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Dive into the research topics where Ardeschir Ghofrani is active.

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Featured researches published by Ardeschir Ghofrani.


European Respiratory Journal | 2015

2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS)Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT)

Nazzareno Galiè; Marc Humbert; Jean-Luc Vachiery; Simon Gibbs; Irene Lang; Adam Torbicki; Gérald Simonneau; Andrew Peacock; Anton Vonk Noordegraaf; Maurice Beghetti; Ardeschir Ghofrani; Miguel Sánchez; Georg Hansmann; Walter Klepetko; Patrizio Lancellotti; Marco Matucci; Theresa McDonagh; Luc Pierard; Pedro T. Trindade; Maurizio Zompatori; Marius M. Hoeper

Guidelines summarize and evaluate all available evidence on a particular issue at the time of the writing process, with the aim of assisting health professionals in selecting the best management strategies for an individual patient with a given condition, taking into account the impact on outcome, as well as the risk–benefit ratio of particular diagnostic or therapeutic means. Guidelines and recommendations should help health professionals to make decisions in their daily practice. However, the final decisions concerning an individual patient must be made by the responsible health professional(s) in consultation with the patient and caregiver as appropriate. 2015 ESC/ERS pulmonary hypertension guidelines incorporate changes and adaptations focusing on clinical management http://ow.ly/RiDLb


European Respiratory Journal | 2015

2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS)Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), Intern…

Nazzareno Galiè; Marc Humbert; Jean-Luc Vachiery; Simon Gibbs; Irene Lang; Adam Torbicki; Gérald Simonneau; Andrew Peacock; Anton Vonk Noordegraaf; Maurice Beghetti; Ardeschir Ghofrani; Miguel Sánchez; Georg Hansmann; Walter Klepetko; Patrizio Lancellotti; Marco Matucci; Theresa McDonagh; Luc Pierard; Pedro T. Trindade; Maurizio Zompatori; Marius M. Hoeper

Guidelines summarize and evaluate all available evidence on a particular issue at the time of the writing process, with the aim of assisting health professionals in selecting the best management strategies for an individual patient with a given condition, taking into account the impact on outcome, as well as the risk–benefit ratio of particular diagnostic or therapeutic means. Guidelines and recommendations should help health professionals to make decisions in their daily practice. However, the final decisions concerning an individual patient must be made by the responsible health professional(s) in consultation with the patient and caregiver as appropriate. 2015 ESC/ERS pulmonary hypertension guidelines incorporate changes and adaptations focusing on clinical management http://ow.ly/RiDLb


Circulation | 2009

Stress Doppler Echocardiography in Relatives of Patients With Idiopathic and Familial Pulmonary Arterial Hypertension Results of a Multicenter European Analysis of Pulmonary Artery Pressure Response to Exercise and Hypoxia

Sylvia Weissmann; Nicola Ehlken; Anna Fijałkowska; Christine Fischer; Thierry Fourme; Nazzareno Galiè; Ardeschir Ghofrani; Rachel Harrison; Sandrine Huez; Marc Humbert; Bart Janssen; Jarosław Kober; Rolf Koehler; Rajiv D. Machado; Derliz Mereles; Robert Naeije; Horst Olschewski; Steeve Provencher; Frank Reichenberger; Kathleen Retailleau; Guido Rocchi; Gérald Simonneau; Adam Torbicki; Richard C. Trembath; Werner Seeger

Background— This large, prospective, multicentric study was performed to analyze the distribution of tricuspid regurgitation velocity (TRV) values during exercise and hypoxia in relatives of patients with idiopathic and familial pulmonary arterial hypertension (PAH) and in healthy control subjects. We tested the hypothesis that relatives of idiopathic/familial PAH patients display an enhanced frequency of hypertensive TRV response to stress and that this response is associated with mutations in the bone morphogenetic protein receptor II (BMPR2) gene. Methods and Results— TRV was estimated by Doppler echocardiography during supine bicycle exercise in normoxia and during 120 minutes of normobaric hypoxia (Fio2=12%; ≈4500 m) in 291 relatives of 109 PAH patients and in 191 age-matched control subjects. Mean maximal TRVs were significantly higher in PAH relatives during both exercise and hypoxia. During exercise, 10% of control subjects but 31.6% of relatives (P<0.0001) exceeded the 90% quantile of mean maximal TRV seen in control subjects. Hypoxia revealed hypertensive TRV in 26% of relatives (P=0.0029). Among control subjects, TRV at rest was not related to age, sex, body mass index, systemic blood pressure, smoking status, or heart rate. Within kindreds identified as harboring deleterious mutations of the BMPR2 gene, a hypertensive TRV response occurred significantly more often compared with those without detected mutations. Conclusions— Pulmonary hypertensive response to exercise and hypoxia in idiopathic/familial PAH relatives appears as a genetic trait with familial clustering, being correlated to but not caused by a BMPR2 mutation. The suitability of this trait to predict manifest PAH development should be addressed in long-term follow-up studies.


Kardiologia Polska | 2015

2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension

Nazzareno Galiè; Marc Humbert; Jean-Luc Vachiery; Simon Gibbs; Irene Lang; Adam Torbicki; Gérald Simonneau; Andrew Peacock; Anton Vonk Noordegraaf; Maurice Beghetti; Ardeschir Ghofrani; Miguel Sánchez; Georg Hansmann; Walter Klepetko; Patrizio Lancellotti; Marco Matucci; Theresa McDonagh; Luc Pierard; Pedro T. Trindade; Maurizio Zompatori; Marius M. Hoeper

Nazzareno Galiè (ESC Chairperson), Marc Humbert (ERS Chairperson), Jean-Luc Vachiery, Simon Gibbs, Irene Lang, Adam Torbicki, Gérald Simonneau, Andrew Peacock, Anton Vonk Noordegraaf, Maurice Beghetti, Ardeschir Ghofrani, Miguel Angel Gomez Sanchez, Georg Hansmann, Walter Klepetko, Patrizio Lancellotti, Marco Matucci, Theresa McDonagh, Luc A. Pierard, Pedro T. Trindade, Maurizio Zompatori and Marius Hoeper The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and of the European Respiratory Society (ERS)


Respiration | 2011

Effect of Exercise and Respiratory Training on Clinical Progression and Survival in Patients with Severe Chronic Pulmonary Hypertension

Nicola Ehlken; Ardeschir Ghofrani; Gerd Staehler; F. Joachim Meyer; Jana Juenger; Christian F. Opitz; Hans Klose; Heinrike Wilkens; Stephan Rosenkranz; Horst Olschewski; Michael Halank

Background: Even though specific agents for the treatment of patients with pulmonary hypertension (PH) are available, in PH patients, physical capacity and quality of life (QoL) are often restricted and survival is reduced. Objectives: This study prospectively investigated the long-term effects of respiratory and exercise training in patients with severe chronic PH regarding safety, time to clinical worsening and survival. Methods: Fifty-eight consecutive patients with severe PH on stable disease-targeted medication received exercise and respiratory training in hospital for 3 weeks and continued at home. They were prospectively followed for 24 ± 12 months. Primary endpoints were time to clinical worsening and survival. Adverse events and changes in the 6-min walking test, QoL, WHO functional class and gas exchange were secondary endpoints and were evaluated at baseline and at weeks 3 and 15. Results: All patients tolerated the exercise training well without severe adverse events. In week 15, 6-min walking test results were significantly improved compared to baseline (by 84 ± 49 m, p < 0.001), as well as QoL scores, WHO functional class (from 2.9 ± 0.5 to 2.6 ± 0.6, p < 0.01), peak oxygen consumption (from 12.5 ± 3.0 to 14.6 ± 3.9 ml/min/kg, p < 0.001), heart rate at rest (from 75 ± 12 to 61 ± 18 beats/min, p < 0.001) and maximal workload (from 65 ± 21 to 80 ± 25 W, p < 0.001). Survival at 1 and 2 years was 100 and 95%, respectively. Fifteen events occurred during the follow-up. Conclusion: This study indicates that exercise and respiratory training as add-on to medical treatment may improve exercise capacity and QoL, and that they have a good long-term safety in the described setting.


Journal of the American College of Cardiology | 2013

New trial designs and potential therapies for pulmonary artery hypertension.

Mardi Gomberg-Maitland; Todd M. Bull; Rajeev Saggar; Robyn J. Barst; Amany Elgazayerly; Thomas R. Fleming; Friedrich Grimminger; Maurizio Rainisio; Duncan J. Stewart; Norman Stockbridge; Carlo Ventura; Ardeschir Ghofrani; Lewis J. Rubin

A greater understanding of the epidemiology, pathogenesis, and pathophysiology of pulmonary artery hypertension (PAH) has led to significant advances, but the disease remains fatal. Treatment options are neither universally available nor always effective, underscoring the need for development of novel therapies and therapeutic strategies. Clinical trials to date have provided evidence of efficacy, but were limited in evaluating the scope and duration of treatment effects. Numerous potential targets in varied stages of drug development exist, in addition to novel uses of familiar therapies. The pursuit of gene and cell-based therapy continues, and device use to help acute deterioration and chronic management is emerging. This rapid surge of drug development has led to multicenter pivotal clinical trials and has resulted in novel ethical and global clinical trial concerns. This paper will provide an overview of the opportunities and challenges that await the development of novel treatments for PAH.


Revista Espanola De Cardiologia | 2016

2015 ESC/ERS Guidelines for the Diagnosis and Treatment of Pulmonary Hypertension.

Nazzareno Galiè; Marc Humbert; Jean-Luc Vachiery; Simon Gibbs; Irene Lang; Adam Torbicki; Gérald Simonneau; Andrew Peacock; Anton Vonk Noordegraaf; Maurice Beghetti; Ardeschir Ghofrani; Miguel Sánchez; Georg Hansmann; Walter Klepetko; Patrizio Lancellotti; Marco Matucci; Theresa McDonagh; Luc Pierard; Pedro T. Trindade; Maurizio Zompatori; Marius M. Hoeper

Published on behalf of the European Society of Cardiology. All rights reserved. & 2015 European Society of Cardiology & European Respiratory Society. This article is being published concurrently in the European Heart Journal (10.1093/eurheartj/ehv317) and the European Respiratory Journal (10.1183/13993003.01032-2015). The articles are identical except for minor stylistic and spelling differences in keeping with each journal’s style. Either citation can be used when citing this article. * Corresponding authors: Nazzareno Galiè, Department of Experimental, Diagnostic and Specialty Medicine–DIMES, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy, Tel: +39 051 349 858, Fax: +39 051 344 859, Email: [email protected].


Journal of Molecular and Cellular Cardiology | 2010

Identification of right heart-enriched genes in a murine model of chronic outflow tract obstruction

Karsten grosse Kreymborg; Shizuka Uchida; Pascal Gellert; André Schneider; Thomas Boettger; Robert Voswinckel; Astrid Wietelmann; Marten Szibor; Norbert Weissmann; Ardeschir Ghofrani; Ralph T. Schermuly; Dietmar Schranz; Werner Seeger; Thomas Braun

The right ventricle (RV) differs in several aspects from the left ventricle (LV) including its embryonic origin, physiological role and anatomical design. In contrast to LV hypertrophy, little is known about the molecular circuits, which are activated upon RV hypertrophy (RVH). We established a highly reproducible model of RVH in mice using pulmonary artery clipping (PAC), which avoids detrimental RV pressure overload and thus allows long-term survival of operated mice. Magnetic resonance imaging revealed pathognomonic changes with striking similarities to human congenital heart disease- or pulmonary arterial hypertension-patients. Comparative, microarray based transcriptome analysis of right- and left-ventricular remodeling identified distinct transcriptional responses to pressure-induced hypertrophy of either ventricle, which were mainly characterized by stronger transcriptional responses of the RV compared to the LV myocardium. Hierarchic cluster analysis revealed a RV- and LV-specific pattern of gene activity after induction of hypertrophy, however, we did not find evidence for qualitatively distinct regulatory pathways in RV compared to LV. Data mining of nearly three thousand RV-enriched genes under PAC disclosed novel potential (co)-regulators of long-term RV remodeling and hypertrophy. We reason that specific inhibitory mechanisms in RV restrict excessive myocardial hypertrophy and thereby contribute to its vulnerability to pressure overload.


BMC Pharmacology | 2009

Acute hemodynamic response to single oral doses of BAY 60-4552, a soluble guanylate cyclase stimulator, in patients with biventricular heart failure

Veselin Mitrovic; B Swidnicki; Ardeschir Ghofrani; Wolfgang Mück; Nina Kirschbaum; Joachim Mittendorf; Johannes-Peter Stasch; Georg Wensing; Reiner Frey; Silvia Lentini

Address: 1Kerckhoff Heart Center, Department of Cardiology, 61231 Bad Nauheim, Germany, 2Department of Internal Medicine, Medical Clinic II/V, University Hospital Giessen and Marburg GmbH, Klinikstrasse 36, 35392 Giessen, Germany, 3Clinical Pharmacology, 42096 Wuppertal, Germany, 4Global Biostatistics, 42096 Wuppertal, Germany, 5Medicinal Chemistry, 42096 Wuppertal, Germany and 6Cardiology Research, Bayer Schering Pharma AG, Pharma Research Centre, 42096 Wuppertal, Germany


Journal of Immunology | 2002

Apical, But Not Basolateral, Endotoxin Preincubation Protects Alveolar Epithelial Cells Against Hydrogen Peroxide-Induced Loss of Barrier Function: The Role of Nitric Oxide Synthesis

Frank Rose; Bernd Guthmann; Tobias Tenenbaum; Ludger Fink; Ardeschir Ghofrani; Norbert Weissmann; Peter König; Leander Ermert; Gabriele Dahlem; Joerg Haenze; Wolfgang Kummer; Werner Seeger; Friedrich Grimminger

The influence of LPS preincubation on hydrogen peroxide (H2O2)-induced loss of epithelial barrier function was investigated in rat alveolar epithelial type II cells (ATII). Both apical and basolateral H2O2 administration caused a manyfold increase in transepithelial [3H]mannitol passage. Apical but not basolateral preincubation of ATII with LPS did not influence control barrier properties but fully abrogated the H2O2-induced leakage response. The effect of apical LPS was CD14 dependent and was accompanied by a strong up-regulation of NO synthase II mRNA and protein and NO release. Inhibition of NO by NG-monomethyl-l-arginine suppressed the LPS effect, whereas it was reproduced by exogenous application of gaseous NO or NO donor agents. Manipulation of the glutathione homeostasis (buthionine-(S,R)-sulfoximine) and the cGMP pathway (1H-(1,2,4)oxadiazolo[4,3-α]quinoxaline-1-one; zaprinast) did not interfere with the protective effect of LPS. Superoxide (O⨪2) generation by ATII cells was reduced by exogenous NO and LPS preincubation. O⨪2 scavenging with exogenous superoxide dismutase, the intracellular superoxide dismutase analog Mn(III)tetrakis(4-benzoic acid) porphyrin, and the superoxide scavenger nitroblue tetrazolium and, in particular, hydroxyl radical scavenging with hydroxyl radical scavenger 1,3-dimethyl-thiourea inhibited the H2O2-induced epithelial leakage response. In conclusion, apical but not basolateral LPS preincubation of ATII cells provides strong protection against H2O2-induced transepithelial leakage, attributable to an up-regulation of epithelial NO synthesis. It is suggested that the LPS-induced NO formation is effective via interaction with reactive oxygen species, including superoxide and hydroxyl radicals. The polarized epithelial response to LPS may be part of the lung innate immune system, activated by inhaled endotoxin or under conditions of pneumonia.

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Adam Torbicki

Medical University of Warsaw

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