Autologous Myoblast Transplantation for Chronic Ischemic Mitral Regurgitation
- Type de publi. : Article dans une revue
- Date de publi. : 01/05/2006
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Auteurs :
Emmanuel MessasAlain BelMiguel Cortes MorichettiClaire CarrionMarc HandschumacherSéverine PeyrardJean-Thomas VilquinMichel DesnosPatrice BrunevalAlain CarpentierPhilippe MenaschéRobert LevineAlbert Hagège
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Organismes :
Therapie Cellulaire en Pathologie Cardio-Vasculaire
Hôpital Européen Georges Pompidou [APHP]
Therapie Cellulaire en Pathologie Cardio-Vasculaire
Hôpital Européen Georges Pompidou [APHP]
Therapie Cellulaire en Pathologie Cardio-Vasculaire
Hôpital Européen Georges Pompidou [APHP]
Physiopathologie et thérapie du muscle strié
Institut de Myologie
CHU Pitié-Salpêtrière [AP-HP]
Harvard Medical School [Boston]
CIC - HEGP
Physiopathologie et thérapie du muscle strié
Institut de Myologie
CHU Pitié-Salpêtrière [AP-HP]
Therapie Cellulaire en Pathologie Cardio-Vasculaire
Hôpital Européen Georges Pompidou [APHP]
Hôpital Européen Georges Pompidou [APHP]
Immunopathologie humaine
Therapie Cellulaire en Pathologie Cardio-Vasculaire
Hôpital Européen Georges Pompidou [APHP]
Therapie Cellulaire en Pathologie Cardio-Vasculaire
Hôpital Européen Georges Pompidou [APHP]
Harvard Medical School [Boston]
Therapie Cellulaire en Pathologie Cardio-Vasculaire
Hôpital Européen Georges Pompidou [APHP]
- Publié dans Journal of the American College of Cardiology le 26/10/2020
Résumé : Objectives: This study was designed to assess whether post-myocardial infarction (MI) in-scar transplantation of skeletal myoblasts (SM) could reduce chronic ischemic mitral regurgitation (MR) by decreasing left ventricular (LV) remodeling. Background: Extensive work has confirmed the relationship between ischemic MR and post-myocardial infarction (MI) remodeling of the LV. Methods: An infero-posterior MI was created in 13 sheep, thereby resulting in increasing MR. Two months post-MI, the animals were randomized and in-scar injected with expanded autologous SM (n = 6, mean: 251 x 10(6) cells) or culture medium only (n = 7). Three-dimensional echocardiography was performed at baseline, before transplantation, and for two months thereafter (sacrifice), with measurements of LV end-diastolic and end-systolic volumes (ESV), ejection fraction (EF), MR stroke volume, and leaflet tethering distance; wall motion score index (WMSi) was assessed by two-dimensional echo. Results: Measurements were similar between groups at baseline and before transplantation. At sacrifice, transplantation was found to have reduced MR progression (regurgitant volume change: -1.83 +/- 0.32 ml vs. 5.9 +/- 0.7 ml in control group, p < 0.0001) and tethering distance (-0.41 +/- 0.09 cm vs. 0.44 +/- 0.12 cm in control group, p < 0.001), with significant improvement of EF (2.01 +/- 0.94% vs. -4.86 +/- 2.23%, p = 0.02), WMSi (-0.25 +/- 0.11 vs. 0.13 +/- 0.03 in controls, p < 0.01) and a trend to a lesser increase in ESV (23.3 +/- 3.5 ml vs. 35.4 +/- 4.2 ml in control group, p = 0.055). Conclusions: Autologous skeletal myoblast transplantation attenuates mild-to-moderate chronic ischemic MR, which otherwise is progressive, by decreasing tethering distance and improving EF and wall motion score, thereby enhancing valve coaptation. These data shed additional light on the mechanism by which skeletal myoblast transplantation may be cardioprotective.
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