Pour savoir comment effectuer et gérer un dépôt de document, consultez le « Guide abrégé – Dépôt de documents » sur le site Web de la Bibliothèque. Pour toute question, écrivez à corpus@ulaval.ca.
 

Personne :
Paquin, Amélie

En cours de chargement...
Photo de profil

Adresse électronique

Date de naissance

Projets de recherche

Structures organisationnelles

Fonction

Nom de famille

Paquin

Prénom

Amélie

Affiliation

Université Laval. Faculté de médecine

ISNI

ORCID

Identifiant Canadiana

ncf13682203

person.page.name

Résultats de recherche

Voici les éléments 1 - 6 sur 6
  • 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.
  • PublicationAccès libre
    Impact de la survenue d'un infarctus aigu du myocarde sur la progression de la sténose aortique
    (2020) Paquin, Amélie; Beaudoin, Jonathan; Clavel, Marie-Annick
    La sténose aortique est l'une des maladies valvulaires cardiaques les plus fréquentes. Il s'agit d'une maladie où la valve aortique s'épaissit et se calcifie progressivement, rendant son ouverture de plus en plus difficile. La sténose aortique a d'importantes conséquences sur le myocarde et peut mener au développement d'angor, d'insuffisance cardiaque, et éventuellement au décès. Aucun traitement ne permet de prévenir ou ralentir le cours de la maladie. La seule option thérapeutique demeure le remplacement de la valve de façon chirurgicale ou percutanée. De plus, l'évolution de la sténose aortique est difficilement prévisible et varie significativement entre les individus. Plusieurs facteurs de risque de développer une sténose aortique ont été identifiés, mais les facteurs qui affectent la vitesse de progression de la maladie sont méconnus. La sténose aortique partage plusieurs similitudes avec la maladie coronarienne athérosclérotique, entre autres au niveau des facteurs de risque et des processus physiopathologiques impliqués. La maladie coronarienne a également des liens étroits avec le développement d'autres maladies valvulaires comme la régurgitation mitrale fonctionnelle suite à un infarctus du myocarde. Au-delà de la déformation géométrique du ventricule gauche occasionnée par l'infarctus, de nouveaux concepts suggèrent aussi l'implication de modifications biologiques pro-inflammatoires et pro-fibrotiques qui affecteraient le tissu valvulaire mitral et contribueraient à son mauvais fonctionnement. Ces conséquences semblent également affecter la valve tricuspide, mais aucune donnée n'existe par rapport à la valve aortique. Il est possible qu'un tel événement ischémique augmente aussi transitoirement la production de fibrose au niveau valvulaire aortique. Nous émettons donc l'hypothèse que la progression de la sténose aortique serait accélérée dans la période qui suit l'infarctus. L'objectif de ce projet de maîtrise est donc d'évaluer l'impact de la survenue d'un infarctus du myocarde sur la vitesse de progression échocardiographique de la sténose aortique, et ce, en comparant à des individus avec sténose aortique n'ayant jamais subi d'infarctus ou avec histoire ancienne d'infarctus. Dans le cadre d'un projet parallèle, des analyses biologiques expérimentales seront également effectuées afin d'évaluer les marqueurs de remodelage de la valve aortique de modèles animaux subissant un infarctus.
  • PublicationAccès libre
    Sex-specific correlates of valvular and arterial calcification burden in patients with moderate aortic stenosis
    (BMJ Group, 2022-12-01) Deslandes, Marianne; Paquin, Amélie; Guzzetti, Ezequiel; Beaudoin, Jonathan; Barriault, Alexandra; Salaun, Erwan; Clavel, Marie-Annick
    Introduction: There are significant sex differences in the prevalence and severity of cardiac calcifying processes. Women harbour more severe mitral annular calcification (MAC), while men exhibit worse aortic valve (AVC) and coronary artery (CAC) calcification. To better understand these differences, we investigated the correlates of cardiac calcification according to sex. Methods: We conducted a cross-sectional study of 406 patients with ≥mild aortic stenosis (AS) defined by an aortic valve area ≤1.5 cm2 , a peak aortic jet velocity >2.0 m/s, or a mean transvalvular gradient >15 mm Hg. Doppler-echocardiography and non-contrast multidetector CT were performed concomitantly to assess AS and cardiac calcifications. Results: Mean age was 71±11 years and 33% were women. The AS haemodynamics were not significantly different between sexes (all p>0.50), with a mean indexed aortic valve area of 0.59±0.21 cm2 /m2 , peak aortic jet velocity of 2.78 (2.37–3.68) m/s, and mean gradient of 17.9 (12.8–31.3) mm Hg for the whole cohort. Compared with men, women harboured lower AVC (480 (222–1191) vs 1003 (484–2329) Agatston unit, AU; p<0.0001) and CAC (366 (50–914) vs 618 (167–1357) AU; p=0.007), but more severe MAC (60 (1–887) vs 48 (0–351) AU; p=0.08) and ascending aorta calcification (227 (43–863) vs 142 (7–493) AU; p=0.03). After comprehensive adjustment, sex remained an independent predictor of each cardiac calcification subtype (all p<0.02) except for the ascending aorta (p=0.32). In multivariable analysis, certain variables, like age or bicuspid aortic valve, were associated with the calcification scores in both sexes. Sexspecific predictors of calcification burden were absence of angiotensin receptor blockers (β=−0.26; p=0.007) and renal impairment (β=0.26; p=0.003) for AVC, and bisphosphonates (β=0.20; p=0.05) for CAC in women; coronary artery disease (β=0.25; p=0.001) for AVC, and angiotensin receptor blockers (β=0.19; p=0.02) and calcium/vitamin D (β=0.15; p=0.02) for MAC in men. Conclusion: In AS, factors associated with cardiac valvular and arterial calcification differ between sexes, suggesting an important contributory role of sex in the pathophysiology of these calcifying processes.
  • 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.
  • PublicationRestreint
    Impact of sex on the management and outcome of aortic stenosis patients
    (2021-05-23) Duval, Raphael; Paquin, Amélie; Magnan, Pierre-Olivier; Voisine, Martine; Tailleur, Mathieu; Fleury, Marie-Ange; Chouinard, Isabelle; Beaudoin, Jonathan; Clavel, Marie-Annick; Bienjonetti-Boudreau, David; Salaun, Erwan
    Objective: The aim of this study was to assess the impact of sex on the management and outcome of patients according to aortic stenosis (AS) severity. Introduction: Sex differences in the management and outcome of AS are poorly understood. Methods: Doppler echocardiography data of patients with at least mild-to-moderate AS [aortic valve area (AVA) ≤1.5 cm2 and peak jet velocity (VPeak) ≥2.5 m/s or mean gradient (MG) ≥25 mmHg] were prospectively collected between 2005 and 2015 and retrospectively analysed. Patients with reduced left ventricular ejection fraction (<50%), or mitral or aortic regurgitation >mild were excluded. Results: Among 3632 patients, 42% were women. The mean indexed AVA (0.48 ± 0.17 cm2/m2), VPeak (3.74 ± 0.88 m/s), and MG (35.1 ± 18.2 mmHg) did not differ between sexes (all P ≥ 0.18). Women were older (72.9 ± 13.0 vs. 70.1 ± 11.8 years) and had more hypertension (75% vs. 70%; P = 0.0005) and less coronary artery disease (38% vs. 55%, P < 0.0001) compared to men. After inverse-propensity weighting (IPW), female sex was associated with higher mortality (IPW-HR: 1.91 [1.14-3.22]; P = 0.01) and less referral to valve intervention (competitive model IPW-HR: 0.88 [0.82-0.96]; P = 0.007) in the whole cohort. This excess mortality in women was blunted in concordant non-severe AS initially treated conservatively (IPW-HR = 1.03 [0.63-1.68]; P = 0.88) or in concordant severe AS initially treated by valve intervention (IPW-HR = 1.25 [0.71-2.21]; P = 0.43). Interestingly, the excess mortality in women was observed in discordant low-gradient AS patients (IPW-HR = 2.17 [1.19-3.95]; P = 0.01) where women were less referred to valve intervention (IPW-Sub-HR: 0.83 [0.73-0.95]; P = 0.009). Conclusion: In this large series of patients, despite similar baseline hemodynamic AS severity, women were less referred to AVR and had higher mortality. This seemed mostly to occur in the patient subset with discordant markers of AS severity (i.e. low-gradient AS) where women were less referred to AVR.
  • 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.