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Hadjadj, Sandra

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Hadjadj

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Sandra

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Université Laval

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ncf13675341

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  • PublicationAccès libre
    Progression of aortic stenosis after an acute myocardial infarction
    (BMJ, 2022-06-21) Clisson, Marine; Paquin, Amélie; Hadjadj, Sandra; Deschênes, Valérie; Rouabhia, Dounia; Robitaille, Charlotte; Beaudoin, Jonathan; Aikawa, Elena; Marsit, Ons; Levine, Robert A; Pibarot, Philippe; Clavel, Marie-Annick
    Background Myocardial infarction (MI) has been shown to induce fibrotic remodelling of the mitral and tricuspid valves. It is unknown whether MI also induces pathological remodelling of the aortic valve and alters aortic stenosis (AS) progression. We thus compared AS progression after an acute MI and in patients with/without history of MI, and assessed post-MI pathobiological changes within the aortic valve leaflets in a sheep model. Methods Serial echocardiograms in human patients with AS were retrospectively analysed and compared between 3 groups: (1) acute MI at baseline (n=68), (2) prior history of MI (n=45) and (3) controls without MI (n=101). Annualised progression rates of AS severity were compared between these 3 groups. In addition, aortic valves were harvested from 15 sheep: (1) induced inferior MI (n=10) and (2) controls without MI (n=5), for biological and histological analyses. Results In humans, the acute MI, previous MI and control groups had comparable baseline AS severity. Indexed aortic valve area (AVAi) declined faster in the acute MI group compared with controls (−0.07±0.06 vs −0.04±0.04 cm²/m²/year; p=0.004). After adjustment, acute MI status was significantly associated with faster AVAi progression (mean difference: −0.013 (95% CI −0.023 to −0.003) cm²/m²/year, p=0.008). In the post-MI experimental animal model, aortic valve thickness and qualitative/quantitative expression of collagen were significantly increased compared with controls. Conclusions The results of this study suggest that AS progression is accelerated following acute MI, which could be caused by increased collagen production and thickening of the aortic valve after the ischaemic event.
  • PublicationRestreint
    Effects of cyproheptadine on mitral valve remodeling and regurgitation after myocardial infarction
    (Elsevier Inc, 2022-07-25) Marsit, Ons; Clavel, Marie-Annick; Paquin, Amélie; Deschênes, Valérie; Hadjadj, Sandra; Sénéchal-Dumais, Isabelle; Couët, Jacques; Arsenault, Marie; Handschumacher, Mark D.; Levine, Robert A.; Aikawa, Elena; Pibarot, Philippe; Beaudoin, Jonathan
    BACKGROUND Ischemic mitral regurgitation (MR) is primarily caused by left ventricle deformation, but leaflet thickening with fibrotic changes are also observed in the valve. Increased levels of 5-hydroxytryptamine (5-HT; ie, serotonin) are described after myocardial infarction (MI); 5-HT can induce valve fibrosis through the 5-HT type 2B receptor (5-HT2BR). OBJECTIVES This study aims to test the hypothesis that post-MI treatment with cyproheptadine (5-HT2BR antagonist) can prevent ischemic MR by reducing the effect of serotonin on mitral biology. METHODS Thirty-six sheep were divided into 2 groups: inferior MI and inferior MI treated with cyproheptadine (0.5 mg/kg/d). Animals were followed for 90 days. Blood 5-HT, infarct size, left ventricular volume and function, MR fraction and mitral leaflet size were assessed. In a complementary in vitro study, valvular interstitial cells were exposed to pre-MI and post-MI serum collected from the experimental animals. RESULTS Increased 5-HT levels were observed after MI in nontreated animals, but not in the group treated with cyproheptadine. Infarct size was similar in both groups (11 ± 3 g vs 9 ± 5 g; P = 0.414). At 90 days, MR fraction was 16% ± 7% in the MI group vs 2% ± 6% in the cyproheptadine group (P = 0.0001). The increase in leaflet size following MI was larger in the cyproheptadine group (+40% ± 9% vs +22% ± 12%; P = 0.001). Mitral interstitial cells overexpressed extracellular matrix genes when treated with post-MI serum, but not when exposed to post-MI serum collected from treated animals. CONCLUSIONS Cyproheptadine given after inferior MI reduces post-MI 5-HT levels, prevents valvular fibrotic remodeling, is associated with larger increase in mitral valve size and less MR.
  • PublicationAccès libre
    Attenuated mitral leaflet enlargement contributes to functional mitral regurgitation after myocardial infarction
    (Elsevier Biomedical, 2020-01-27) Clisson, Marine; Hadjadj, Sandra; Couët, Jacques; Boulanger, Marie-Chloé; Beaudoin, Jonathan; Handschumacher, Mark D.; Marsit, Ons; Pibarot, Philippe; Drolet, Marie-Claude.; Clavel, Marie-Annick; Kim, Dae-Hee; Côté-Laroche, Claudia; Guerrero, J. Luis; Bouchard, Marc; Bartko, Philipp Emanuel; Mathieu, Patrick; Arsenault, Marie; Aïkawa, Elena; Bischoff, Joyce; Levine, Robert A.
    Background: Mitral leaflet enlargement has been identified as an adaptive mechanism to prevent mitral regurgitation in dilated left ventricles (LVs) caused by chronic aortic regurgitation (AR). This enlargement is deficient in patients with functional mitral regurgitation, which remains frequent in the population with ischemic cardiomyopathy. Maladaptive fibrotic changes have been identified in post-myocardial infarction (MI) mitral valves. It is unknown if these changes can interfere with valve growth and whether they are present in other valves. Objectives: This study sought to test the hypothesis that MI impairs leaflet growth, seen in AR, and induces fibrotic changes in mitral and tricuspid valves. Methods: Sheep models of AR, AR + MI, and controls were followed for 90 days. Cardiac magnetic resonance, echocardiography, and computed tomography were performed at baseline and 90 days to assess LV volume, LV function, mitral regurgitation and mitral leaflet size. Histopathology and molecular analyses were performed in excised valves. Results: Both experimental groups developed similar LV dilatation and dysfunction. At 90 days, mitral valve leaflet size was smaller in the AR + MI group (12.8 ± 1.3 cm2 vs. 15.1 ± 1.6 cm2, p = 0.03). Mitral regurgitant fraction was 4% ± 7% in the AR group versus 19% ± 10% in the AR + MI group (p = 0.02). AR + MI leaflets were thicker compared with AR and control valves. Increased expression of extracellular matrix remodeling genes was found in both the mitral and tricuspid leaflets in the AR + MI group. Conclusions: In these animal models of AR, the presence of MI was associated with impaired adaptive valve growth and more functional mitral regurgitation, despite similar LV size and function. More pronounced extracellular remodeling was observed in mitral and tricuspid leaflets, suggesting systemic valvular remodeling after MI.
  • PublicationRestreint
    Echocardiographic variables associated with transvalvular gradient after a transcatheter edge-to-edge mitral valve repair
    (C.V. Mosby, 2021-10-12) O'Connor, Kim; Paquin, Amélie; Hadjadj, Sandra; Rodés-Cabau, Josep; Paradis, Jean-Michel; Beaudoin, Jonathan; Bernier, Mathieu; Pibarot, Philippe; Clavel, Marie-Annick; Simard, Serge; Rouleau, Zachary; Freitas-Ferraz, Afonso; Salaun, Erwan
    Background: Transcatheter edge-to-edge mitral valve repair may lead to a reduction in mitral valve area (MVA) and elevated mean transmitral gradient (TMG). The objectives of this study were to assess the value of baseline MVA by different imaging methods and to explore the associations between MVA indexed to body surface area or left ventricular forward stroke volume and postprocedural TMG. Methods: Preprocedural echocardiographic images from 76 consecutive patients were retrospectively reviewed. MVA planimetry from two-dimensional (2D) transthoracic echocardiography (MVATTE), 2D transesophageal echocardiography in the transgastric view (MVA₂D TEE), and three-dimensional (3D) transesophageal echocardiography (MVA₃D) were measured. Postprocedural TMGs were assessed at 1 to 3 months and all-cause mortality at 1 year. Results: Postprocedural mean TMG > 5 mm Hg was associated with a 3.42-fold (95% confidence interval [CI], 1.08–10.87; P = .04) increased risk for 1-year all-cause mortality. Patients with postprocedural TMG > 5 mm Hg (25% [19 of 76]) had significantly smaller preprocedural MVA3D (3.9 ± 0.8 vs 5.2 ± 1.3 cm2 , P < .01) and MVATTE (4.9 ± 1.1 vs 5.8 ± 1.5 cm² , P = .01) compared with patients without elevated TMG. No significant difference was found for MVA₂D TEE (P = .20). The best threshold values for MVA₃D and MVATTE to be associated with postprocedural TMG > 5 mm Hg were, respectively, 3.9 cm² (area under the curve [AUC] = 0.80; 95% CI, 0.66–0.94; sensitivity 62%, specificity 87%) and 4.6 cm² (AUC = 0.68; 95% CI, 0.54–0.82; sensitivity 53%, specificity 80%). MVA₃D indexed to body surface area and to stroke volume showed overall the best associations with postprocedural mean TMG > 5 mm Hg, with optimal thresholds, respectively, of 2.5 cm² /m² (AUC = 0.88; 95% CI, 0.77–0.98; sensitivity 92%, specificity 74%) and 95 cm² /L (AUC = 0.87; 95% CI, 0.77–0.97; sensitivity 85%, specificity 82%). Conclusions: Elevated TMG following transcatheter edge-to-edge mitral valve repair was associated with increased mortality. The present results indicate that MVA₃D, MVA₃D indexed to body surface area, and MVA₃D indexed to stroke volume may be considered potential predictors of postprocedural TMG > 5 mm Hg and could help optimize patient selection, while the use of 2D methods for valve area were poorly associated with TMG.