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Dive into the research topics where Claire Bouleti is active.

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Featured researches published by Claire Bouleti.


Journal of the American College of Cardiology | 2015

Late Cardiac Death in Patients Undergoing Transcatheter Aortic Valve Replacement Incidence and Predictors of Advanced Heart Failure and Sudden Cardiac Death

Marina Urena; John G. Webb; Hélène Eltchaninoff; Antonio J. Muñoz-García; Claire Bouleti; Corrado Tamburino; Luis Nombela-Franco; Fabian Nietlispach; César Morís; Marc Ruel; Antonio E. Dager; Vicenç Serra; Asim N. Cheema; Ignacio J. Amat-Santos; Fabio Sandoli de Brito; Pedro A. Lemos; Alexandre Abizaid; Rogério Sarmento-Leite; Henrique B. Ribeiro; Eric Dumont; Marco Barbanti; Eric Durand; Juan H. Alonso Briales; Dominique Himbert; Alec Vahanian; Sebastien Immè; Eulogio García; Francesco Maisano; Raquel del Valle; Luis Miguel Benitez

BACKGROUND Little evidence exists of the burden and predictors of cardiac death after transcatheter aortic valve replacement (TAVR). OBJECTIVES The purpose of this study was to assess the incidence and predictors of cardiac death from advanced heart failure (HF) and sudden cardiac death (SCD) in a large patient cohort undergoing TAVR. METHODS The study included a total of 3,726 patients who underwent TAVR using balloon (57%) or self-expandable (43%) valves. Causes of death were defined according to the Valve Academic Research Consortium-2. RESULTS At a mean follow-up of 22 ± 18 months, 155 patients had died due to advanced HF (15.2% of total deaths, 46.1% of deaths from cardiac causes) and 57 had died due to SCD (5.6% of deaths, 16.9% of cardiac deaths). Baseline comorbidities (chronic obstructive pulmonary disease, atrial fibrillation, left ventricular ejection fraction ≤40%, lower mean transaortic gradient, pulmonary artery systolic pressure >60 mm Hg; p < 0.05 for all) and 2 procedural factors (transapical approach, hazard ratio [HR]: 2.38, 95% confidence interval [CI]: 1.60 to 3.54; p < 0.001; presence of moderate or severe aortic regurgitation after TAVR, HR: 2.79, 95% CI: 1.82 to 4.27; p < 0.001) independently predicted death from advanced HF. Left ventricular ejection fraction ≤40% (HR: 1.93, 95% CI: 1.05 to 3.55; p = 0.033) and new-onset persistent left bundle-branch block following TAVR (HR: 2.26, 95% CI: 1.23 to 4.14; p = 0.009) were independently associated with an increased risk of SCD. Patients with new-onset persistent left bundle-branch block and a QRS duration >160 ms had a greater SCD risk (HR: 4.78, 95% CI: 1.56 to 14.63; p = 0.006). CONCLUSIONS Advanced HF and SCD accounted for two-thirds of cardiac deaths in patients after TAVR. Potentially modifiable or treatable factors leading to increased risk of mortality for HF and SCD were identified. Future studies should determine whether targeting these factors decreases the risk of cardiac death.


Circulation | 2012

Protection Against Myocardial Infarction and No-Reflow Through Preservation of Vascular Integrity by Angiopoietin-Like 4

Ariane Galaup; Elisa Gomez; Rachid Souktani; Mélanie Durand; Aurélie Cazes; Catherine Monnot; Jérémie Teillon; Sebastien Jan; Claire Bouleti; Gaëlle Briois; Josette Philippe; Sandrine Pons; Valérie Martin; Rana Assaly; Philippe Bonnin; Philippe Ratajczak; Anne Janin; Gavin Thurston; David M. Valenzuela; Andrew J. Murphy; George D. Yancopoulos; Renaud Tissier; Alain Berdeaux; Bijan Ghaleh; Stéphane Germain

Background— Increased permeability, predominantly controlled by endothelial junction stability, is an early event in the deterioration of vascular integrity in ischemic disorders. Hemorrhage, edema, and inflammation are the main features of reperfusion injuries, as observed in acute myocardial infarction (AMI). Thus, preservation of vascular integrity is fundamental in ischemic heart disease. Angiopoietins are pivotal modulators of cell–cell junctions and vascular integrity. We hypothesized that hypoxic induction of angiopoietin-like protein 4 (ANGPTL4) might modulate vascular damage, infarct size, and no-reflow during AMI. Methods and Results— We showed that vascular permeability, hemorrhage, edema, inflammation, and infarct severity were increased in angptl4-deficient mice. We determined that decrease in vascular endothelial growth factor receptor 2 (VEGFR2) and VE-cadherin expression and increase in Src kinase phosphorylation downstream of VEGFR2 were accentuated after ischemia-reperfusion in the coronary microcirculation of angptl4-deficient mice. Both events led to altered VEGFR2/VE-cadherin complexes and to disrupted adherens junctions in the endothelial cells of angptl4-deficient mice that correlated with increased no-reflow. In vivo injection of recombinant human ANGPTL4 protected VEGF-driven dissociation of the VEGFR2/VE-cadherin complex, reduced myocardial infarct size, and the extent of no-reflow in mice and rabbits. Conclusions— These data showed that ANGPTL4 might constitute a relevant target for therapeutic vasculoprotection aimed at counteracting the effects of VEGF, thus being crucial for preventing no-reflow and conferring secondary cardioprotection during AMI.


Circulation | 2012

Late Results of Percutaneous Mitral Commissurotomy up to 20 Years: Development and Validation of a Risk Score Predicting Late Functional Results from a Series of 912 Patients

Claire Bouleti; Bernard Iung; Cédric Laouénan; Dominique Himbert; Eric Brochet; David Messika-Zeitoun; Delphine Detaint; Eric Garbarz; Bertrand Cormier; Pierre-Louis Michel; Alec Vahanian

Background— Long-term follow-up after percutaneous mitral commissurotomy enables predictive factors of late results to be identified. Methods and Results— Late results of percutaneous mitral commissurotomy were assessed in 1024 consecutive patients. Good immediate results, defined as valve area ≥1.5 cm2 without mitral regurgitation >2/4, were obtained in 912 patients (89%). These 912 patients were randomly split into 2 cohorts comprising 609 and 303 patients that were used to develop and validate, respectively, a scoring system predicting late functional results. The 20-year rate of good functional results (survival without cardiovascular death, mitral surgery, or repeat percutaneous mitral commissurotomy and in New York Heart Association class I or II) was 30.2±2.0%. A multivariable Cox model identified 7 predictive factors of poor late functional results: higher final mean gradient ( P <0.0001), interaction between age and final mitral valve area ( P <0.0001) showing that the impact of valve area decreases with age, interaction between sex and valve calcification ( P <0.0001) showing that the impact of valve anatomy is stronger in men, and interaction between rhythm and New York Heart Association class showing an impact of New York Heart Association class only in patients in atrial fibrillation ( P <0.0001). A 13-point score enabled 3 risk groups to be defined, corresponding to predicted good functional results of 55.1%, 29.1%, and 10.5% at 20 years in the validation cohort. Conclusions— Twenty years after percutaneous mitral commissurotomy in a population of patients with varied characteristics, 30% still had good functional results. Prediction of late functional results is multifactorial and strongly determined by age and the quality of immediate results. A simple validated scoring system is useful for estimating individual patient outcome. # Clinical Perspective {#article-title-40}Background— Long-term follow-up after percutaneous mitral commissurotomy enables predictive factors of late results to be identified. Methods and Results— Late results of percutaneous mitral commissurotomy were assessed in 1024 consecutive patients. Good immediate results, defined as valve area ≥1.5 cm2 without mitral regurgitation >2/4, were obtained in 912 patients (89%). These 912 patients were randomly split into 2 cohorts comprising 609 and 303 patients that were used to develop and validate, respectively, a scoring system predicting late functional results. The 20-year rate of good functional results (survival without cardiovascular death, mitral surgery, or repeat percutaneous mitral commissurotomy and in New York Heart Association class I or II) was 30.2±2.0%. A multivariable Cox model identified 7 predictive factors of poor late functional results: higher final mean gradient (P<0.0001), interaction between age and final mitral valve area (P<0.0001) showing that the impact of valve area decreases with age, interaction between sex and valve calcification (P<0.0001) showing that the impact of valve anatomy is stronger in men, and interaction between rhythm and New York Heart Association class showing an impact of New York Heart Association class only in patients in atrial fibrillation (P<0.0001). A 13-point score enabled 3 risk groups to be defined, corresponding to predicted good functional results of 55.1%, 29.1%, and 10.5% at 20 years in the validation cohort. Conclusions— Twenty years after percutaneous mitral commissurotomy in a population of patients with varied characteristics, 30% still had good functional results. Prediction of late functional results is multifactorial and strongly determined by age and the quality of immediate results. A simple validated scoring system is useful for estimating individual patient outcome.


Journal of the American College of Cardiology | 2014

Transcatheter valve replacement in patients with severe mitral valve disease and annular calcification.

Dominique Himbert; Claire Bouleti; Bernard Iung; Mohammed Nejjari; Eric Brochet; Jean-Pol Depoix; Walid Ghodbane; Amir-Ali Fassa; Patrick Nataf; Alec Vahanian

Patients with extensive mitral annular calcification (MAC) may have an inoperable condition because of insurmountable technical issues. Four cases have suggested the feasibility of transcatheter mitral valve replacement (TMVR) in these patients [(1–4)][1]. We report here the first series of


Archives of Cardiovascular Diseases | 2015

The no-reflow phenomenon: State of the art.

Claire Bouleti; Nathan Mewton; Stéphane Germain

Primary percutaneous coronary intervention (PCI) is the best available reperfusion strategy for acute ST-segment elevation myocardial infarction (STEMI), with nearly 95% of occluded coronary vessels being reopened in this setting. Despite re-establishing epicardial coronary vessel patency, primary PCI may fail to restore optimal myocardial reperfusion within the myocardial tissue, a failure at the microvascular level known as no-reflow (NR). NR has been reported to occur in up to 60% of STEMI patients with optimal coronary vessel reperfusion. When it does occur, it significantly attenuates the beneficial effect of reperfusion therapy, leading to poor outcomes. The pathophysiology of NR is complex and incompletely understood. Many phenomena are known to contribute to NR, including leukocyte infiltration, vasoconstriction, activation of inflammatory pathways and cellular oedema. Vascular damage and haemorrhage may also play important roles in the establishment of NR. In this review, we describe the pathophysiological mechanisms of NR and the tools available for diagnosing it. We also describe the microvasculature and the endothelial mechanisms involved in NR, which may provide relevant therapeutic targets for reducing NR and improving the prognosis for patients.


European Heart Journal | 2013

Protective effects of angiopoietin-like 4 on cerebrovascular and functional damages in ischaemic stroke

Claire Bouleti; Thomas Mathivet; Bérard Coqueran; Jean-Michel Serfaty; Mathieu Lesage; Elodie Berland; Corinne Ardidie-Robouant; Gilles Kauffenstein; Daniel Henrion; Bertrand Lapergue; Mikael Mazighi; Charles Duyckaerts; Gavin Thurston; David M. Valenzuela; Andrew J. Murphy; George D. Yancopoulos; Catherine Monnot; Isabelle Margaill; Stéphane Germain

AIMS Given the impact of vascular injuries and oedema on brain damage caused during stroke, vascular protection represents a major medical need. We hypothesized that angiopoietin-like 4 (ANGPTL4), a regulator of endothelial barrier integrity, might exert a protective effect during ischaemic stroke. METHODS AND RESULTS Using a murine transient ischaemic stroke model, treatment with recombinant ANGPTL4 led to significantly decreased infarct size and improved behaviour. Quantitative characteristics of the vascular network (density and branchpoints) were preserved in ANGPTL4-treated mice. Integrity of tight and adherens junctions was also quantified and ANGPTL4-treated mice displayed increased VE-cadherin and claudin-5-positive areas. Brain oedema was thus significantly decreased in ANGPTL4-treated mice. In accordance, vascular damage and infarct severity were increased in angptl4-deficient mice thus providing genetic evidence that ANGPTL4 preserves brain tissue from ischaemia-induced alterations. Altogether, these data show that ANGPTL4 protects not only the global vascular network, but also interendothelial junctions and controls both deleterious inflammatory response and oedema. Mechanistically, ANGPTL4 counteracted VEGF signalling and thereby diminished Src-signalling downstream from VEGFR2. This led to decreased VEGFR2-VE-cadherin complex disruption, increased stability of junctions and thus increased endothelial cell barrier integrity of the cerebral microcirculation. In addition, ANGPTL4 prevented neuronal loss in the ischaemic area. CONCLUSION These results, therefore, show ANGPTL4 counteracts the loss of vascular integrity in ischaemic stroke, by restricting Src kinase signalling downstream from VEGFR2. ANGPTL4 treatment thus reduces oedema, infarct size, neuronal loss, and improves mice behaviour. These results suggest that ANGPTL4 constitutes a relevant target for vasculoprotection and cerebral protection during stroke.


Heart | 2015

Long-term outcome after transcatheter aortic valve implantation

Claire Bouleti; Dominique Himbert; Bernard Iung; Benjamin Alos; Caroline Kerneis; Walid Ghodbane; David Messika-Zeitoun; Eric Brochet; Amir-Ali Fassa; Jean-Pol Depoix; Phalla Ou; Patrick Nataf

Objective To assess late outcome after transcatheter aortic valve implantation (TAVI) up to 6 years and to analyse its predictive factors with a particular emphasis on functional status. Very few data exist on the long-term results of TAVI, and these data are crucial for decision making. Methods Between October 2006 and December 2009, 123 consecutive patients were discharged alive after TAVI in our institution. Mean age was 82±8 years, and 88% of patients were highly symptomatic in New York Heart Association (NYHA) class III–IV. Results Follow-up was complete in 122 patients (99%). The overall 6-year survival rate was 31%±5%, the majority of deaths being non-cardiac. Predictive factors of late mortality were the presence of lower limb arteritis (p=0.009), a higher Charlson comorbidity index (p=0.03) and post-TAVI paraprosthetic aortic regurgitation ≥2/4 (p=0.01). Late outcomes according to Valve Academic Research Consortium-2 criteria were analysed, and the 5-year event-free survival rate was 28%±4%. Finally, the rate of good functional results, defined as survival in NYHA class I or II, was 32%±5% at 5-year follow-up. In the survivors, the EQ-5D questionnaire further confirmed the benefit in terms of quality of life. Conclusions About one-third of patients discharged alive after TAVI were alive at 6-year follow-up, and the survivors exhibited good functional results assessed by NYHA class and quality-of-life standardised evaluation.


European Heart Journal | 2013

Reinterventions after percutaneous mitral commissurotomy during long-term follow-up, up to 20 years: the role of repeat percutaneous mitral commissurotomy

Claire Bouleti; Bernard Iung; Dominique Himbert; Eric Brochet; David Messika-Zeitoun; Delphine Detaint; Eric Garbarz; Bertrand Cormier; Alec Vahanian

AIMS We analysed reinterventions performed during long-term follow-up after percutaneous mitral commissurotomy (PMC) with a particular focus on freedom from mitral surgery and late results of repeat PMC. METHODS AND RESULTS In 912 patients who had good immediate results of PMC (valve area ≥1.5 cm² with mitral regurgitation ≤2/4), we analysed survival without reintervention (surgery or repeat PMC) and survival without surgery alone, with a follow-up up to 20 years. The median age was 48 years, and 251 patients (27%) had calcified valves. During a median follow-up of 12 years, 351 patients (38%) underwent a reintervention: surgery was performed in 266 (76%) patients and repeat PMC in 85 (24%). Cardiovascular survival without reintervention (surgery or repeat PMC) was 38 ± 2% at 20 years. When analysing cardiovascular survival without surgery, this rate increased to 46 ± 2% at 20 years. In the 504 patients aged <50 years at the time of their initial PMC, 20-year rates were 45 ± 3% for cardiovascular survival without reintervention and 57 ± 3% for cardiovascular survival without surgery. Of the 85 patients who underwent repeat PMC, cardiovascular survival without surgery was 60 ± 7% at 10 years. CONCLUSION After successful PMC, reintervention is frequently needed. However, almost half of the patients remained free from surgery at 20 years. Repeat PMC was performed in one out of four cases of reintervention in this study, thereby allowing for postponement of surgery in a substantial number of patients.


Critical Care Medicine | 2013

Connection between cardiac vascular permeability, myocardial edema, and inflammation during sepsis: role of the α1AMP-activated protein kinase isoform.

Diego Castanares-Zapatero; Claire Bouleti; Caroline Sommereyns; Bernhard Gerber; Christelle Lecut; Thomas Mathivet; Michael Horckmans; Didier Communi; Marc Foretz; Jean-Louis Vanoverschelde; Stéphane Germain; Luc Bertrand; Pierre-François Laterre; Cécile Oury; Benoit Viollet; Sandrine Horman; Christophe Beauloye

Objective:As adenosine monophosphate (AMP)-activated protein kinase both controls cytoskeleton organization in endothelial cells and exerts anti-inflammatory effects, we here postulated that it could influence vascular permeability and inflammation, thereby counteracting cardiac wall edema during sepsis. Design:Controlled animal study. Settings:University research laboratory. Subjects:C57BL/6J, &agr;1AMPK–/–, and &agr;1AMPK+/+ mice. Intervention:Sepsis was triggered in vivo using a sublethal injection of lipopolysaccharide (O55B5, 10 mg/kg), inducing systolic left ventricular dysfunction. Left ventricular function, edema, vascular permeability, and inflammation were assessed in vivo in both wild-type mice (&agr;1AMPK+/+) and &agr;1AMP-activated protein kinase–deficient mice (&agr;1AMPK–/–). The 5-aminoimidazole-4-carboxamide riboside served to study the impact of AMP-activated protein kinase activation on vascular permeability in vivo. The integrity of endothelial cell monolayers was also examined in vitro after lipopolysaccharide challenge in the presence of aminoimidazole-4-carboxamide riboside and/or after &agr;1AMP-activated protein kinase silencing. Measurements and Main Results:&agr;1AMP-activated protein kinase deficiency dramatically impaired tolerance to lipopolysaccharide challenge. Indeed, &agr;1AMPK–/– exhibited heightened cardiac vascular permeability after lipopolysaccharide challenge compared with &agr;1AMPK+/+. Consequently, an increase in left ventricular mass corresponding to exaggerated wall edema occurred in &agr;1AMPK–/–, without any further decrease in systolic function. Mechanistically, the lipopolysaccharide-induced &agr;1AMPK–/– cardiac phenotype could not be attributed to major changes in the systemic inflammatory response but was due to an increased disruption of interendothelial tight junctions. Accordingly, AMP-activated protein kinase activation by aminoimidazole-4-carboxamide riboside counteracted lipopolysaccharide-induced hyperpermeability in wild-type mice in vivo as well as in endothelial cells in vitro. This effect was associated with a potent protection of zonula occludens-1 linear border pattern in endothelial cells. Conclusions:Our results demonstrate for the first time the involvement of a signaling pathway in the control of left ventricular wall edema during sepsis. AMP-activated protein kinase exerts a protective action through the preservation of interendothelial tight junctions. Interestingly, exaggerated left ventricular wall edema was not coupled with aggravated systolic dysfunction. However, it could contribute to diastolic dysfunction in patients with sepsis.


Archives of Cardiovascular Diseases | 2016

Tricuspid valve and percutaneous approach: No longer the forgotten valve!

Claire Bouleti; Jean-Michel Juliard; Dominique Himbert; Bernard Iung; E. Brochet; Marina Urena; Marie-Pierre Dilly; Phalla Ou; Patrick Nataf; Alec Vahanian

Tricuspid valve disease is mainly represented by tricuspid regurgitation (TR), which is a predictor of poor outcome. TR is usually secondary, caused by right ventricle pressure or volume overload, the leading cause being left-sided heart valve diseases. Tricuspid surgery for severe TR is recommended during left valve surgery, and consists of either a valve replacement or, most often, a tricuspid repair with or without prosthetic annuloplasty. When TR persists or worsens after left valvular surgery, redo isolated tricuspid surgery is associated with high mortality. In addition, a sizeable proportion of patients present with tricuspid surgery deterioration over time, and need a reintervention, which is associated with high morbi-mortality rates. In this context, and given the recent major breakthrough in the percutaneous treatment of aortic and mitral valve diseases, the tricuspid valve appears an appealing challenge, although it raises specific issues. The first applications of transcatheter techniques for tricuspid valve disease were valve-in-valve and valve-in-ring implantation for degenerated bioprosthesis or ring annuloplasty. Some concerns remain regarding prosthesis sizing, rapid ventricular pacing and the best approach, but these procedures appear to be safe and effective. More recently, bicuspidization using a transcatheter approach for the treatment of native tricuspid valve has been published, in two patients. Finally, other devices are in preclinical development.

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Thomas Mathivet

Katholieke Universiteit Leuven

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