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34 results on '"Guyomarch, Beatrice"'

3. Predictive Factors of Stent Patency in Iliofemoral Venous Diseases in a Multicentre Cohort Study

Author

Thouveny, Francine, David, Arthur, Henni, Samir, Guédon, Alexis F., de Préville, Agathe, Rousseau, Hervé, Revel-Mouroz, Paul, Guyomarch, Béatrice, Mahé, Guillaume, Gautier, Giovanni, Maurel, Blandine, Espitia, Olivier, Douane, Frédéric, Hersant, Jeanne, Abbadie, Fabrice, Sobocinski, Jonathan, Heautot, Jean-François, Miossec, Annaïg, Lapébie, François-Xavier, and Hartung, Olivier

Published
2023
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12. Sodium-channel blocker challenge in the familial screening of Brugada syndrome: Safety and predictors of positivity

Author

Therasse, Dylan, Sacher, Frederic, Petit, Bertrand, Babuty, Dominique, Mabo, Philippe, Martins, Raphael, Jesel, Laurence, Maury, Philippe, Pasquie, Jean Luc, Mansourati, Jacques, Dupuis, Jean Marc, Kyndt, Florence, Thollet, Aurélie, Guyomarch, Beatrice, Barc, Julien, Schott, Jean Jacques, Le Marec, Herve, Redon, Richard, Probst, Vincent, and Gourraud, Jean-Baptiste

Published
2017
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18. Symptomatic Aortitis at Giant Cell Arteritis Diagnosis: A Prognostic Factor of Aortic Event.

Author

Espitia, Olivier, primary, Blonz, Gautier, additional, Urbanski, Geoffrey, additional, Landron, Cédric, additional, Connault, Jerome, additional, Lavigne, Christian, additional, Roblot, Pascal, additional, Maillot, Francois, additional, Audemard, Alexandra, additional, Artifoni, Mathieu, additional, Durant, Cecile, additional, Guyomarch, Beatrice, additional, Hamidou, Mohamed, additional, Magnant, Julie, additional, and Agard, Christian, additional

Published
2020
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19. Identification of genomic differences among peripheral arterial beds in atherosclerotic and healthy arteries

Author

Steenman, Marja, Espitia, Olivier, Maurel, Blandine, Guyomarch, Beatrice, Heymann, Marie-Françoise, Pistorius, Marc-Antoine, Ory, Benjamin, Heymann, Dominique, Houlgatte, Rémi, Gouëffic, Yann, Quillard, Thibaut, Unité de recherche de l'institut du thorax (ITX-lab), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Sarcomes osseux et remodelage des tissus calcifiés - Phy-Os [Nantes - INSERM U1238] (Phy-Os), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Bretagne Loire (UBL)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Service de médecine interne [Nantes], Université de Nantes (UN)-Hôtel-Dieu-Centre hospitalier universitaire de Nantes (CHU Nantes), Département de chirurgie vasculaire [CHU Nantes], Centre hospitalier universitaire de Nantes (CHU Nantes), Apoptosis and Tumor Progression (CRCINA-ÉQUIPE 9), Centre de Recherche en Cancérologie et Immunologie Nantes-Angers (CRCINA), Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes), Department of Oncology and Metabolism [Sheffield, UK] (INSERM European Associated Laboratory 'Sarcoma Research Unit'), The University of Sheffield [Sheffield, U.K.], Nutrition-Génétique et Exposition aux Risques Environnementaux (NGERE), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL), Délégation à la Recherche Clinique et à l'Innovation [CHRU Nancy] (DRCI), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), This work was funded by an Allocation Nationale de Recherche (ANR) for physiopathology and by an inter-regional Programme Hospitalier de Recherche Clinique (PHRC). T. Quillard received financial support from the European commission (Marie Sklodowska-Curie Actions, Individual Fellowships), the Fondation de l’Avenir (Paris, France), the University Hospital of Nantes (CHU Nantes, Nantes, France), and the Fédération Francaise de Cardiologie (Paris, France)., maurice, sandrine, unité de recherche de l'institut du thorax UMR1087 UMR6291 (ITX), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), and Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)

Subjects
Male, [SDV.MHEP.RSOA] Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system, Genome, Human, Gene Expression Profiling, lcsh:R, Calcinosis, lcsh:Medicine, Arteries, Middle Aged, Atherosclerosis, Article, Plaque, Atherosclerotic, [SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, [SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Risk Factors, Case-Control Studies, Humans, Female, lcsh:Q, lcsh:Science, Aged
Abstract

International audience; Calcification is independently associated with cardiovascular events and morbidity. The calcification burden in atherosclerotic lesions quantitatively and qualitatively differs between arterial beds. Cardiovascular risk factors (CVRF) differentially affect plaque development between arterial beds. The aim of this study was to evaluate the impact of CVRF on atherosclerotic plaque calcification and to further study the molecular arterial heterogeneity that could account for these differences. Histological analysis was performed on atherosclerotic plaques from 153 carotid, 97 femoral and 28 infrapopliteal arteries. CVRF showed minor associations with plaque calcification: age and hypertension affected only the overall presence of calcification but not the type of the calcification, which significantly differed between arterial beds. Transcriptome analysis revealed distinct gene expression profiles associated with each territory in atherosclerotic and healthy arteries. Canonical pathway analysis showed the preferential involvement of immune system-related processes in both atherosclerotic and healthy carotid arteries. Bone development-related genes were among those mostly enriched in atherosclerotic and healthy femoral arteries, which are more prone to developing endochondral calcification. This study highlights the heterogeneous nature of arteries from different peripheral vascular beds and contributes to a better understanding of atherosclerosis formation and evolution. Vascular calcification is an independent predicting factor for cardiovascular events and morbidity 1. Vascular calcification is associated with a worse prognosis after lower limb artery endovascular revascularization: multi-variate analysis reported that the percentage of calcified plaque is an independent predictor of binary restenosis at 12 months 2. Vascular calcification favors plaque rupture and contributes to hypertension depending on its localization and extent. Anatomo-histological studies have shown that atherosclerotic plaque compositions largely differ between anatomical locations in peripheral arterial diseases (PAD). Plaque calcifications are heterogeneous with various types of calcifications, including predominantly microcalcifications in carotid arteries (CA) and bone tissue (osteoid metaplasia) in femoral arteries (FA) 3,4. These differences do not derive from distinct stages of plaque progression , as femoral plaques tend to develop later than those in CA 5. The discrepancies in calcification burden could therefore derive from different shear stress conditions 6 , intrinsic biological differences between vascular cells as suggested by their diverse embryological origins 7,8 , or exposure to different cardiovascular risk factors (CVRF), as CVRF also differentially affect plaque development differentially between arterial beds 9–12 .

Published
2018
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20. TCT-62 A Polymer-Free Paclitaxel-Eluting Stent (Zilver PTX) Versus a Bare-Metal Stent (Misago) for De Novo Femoropopliteal Lesions (BATTLE): A Randomized Trial

Author

Goueffic, Yann, primary, Sauguet, Antoine, additional, Desgranges, Pascal, additional, Feugier, Patrick, additional, Rosset, Eugenio, additional, Ducasse, Eric, additional, Cardon, Alain, additional, Salomon du Mont, Lucie, additional, Pernes, Jean Marc, additional, Commeau, Philippe, additional, Lermusiaux, Patrick, additional, Leclere, Brice, additional, Guyomarch, Beatrice, additional, Hoffmann, Clement, additional, and Maurel, Blandine, additional

Published
2019
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21. Clinical Yield of Familial Screening After Sudden Death in Young Subjects

Author

Quenin, Pauline, Kyndt, Florence, Mabo, Philippe, Mansourati, Jacques, Babuty, Dominique, Thollet, Aurélie, Guyomarch, Beatrice, Redon, Richard, Barc, Julien, Schott, Jean-Jacques, Sacher, Frédéric, Probst, Vincent, Gourraud, Jean Baptiste, unité de recherche de l'institut du thorax UMR1087 UMR6291 (ITX), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Service de cardiologie et maladies vasculaires [Rennes] = Cardiac, Thoracic, and Vascular Surgery [Rennes], CHU Pontchaillou [Rennes], Optimisation des régulations physiologiques (ORPHY (EA 4324)), Institut Brestois Santé Agro Matière (IBSAM), Université de Brest (UBO)-Université de Brest (UBO)-Université de Brest (UBO)-Centre Hospitalier Régional Universitaire de Brest (CHRU Brest), Service de Cardiologie B, Centre Hospitalier Régional Universitaire de Tours (CHRU Tours)-CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] (CRCTB), Université Bordeaux Segalen - Bordeaux 2-CHU Bordeaux [Bordeaux]-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service de cardiologie et maladies vasculaires, Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Hôpital Pontchaillou-CHU Pontchaillou [Rennes], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université, Université de Brest (UBO)-Centre Hospitalier Régional Universitaire de Brest (CHRU Brest)-Institut Brestois Santé Agro Matière (IBSAM), Université de Brest (UBO)-Université de Brest (UBO), Unité de recherche de l'institut du thorax (ITX-lab), and Abramatic, Séverine

Subjects
sudden, [SDV.GEN]Life Sciences [q-bio]/Genetics, cardiac, death, long QT syndrome, Brugada syndrome, [SDV.GEN] Life Sciences [q-bio]/Genetics, humans, prospective studies
Abstract

International audience; BACKGROUND:After sudden cardiac death with negative autopsy, clinical screening of relatives identifies a high proportion of inherited arrhythmia syndrome. However, the efficacy of this screening in families not selected by autopsy has never been assessed. We aim to investigate the value of clinical screening in relatives of all subjects who died suddenly before 45 years of age.METHODS AND RESULTS:One hundred and three consecutive families who experienced unexplained sudden cardiac death before 45 years of age were included from May 2009 to December 2014 in a prospective multicenter registry. Clinical screening was provided to all relatives and performed in 64 families (230 relatives, 80 unexplained sudden cardiac death). Diagnosis was established in 16 families (25%), including Brugada syndrome (7), long QT syndromes (5), dilated cardiomyopathy (2), and hypertrophic cardiomyopathy (2). The diagnostic yield was mainly dependent on the number of screened relatives (3.8±3.4 screened relatives in diagnosed families versus 2.0±1.5; P

Published
2017
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27. Transcatheter closure of coronary artery fistulas in infants and children: A French multicenter study

Author

Mottin, Benoît, primary, Baruteau, Alban, additional, Boudjemline, Younes, additional, Piéchaud, François J., additional, Godart, François, additional, Lusson, Jean-René, additional, Hascoet, Sebastien, additional, Le Gloan, Laurianne, additional, Fresse, Karine Warin, additional, Guyomarch, Beatrice, additional, Bouzguenda, Ivan, additional, Malekzadeh-Milani, Sophie, additional, Petit, Jerome, additional, and Guérin, Patrice, additional

Published
2015
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31. Search for Rare Copy-Number Variants in Congenital Heart Defects Identifies Novel Candidate Genes and a Potential Role for FOXC1 in Patients With Coarctation of the Aorta.

Author

Sanchez-Castro, Marta, Eldjouzi, Hadja, Charpentier, Eric, Busson, Pierre-Francois, Hauet, Quentin, Lindenbaum, Pierre, Delasalle-Guyomarch, Beatrice, Baudry, Adrien, Pichon, Olivier, Pascal, Cecile, Lefort, Bruno, Bajolle, Fanny, Pezard, Philippe, Schott, Jean-Jacques, Dina, Christian, Redon, Richard, Gournay, Veronique, Bonnet, Damien, and Le Caignec, Cedric

Subjects
CONGENITAL heart disease, POLYMERASE chain reaction, DISEASE risk factors
Abstract

Background--Congenital heart defects are the most frequent malformations among newborns and a frequent cause of morbidity and mortality. Although genetic variation contributes to congenital heart defects, their precise molecular bases remain unknown in the majority of patients. Methods and Results--We analyzed, by high-resolution array comparative genomic hybridization, 316 children with sporadic, nonsyndromic congenital heart defects, including 76 coarctation of the aorta, 159 transposition of the great arteries, and 81 tetralogy of Fallot, as well as their unaffected parents. We identified by array comparative genomic hybridization, and validated by quantitative real-time polymerase chain reaction, 71 rare de novo (n=8) or inherited (n=63) copy-number variants (CNVs; 50 duplications and 21 deletions) in patients. We identified 113 candidate genes for congenital heart defects within these CNVs, including BTRC, CHRNB3, CSRP2BP, ERBB2, ERMARD, GLIS3, PLN, PTPRJ, RLN3, and TCTE3. No de novo CNVs were identified in patients with transposition of the great arteries in contrast to coarctation of the aorta and tetralogy of Fallot (P=0.002; Fisher exact test). A search for transcription factor binding sites showed that 93% of the rare CNVs identified in patients with coarctation of the aorta contained at least 1 gene with FOXC1-binding sites. This significant enrichment (P<0.0001; permutation test) was not observed for the CNVs identified in patients with transposition of the great arteries and tetralogy of Fallot. We hypothesize that these CNVs may alter the expression of genes regulated by FOXC1. Foxc1 belongs to the forkhead transcription factors family, which plays a critical role in cardiovascular development in mice. Conclusions--These data suggest that deregulation of FOXC1 or its downstream genes play a major role in the pathogenesis of coarctation of the aorta in humans. [ABSTRACT FROM AUTHOR]

Published
2016
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33. Abstract 14257: De Novo Onset of Atrial Fibrillation in Heart Failure Patients is Predicted by the Blood Transcriptome

Author

Steenman, Marja, Lamirault, Guillaume, Chevalier, Catherine, Guisle, Isabelle, Guyomarch, Beatrice, Fellah-Hebia, Imen, Solnon, Aude, Gourraud, Jean Baptiste, Desprets, Laurent, Abbey, Selim, Leclercq, Christophe, Bru, Paul, Milhem, Antoine, Billon, Olivier, Anselme, Fr?deric, Savour?, Arnaud, Trochu, Jean Noel, Houlgatte, R?mi, and Lande, Gilles

Abstract

Introduction:Heart failure increases the risk of developing atrial fibrillation. Better prediction of this risk may improve treatment strategies. Thus far no transcriptome-based predictor of atrial fibrillation incidence in heart failure has been identified.Hypothesis:We hypothesized that the blood transcriptome profile of heart failure patients is associated with atrial fibrillation incidence.Methods:We enrolled 139 heart failure patients without a history of atrial fibrillation. Coronary sinus blood samples were obtained during biventricular cardioverter defibrillator implantation and were used for whole genome expression profiling using microarrays. Patients were followed up during one year and paroxysmal or persistent atrial fibrillation occurrence was based on interrogation of the defibrillator. Two-class statistical analysis was used to identify genes differentially expressed in patients developing atrial fibrillation during follow-up vs. patients remaining in sinus rhythm. The predictive value of the expression profile was determined using a Mann-Whitney Test.Results:Both clinical and gene expression data could be analyzed for 115 patients: 102 patients stayed in sinus rhythm throughout follow-up while 13 patients developed atrial fibrillation at 1 year follow-up (paroxysmal n=10, persistent n=3). A total of 155 genes was down-regulated in patients developing atrial fibrillation at 1 year follow-up (FDR=0%). The expression levels of these 155 genes were combined to obtain a molecular atrial fibrillation prediction score for each patient. This prediction score distinguished patients that would develop atrial fibrillation within 1 year from patients staying in sinus rhythm (p<0.0001).Conclusions:The blood transcriptome of heart failure patients is a promising tool for the prediction of de novo onset of atrial fibrillation. In line with precision medicine development, the hereby identified high risk patients may benefit from more aggressive clinical management.

Published
2019
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34. Identification of genomic differences among peripheral arterial beds in atherosclerotic and healthy arteries.

Author

Steenman M, Espitia O, Maurel B, Guyomarch B, Heymann MF, Pistorius MA, Ory B, Heymann D, Houlgatte R, Gouëffic Y, and Quillard T

Subjects
Aged, Atherosclerosis pathology, Calcinosis, Case-Control Studies, Female, Gene Expression Profiling, Humans, Male, Middle Aged, Plaque, Atherosclerotic pathology, Risk Factors, Arteries metabolism, Atherosclerosis genetics, Genome, Human
Abstract

Calcification is independently associated with cardiovascular events and morbidity. The calcification burden in atherosclerotic lesions quantitatively and qualitatively differs between arterial beds. Cardiovascular risk factors (CVRF) differentially affect plaque development between arterial beds. The aim of this study was to evaluate the impact of CVRF on atherosclerotic plaque calcification and to further study the molecular arterial heterogeneity that could account for these differences. Histological analysis was performed on atherosclerotic plaques from 153 carotid, 97 femoral and 28 infrapopliteal arteries. CVRF showed minor associations with plaque calcification: age and hypertension affected only the overall presence of calcification but not the type of the calcification, which significantly differed between arterial beds. Transcriptome analysis revealed distinct gene expression profiles associated with each territory in atherosclerotic and healthy arteries. Canonical pathway analysis showed the preferential involvement of immune system-related processes in both atherosclerotic and healthy carotid arteries. Bone development-related genes were among those mostly enriched in atherosclerotic and healthy femoral arteries, which are more prone to developing endochondral calcification. This study highlights the heterogeneous nature of arteries from different peripheral vascular beds and contributes to a better understanding of atherosclerosis formation and evolution.

Published
2018
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