Albert Hagège

ORCID: 0000-0003-4685-6077
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About
Contact & Profiles
Research Areas
  • Cardiomyopathy and Myosin Studies
  • Cardiovascular Function and Risk Factors
  • Cardiac Valve Diseases and Treatments
  • Cardiac Structural Anomalies and Repair
  • Tissue Engineering and Regenerative Medicine
  • Cardiovascular Effects of Exercise
  • Congenital heart defects research
  • Cardiac pacing and defibrillation studies
  • Cardiac Imaging and Diagnostics
  • Trypanosoma species research and implications
  • Viral Infections and Immunology Research
  • Infective Endocarditis Diagnosis and Management
  • Heart Failure Treatment and Management
  • Mesenchymal stem cell research
  • Mechanical Circulatory Support Devices
  • Muscle Physiology and Disorders
  • Lysosomal Storage Disorders Research
  • Congenital Heart Disease Studies
  • Transplantation: Methods and Outcomes
  • Electrospun Nanofibers in Biomedical Applications
  • Cardiac Arrhythmias and Treatments
  • Cardiac Ischemia and Reperfusion
  • Pluripotent Stem Cells Research
  • Connective tissue disorders research
  • Extracellular vesicles in disease

Hôpital Européen Georges-Pompidou
2016-2025

Inserm
2014-2024

Université Paris Cité
2014-2024

Sorbonne Paris Cité
2014-2024

Paris Cardiovascular Research Center
2015-2024

Hôpital Européen
2015-2024

Assistance Publique – Hôpitaux de Paris
2015-2024

Massachusetts General Hospital
1988-2024

Favaloro University
2024

Sequoia (United States)
2024

The ESC Guidelines represent the views of and were produced after careful consideration scientific medical knowledge evidence available at time their dating.The is not responsible in event any contradiction, discrepancy and/or ambiguity between other official recommendations or guidelines issued by relevant public health authorities, particular relationship to good use healthcare therapeutic strategies.Health professionals are encouraged take fully into account when exercising clinical...

10.1093/eurheartj/ehu284 article EN European Heart Journal 2014-08-29

Phase I clinical studies have demonstrated the feasibility of implanting autologous skeletal myoblasts in postinfarction scars. However, they failed to determine whether this procedure was functionally effective and arrhythmogenic.This multicenter, randomized, placebo-controlled, double-blind study included patients with left ventricular (LV) dysfunction (ejection fraction < or = 35%), myocardial infarction, indication for coronary surgery. Each patient received either cells grown from a...

10.1161/circulationaha.107.734103 article EN Circulation 2008-02-20
Iacopo Olivotto Artur Oręziak Roberto Barriales‐Villa Theodore P. Abraham Ahmad Masri and 94 more Pablo García‐Pavía Sara Saberi Neal K. Lakdawala Matthew T. Wheeler Anjali Owens Miloš Kubánek Wojciech Wojakowski Morten K. Jensen Juan R. Gimeno Jonathan Myers Jonathan Myers Sheila M. Hegde Scott D. Solomon Amy J. Sehnert David Zhang Wanying Li Mondira Bhattacharya Jay M. Edelberg Cynthia Burstein Waldman Steven J. Lester Carolyn Y. Ho Carolyn Y. Ho Jozef Bartúnek Jozef Bartúnek Antoine Bondue Emeline M. Van Craenenbroeck Miloš Kubánek David Zemánek Morten K. Jensen Jens Mogensen Jens Jakob Thune Philippe Charron Albert Hagège Olivier Lairez Jean‐Noël Trochu Christoph Axthelm H DUENGEN Norbert Frey Veselin Mitrović Michael Preusch Jeanette Schulz‐Menger Tim Seidler Michael Arad Majdi Halabi Amos Katz Daniel Monakier Offir Paz Samuel Viskin Donna R. Zwas Iacopo Olivotto Hans‐Peter Brunner‐La Rocca Michelle Michels Dariusz Dudek Zofia Oko−Sarnowska Artur Oręziak Wojciech Wojakowski Nuno Cardim Helder Pereira Roberto Barriales‐Villa Pablo García Pavía Juan Gimeno Blanes Rafael Hidalgo Urbano Leonardo Mejia Rincon Perry Elliott Zaheer Yousef Theodore P. Abraham Jonathan Myers Paulino Álvarez Richard G. Bach Richard C. Becker Lubna Choudhury David Fermin Jozef Bartúnek John L. Jefferies Christopher M. Kramer Neal K. Lakdawala Steven J. Lester Ali J. Marian Ahmad Masri Matthew J. Maurer Sherif F. Nagueh Anjali Owens David S. Owens Florian Rader Sara Saberi Mark V. Sherrid Jamshid Shirani John D. Symanski Aslan T. Turer Carolyn Y. Ho Omar Wever‐Pinzon Matthew T. Wheeler Timothy C. Wong Mohamad H. Yamani

10.1016/s0140-6736(20)31792-x article EN The Lancet 2020-08-29

Background— Clinical trials in heart failure have focused on the improvement symptoms or decreases risk of death and other cardiovascular events. Little is known about effect drugs clinical deterioration surviving patients. Methods Results— We compared angiotensin-neprilysin inhibitor LCZ696 (400 mg daily) with angiotensin-converting enzyme enalapril (20 8399 patients reduced ejection fraction a double-blind trial. The analyses prespecified measures nonfatal deterioration. In comparison...

10.1161/circulationaha.114.013748 article EN Circulation 2014-11-18

Mitral valve prolapse has been diagnosed by two-dimensional echocardiographic criteria with surprising frequency in the general population, even when preselected normal subjects are examined. In most of these individuals, however, appears apical four-chamber view and is absent roughly orthogonal long-axis views. Previous studies vitro models nonplanar rings have shown that systolic mitral annular nonplanarity can potentially produce this discrepancy. However, to prove directly apparent...

10.1161/01.cir.80.3.589 article EN Circulation 1989-09-01

Comparative studies suggest that stem cells committed to a cardiac lineage are more effective for improving heart function than those featuring an extra-cardiac phenotype. We have therefore developed population of human embryonic cell (ESC)-derived progenitor cells. Undifferentiated ESCs (I6 line) were amplified and cardiac-committed by exposure bone morphogenetic protein-2 fibroblast growth factor receptor inhibitor. Cells responding these cardio-instructive cues express the transcription...

10.1093/eurheartj/ehv189 article EN European Heart Journal 2015-05-19

Fabry disease ( FD ) is an X‐linked genetic disorder caused by the deficient activity of lysosomal α‐galactosidase (α‐Gal). While males are usually severely affected, clinical presentation in female patients may be more variable ranging from asymptomatic to, occasionally, as affected male patients. The aim this study was to evaluate existence skewed X‐chromosome inactivation XCI females with , its concordance between tissues, and contribution phenotype. Fifty‐six were enrolled. Clinical...

10.1111/cge.12613 article EN Clinical Genetics 2015-05-14

Cell therapy holds promise for tissue regeneration, including in individuals with advanced heart failure. However, treatment of disease bone marrow cells and skeletal muscle progenitors has had only marginal positive benefits clinical trials, perhaps because adult stem have limited plasticity. The identification, among human pluripotent cells, early cardiovascular cell required the development first cardiac lineage would shed light on cardiogenesis might pave way degenerative diseases. Here,...

10.1172/jci40120 article EN Journal of Clinical Investigation 2010-03-24

2D : two-dimensional 99mTc-DPD : 99mTechnetium-3,3-diphosphono- 1,2-propanodi-carboxylic acid ACE : angiotensin-converting enzyme AF : atrial fibrillation AL : amyloid light chain AR : aortic regurgitation ARB : angiotensin receptor blocker ATTR : amyloidosis-transthyretin type AV : atrioventricular BiVAD : biventricular assist device BNP : brain natriuretic peptide BPM : Beats per minute CCS : Canadian Cardiovascular Society CFC : cardiofacialcutaneous CHA2DS2-VASc : Congestive Heart...

10.5603/kp.2014.0212 article EN Kardiologia Polska 2014-11-14

AimsIncreased left ventricular wall thickness (LVWT) is a common finding in cardiology. It not known how often hereditary transthyretin-related familial amyloid cardiomyopathy (mTTR-FAC) responsible for LVWT. Several therapeutic modalities mTTR-FAC are currently clinical trials; thus, it important to establish the prevalence of TTR mutations (mTTR) and characteristics patients with mTTR-FAC.

10.1093/eurheartj/ehv583 article EN European Heart Journal 2015-11-03
Karim Wahbi Rabah Ben Yaou Estelle Gandjbakhch Frédéric Anselme Thomas Gossios and 95 more Neal K. Lakdawala Caroline Stalens Frédéric Sacher Dominique Babuty Jean‐Noël Trochu Ghassan Moubarak Kostantinos Savvatis Raphaël Porcher Pascal Laforêt Abdallah Fayssoil Éloi Marijon Tanya Stojkovic Anthony Béhin Sarah Léonard-Louis Guilhem Solé Fabien Labombarda Pascale Richard Corinne Métay Susana Quijano-Roy Ivana Dabaj Didier Klug Marie‐Christine Vantyghem Philippe Chevalier Pı̈erre Ambrosi Emmanuelle Salort Nicolas Sadoul Xavier Waintraub Khadija Chikhaoui Philippe Mabo Nicolas Combes Philippe Maury Jean‐Marc Sellal Usha B. Tedrow Jonathan M. Kalman Jitendra K. Vohra Alexander F.A. Androulakis Katja Zeppenfeld T. Thompson Christine Barnérias Henri-Marc Bécane Éric Bieth Franck Boccara Damien Bonnet Françoise Bouhour Stéphane Boulé Anne‐Claire Bréhin Françoise Chapon Pascal Cintas Jean‐Marie Cuisset Jean‐Marc Davy Annachiara De Sandre‐Giovannoli Florence Démurger Isabelle Desguerre Klaus Dieterich Julien Durigneux Andoni Echaniz‐Laguna Romain Eschalier Ana Ferreiro Xavier Ferrer Christine Francannet Mélanie Fradin Bénédicte Gaborit Arnaud Gay Albert Hagège Arnaud Isapof Isabelle Jéru Raúl Juntas Morales Emmanuelle Lagrue Nicolas Lamblin Olivier Lascols Vincent Laugel Arnaud Lazarus France Leturcq Nicolas Lévy Armelle Magot Véronique Manel Raphaël P. Martins M. Mayer Sandra Mercier Christophe Meune Maud Michaud Marie-Christine Minot-Myhié Antoine Muchir Aleksandra Nadaj‐Pakleza Yann Péréon Philippe Petiot Florence Petit Julien Praline Anne Rollin Pascal Sabouraud Catherine Sarret S. Schaeffer Frédéric Taithe Céline Tard V. Tiffreau

Background: An accurate estimation of the risk life-threatening (LT) ventricular tachyarrhythmia (VTA) in patients with LMNA mutations is crucial to select candidates for implantable cardioverter-defibrillator implantation. Methods: We included 839 adult mutations, including 660 from a French nationwide registry development sample, and 179 other countries, referred 5 tertiary centers cardiomyopathies, validation sample. LTVTA was defined as (1) sudden cardiac death or (2) cardioverter...

10.1161/circulationaha.118.039410 article EN Circulation 2019-06-03

Fabry disease (FD) is an X‐linked lysosomal storage disorder caused by pathogenic variants in the α‐galactosidase A ( GLA ) gene that leads to reduced or undetectable enzyme activity and progressive accumulation of globotriaosylceramide its deacylated form globotriaosylsphingosine cells throughout body. FD can be multisystemic with neurological, renal, cutaneous cardiac involvement limited heart. Cardiac characterized hypertrophy, fibrosis, arrhythmias, heart failure sudden death. The...

10.1002/ejhf.1960 article EN cc-by-nc European Journal of Heart Failure 2020-07-01

BackgroundOne of the major determinants exercise intolerance and limiting symptoms among patients with obstructive hypertrophic cardiomyopathy (HCM) is an elevated intracardiac pressure resulting from left ventricular outflow tract obstruction. Aficamten oral selective cardiac myosin inhibitor that reduces gradients by mitigating hypercontractility.MethodsIn this phase 3, double-blind trial, we randomly assigned adults symptomatic HCM to receive aficamten (starting dose, 5 mg; maximum 20 mg)...

10.1056/nejmoa2401424 article EN New England Journal of Medicine 2024-05-13

Long-term safety and efficacy of mavacamten in patients with obstructive hypertrophic cardiomyopathy (HCM) are unknown. MAVA-LTE (NCT03723655) is an ongoing, 5-year, open-label extension study designed to evaluate the long-term effects mavacamten.

10.1093/eurheartj/ehae579 article EN cc-by-nc European Heart Journal 2024-09-01

Cardiac myosin binding protein C (MyBP-C) is a sarcomeric belonging to the intracellular immunoglobulin superfamily. Its function uncertain, but for decade evidence has existed both structural and regulatory roles. The gene encoding cardiac MyBP-C (MYBPC3) in humans located on chromosome 11p11.2, mutations have been identified this unrelated families with familial hypertrophic cardiomyopathy (FHC). Detailed characterization of MYBPC3 essential studies regulation, analysis role contraction...

10.1161/01.res.0000435859.24609.b3 article EN Circulation Research 1997-03-01

Background —Little information is available on phenotype-genotype correlations in familial hypertrophic cardiomyopathy that are related to the cardiac myosin binding protein C ( MYBPC3 ) gene. The aim of this study was perform type analysis. Methods and Results —We studied 76 genetically affected subjects from nine families with seven recently identified mutations (SASint20, SDSint7, SDSint23, branch point int23, Glu542Gln, a deletion exon 25, duplication/deletion 33) Detailed clinical, ECG,...

10.1161/01.cir.97.22.2230 article EN Circulation 1998-06-09
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