than industry): Hossein A. Ghofrani has received sponsored grants over the past 3 years from the German Research Foundation, Excellence Cluster Cardiopulmonary Research and Germany Ministry for Education and Research, Grant monies (from industry related sources): Hossein A. Ghofrani has received industry-sponsored grants over the past 3 years from Bayer HealthCare AG, Aires, Encysive/Pfizer and Novartis, Consultant fee, speaker bureau, advisory committee, etc.: Hossein A. Ghofrani has relationships with the following drug companies: Bayer HealthCare AG, Actelion, Encysive, Pfizer, Ergonex, Novartis and GlaxoSmithKlineFriedrich Grimminger: Consultant fee, speaker bureau, advisory committee, etc.: Friedrich Grimminger has relationships with Bayer AGMarius Hoeper: Consultant fee, speaker bureau, advisory committee, etc.: Marius Hoeper has relationships with the following drug companies: Actelion, Bayer, Gilead, GlaxoSmithKline, Lilly, Novartis and PfizerNick Kim: Grant monies (from industry related sources): Nick H. Kim has received industry related grant monies from the following drug companies: Actelion, Gilead and United Therapeutics, Consultant fee, speaker bureau, advisory committee, etc.: Nick H. Kim has relationships with the following drug companies: Bayer (consultant), Gilead, United Therapeutics (advisory meeting)Eckhard Mayer: Consultant fee, speaker bureau, advisory committee, etc.: Eckhard Mayer has relationships with the following drug companies: Bayer Schering, Pfizer, ActelionDieter Neuser: Employee: Dieter Neuser is an employee of Bayer Pharma AGJanethe Pena: Employee: Janethe Pena is an employee of Bayer HealthCareGerald Simonneau: University grant monies: Gerald Simonneau has received university grant monies from the following drug companies: Actelion, Bayer, GlaxoSmithKline, Lilly, Novartis and Pfizer, Grant monies (from industry related sources): Gerald Simonneau has received industry related grant monies from the following drug companies: Actelion, Bayer, GlaxoSmithKline, Lilly, Novartis and Pfizer, Consultant fee, speaker bureau, advisory committee, etc.: Gerald Simonneau has relationships with the following drug companies: Actelion, Bayer, GlaxoSmithKline, Lilly, Novartis and PfizerMartin Wilkins: Grant monies (from industry related sources): Martin Wilkins has received grant monies from Bayer, Consultant fee, speaker bureau, advisory committee, etc.: Martin Wilkins is a Chair on a research abstract panel for BayerRiociguat is an investigational new drug currently in process for registration submission to health authorities, after successful finalisation of an RCT in patients with PAH.Department of Internal Medicine, University Hospital Giessen and Marburg, Giessen, Germany.
    Chest 10/2012; 142(4_MeetingAbstracts):1023A. DOI:10.1378/chest.1462924 · 7.13 Impact Factor
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    ABSTRACT: SESSION TYPE: Late-Breaking AbstractsPRESENTED ON: Tuesday, October 23, 2012 at 04:30 PM - 05:45 PMPURPOSE: Current oral PAH therapies have been approved based on short-term trials with exercise capacity as the primary endpoint. In this event-driven trial, the effect of macitentan, a novel dual endothelin receptor antagonist (ERA) with enhanced tissue penetration, was assessed on a primary endpoint of morbidity and mortality in PAH patients.METHODS: In this double-blind, placebo-controlled, Phase III, event-driven study, patients (≥12 years) with symptomatic PAH were randomized (1:1:1) to placebo, macitentan 3mg or macitentan 10mg, once daily. Stable background oral or inhaled PAH therapy, other than an ERA, was allowed. The primary endpoint was time from treatment initiation to first morbidity or mortality event in all randomized patients. This composite endpoint, defined as death, atrial septostomy, lung transplantation, initiation of intravenous/subcutaneous prostanoids or worsening of PAH, was blindly and independently adjudicated. Secondary endpoints included the composite of mortality due to PAH or hospitalization for PAH.RESULTS: 742 patients with PAH were randomized to placebo (n=250), macitentan 3mg (n=250) or macitentan 10mg (n=242); mean treatment duration was 85.3, 99.5 and 103.9 weeks, respectively. Macitentan reduced the risk of occurrence of morbidity and mortality events versus placebo by 30% in the 3mg group (97.5%CI:4-48%;P=0.0108) and 45% in the 10 mg group (97.5%CI:24-61%;P<0.0001). The effect of macitentan on this endpoint was observed irrespective of background PAH therapy (mainly phosphodiesterase type-5 inhibitors); risk reduction for macitentan 3mg and 10mg was 17% (95%CI:-16-41%) and 38% (95%CI:11-57%) in the presence of background PAH therapy and 47% (95%CI:15-66%) and 55% (95%CI:28-72%) in the absence of background PAH therapy. Macitentan 3mg and 10mg also reduced the risk of the secondary endpoint, mortality due to PAH/hospitalization for PAH, by 33% (97.5%CI:3-54%;P=0.0146) and 50% (97.5%CI:25-67%;P<0.0001), respectively. Macitentan was well tolerated, with similar incidences of elevated liver aminotransferases and peripheral edema across all groups. Adverse events more frequently associated with macitentan versus placebo were headache, nasopharyngitis and anemia.CONCLUSIONS: Macitentan demonstrated a significant effect on the combined endpoint of morbidity and mortality, with a favorable safety profile, in the largest and longest randomized controlled trial of therapy in PAH to date.CLINICAL IMPLICATIONS: Macitentan has the potential to improve long-term outcomes in PAH patients.DISCLOSURE: Lewis Rubin: Consultant fee, speaker bureau, advisory committee, etc.: Actelion Pharmaceuticals Ltd, Consultant fee, speaker bureau, advisory committee, etc.: Pfizer, Consultant fee, speaker bureau, advisory committee, etc.: United Therapeutics, Consultant fee, speaker bureau, advisory committee, etc.: Lung LLC, Consultant fee, speaker bureau, advisory committee, etc.: Gilead, Consultant fee, speaker bureau, advisory committee, etc.: GlaxoSmithKline, Consultant fee, speaker bureau, advisory committee, etc.: Bayer, Consultant fee, speaker bureau, advisory committee, etc.: GeNoTomás Pulido: Consultant fee, speaker bureau, advisory committee, etc.: Actelion , Consultant fee, speaker bureau, advisory committee, etc.: Pfizer, Consultant fee, speaker bureau, advisory committee, etc.: Lily, Consultant fee, speaker bureau, advisory committee, etc.: Bayer, Grant monies (from sources other than industry): National Heart Insitute, Grant monies (from industry related sources): Actelion, Grant monies (from industry related sources): Bayer, Grant monies (from industry related sources): United TherapeuticsRichard Channick: Grant monies (from industry related sources): Actelion, Consultant fee, speaker bureau, advisory committee, etc.: ActelionMarion Delcroix: Grant monies (from industry related sources): Actelion, Grant monies (from industry related sources): GlaxoSmithKline, Consultant fee, speaker bureau, advisory committee, etc.: Actelion, Consultant fee, speaker bureau, advisory committee, etc.: GlaxoSmithKline, Consultant fee, speaker bureau, advisory committee, etc.: Pfizer, Consultant fee, speaker bureau, advisory committee, etc.: United Therapeutics, Consultant fee, speaker bureau, advisory committee, etc.: BayerNazzareno Galie: Grant monies (from industry related sources): Actelion, Grant monies (from industry related sources): Pfizer, Grant monies (from industry related sources): Eli Lilly, Grant monies (from industry related sources): Bayer, Grant monies (from industry related sources): GlaxoSmithKline, Consultant fee, speaker bureau, advisory committee, etc.: Actelion, Consultant fee, speaker bureau, advisory committee, etc.: Pfizer, Consultant fee, speaker bureau, advisory committee, etc.: Eli Lilly, Consultant fee, speaker bureau, advisory committee, etc.: GlaxoSmithKline, Consultant fee, speaker bureau, advisory committee, etc.: BayerHossein-Ardeschir Ghofrani: Grant monies (from industry related sources): Actelion, Grant monies (from industry related sources): Pfizer, Grant monies (from industry related sources): Bayer, Grant monies (from industry related sources): Ergonex, Consultant fee, speaker bureau, advisory committee, etc.: Actelion, Consultant fee, speaker bureau, advisory committee, etc.: Pfizer, Consultant fee, speaker bureau, advisory committee, etc.: Bayer, Consultant fee, speaker bureau, advisory committee, etc.: Ergonex, Consultant fee, speaker bureau, advisory committee, etc.: Gilead, Consultant fee, speaker bureau, advisory committee, etc.: GlaxoSmithKline, Consultant fee, speaker bureau, advisory committee, etc.: Merck, Consultant fee, speaker bureau, advisory committee, etc.: NovartisPavel Jansa: Grant monies (from industry related sources): Actelion, Consultant fee, speaker bureau, advisory committee, etc.: United Therapeutics, Consultant fee, speaker bureau, advisory committee, etc.: Actelion, Consultant fee, speaker bureau, advisory committee, etc.: AOP Orphan, Consultant fee, speaker bureau, advisory committee, etc.: GlaxoSmithKline, Consultant fee, speaker bureau, advisory committee, etc.: BayerFranck-Olivier Le Brun: Employee: Actelion, Consultant fee, speaker bureau, advisory committee, etc.: ActelionSanjay Mehta: Grant monies (from industry related sources): Actelion, Consultant fee, speaker bureau, advisory committee, etc.: Actelion, Consultant fee, speaker bureau, advisory committee, etc.: Takeda Nycomed, Grant monies (from sources other than industry): Heart & Stroke Foundation of Ontario/Canada (HSFO/C), Grant monies (from industry related sources): Canadian Institute of Health Research / CIHR, Grant monies (from sources other than industry): Ontario Thoracic Society (OTS), Consultant fee, speaker bureau, advisory committee, etc.: Actelion Pharmaceuticals Canada, Consultant fee, speaker bureau, advisory committee, etc.: Takeda - Nycomed, Consultant fee, speaker bureau, advisory committee, etc.: Boehringer-Ingelheim CanadaCamilla Mittelholzer: Employee: Actelion, Shareholder: ActelionLoic Perchenet: Employee: Actelion, Shareholder: ActelionBkS Sastry: Consultant fee, speaker bureau, advisory committee, etc.: Actelion, Consultant fee, speaker bureau, advisory committee, etc.: GlaxoSmithKlineOlivier Sitbon: Grant monies (from industry related sources): GlaxoSmithKline, Grant monies (from industry related sources): Actelion, Grant monies (from industry related sources): Pfizer, Grant monies (from industry related sources): bayer, Grant monies (from industry related sources): Eli Lilly, Consultant fee, speaker bureau, advisory committee, etc.: GlaxoSmithKline, Consultant fee, speaker bureau, advisory committee, etc.: Actelion, Consultant fee, speaker bureau, advisory committee, etc.: Pfizer, Consultant fee, speaker bureau, advisory committee, etc.: United Therapuetics, Consultant fee, speaker bureau, advisory committee, etc.: Eli Lilly, Consultant fee, speaker bureau, advisory committee, etc.: United Therapuetics, Consultant fee, speaker bureau, advisory committee, etc.: BayerRogerio Souza: Grant monies (from industry related sources): Actelion, Consultant fee, speaker bureau, advisory committee, etc.: ActelionAdam Torbicki: Grant monies (from industry related sources): Actelion, Consultant fee, speaker bureau, advisory committee, etc.: Actelion, Consultant fee, speaker bureau, advisory committee, etc.: Eli Lilly, Consultant fee, speaker bureau, advisory committee, etc.: Bayer, Consultant fee, speaker bureau, advisory committee, etc.: GlaxoSmithKline, Consultant fee, speaker bureau, advisory committee, etc.: AOP Orphan Pharmaceutics, Grant monies (from industry related sources): Bayer, Grant monies (from industry related sources): United Therapeutics, Grant monies (from industry related sources): AOP Orphan Pharmaceutics, Grant monies (from industry related sources): Pfizer, Consultant fee, speaker bureau, advisory committee, etc.: Bristol Myers SquibbGerald Simonneau: Grant monies (from industry related sources): Actelion, Grant monies (from industry related sources): GlaxoSmithKline, Grant monies (from industry related sources): Pfizer, Grant monies (from industry related sources): Eli Lilly, Consultant fee, speaker bureau, advisory committee, etc.: Actelion, Consultant fee, speaker bureau, advisory committee, etc.: GlaxoSmithKline, Consultant fee, speaker bureau, advisory committee, etc.: Pfizer, Consultant fee, speaker bureau, advisory committee, etc.: Eli Lilly, Consultant fee, speaker bureau, advisory committee, etc.: United Therapeutics, Consultant fee, speaker bureau, advisory committee, etc.: NovartisMacitentan is under investigation for the treatment of pulmonary arterial hypertension. SERAPHIN, the Phase 3 study reported here, is the registration trial for macitentan in this indication. University of California, San Diego, CA.
    Chest 10/2012; 142(4_MeetingAbstracts):1026A. DOI:10.1378/chest.1456207 · 7.13 Impact Factor

Publication Stats

36k Citations
4,339.72 Total Impact Points

Institutions

  • 2013–2015
    • Hôpital Bicêtre (Hôpitaux Universitaires Paris-Sud)
      Lutetia Parisorum, Île-de-France, France
    • Mater Misericordiae University Hospital
      • Department of Respiratory Medicine
      Dublin, Leinster, Ireland
  • 2002–2015
    • Unité Inserm U1077
      Caen, Lower Normandy, France
    • McGill University
      Montréal, Quebec, Canada
    • Baylor College of Medicine
      Houston, Texas, United States
  • 1990–2015
    • Centre Chirurgical Marie Lannelongue
      Plessis-Robinson, Île-de-France, France
  • 1989–2015
    • Université Paris-Sud 11
      • • Faculty of Medicine
      • • Service de Pneumologie
      Orsay, Île-de-France, France
  • 1986–2014
    • Hôpital Antoine-Béclère – Hôpitaux universitaires Paris-Sud
      Clamart, Île-de-France, France
  • 2010
    • Université Libre de Bruxelles
      Bruxelles, Brussels Capital Region, Belgium
  • 2009
    • Université René Descartes - Paris 5
      • Faculté de Médecine
      Lutetia Parisorum, Île-de-France, France
    • Palmelit Francia
      Montferrier, Languedoc-Roussillon, France
    • Centre Hospitalier Universitaire de Brest
      Brest, Brittany, France
  • 2007–2009
    • Assistance Publique – Hôpitaux de Paris
      Lutetia Parisorum, Île-de-France, France
  • 2002–2009
    • University of Bologna
      • Institute of Cardiology
      Bologna, Emilia-Romagna, Italy
  • 2006
    • Vanderbilt University
      • Division of Allergy, Pulmonary and Critical Care
      Нашвилл, Michigan, United States
    • University of Leicester
      • Department of Genetics
      Leicester, ENG, United Kingdom
  • 1984–2006
    • Hôpital Henri Mondor (Hôpitaux Universitaires Henri Mondor)
      Créteil, Île-de-France, France
  • 2005
    • Hôtel-Dieu de Paris – Hôpitaux universitaires Paris Centre
      Lutetia Parisorum, Île-de-France, France
  • 2004
    • CHRU de Strasbourg
      Strasburg, Alsace, France
  • 2001
    • Arkansas Children's Hospital
      Little Rock, Arkansas, United States
  • 1991
    • University of Tours
      Tours, Centre, France