Alain Manrique1,2,3, Patricia Lemarchand4,5,6,7, Béatrice Delasalle4,5,6,7, Olivier Lairez8, Catherine Sportouch-Duckan9,10, Guillaume Lamirault4,5,6,7, Philippe Le Corvoisier11, Yannick Neuder12, Marjorie Richardson13, Alain Lebon14, Jérome Roncalli8, Christophe Piot9,10, Jean-Noel Trochu4,5,6,7, Emmanuel Teiger15, Claude Hossein-Foucher16,17, Thierry Le Tourneau4,5,6,7. 1. Nuclear Medicine, CHU de Caen, Caen, F-14000, France. manrique@cyceron.fr. 2. EA 4650, Université de Caen Normandie, Caen, F-14000, France. manrique@cyceron.fr. 3. CHU de Caen et GIP Cyceron, Campus Jules Horowitz, BP 5229, 14074, Caen cedex 6, France. manrique@cyceron.fr. 4. INSERM, UMR1087, l'institut du thorax, Nantes, F-44000, France. 5. CNRS, UMR 6291, Nantes, F-44000, France. 6. Université de Nantes, Nantes, F-44000, France. 7. CHU de Nantes, Nantes, F-44000, France. 8. Cardiac Imaging Center, CIC Biothérapies, CHU de Toulouse, Institut CARDIOMET-Toulouse, Toulouse, France. 9. Institut de Génomique Fonctionnelle, INSERM U661, CNRS UMR 5203, Université Montpellier, Montpellier, France. 10. Clinique du Millénaire, Montpellier, France. 11. INSERM, Centre d'Investigation Clinique 1430 et U955 équipe 3, Hôpital Henri Mondor, Créteil, France. 12. Pole Thorax et Vaisseaux, CHU de Grenoble, Grenoble, France. 13. Service d'Explorations Fonctionnelles Cardiovasculaires, Hôpital Cardiologique, CHRU Lille, Lille, France. 14. Service de Cardiologie, CHU de Caen, Caen, F-14000, France. 15. AP-HP, unité de cardiologie interventionnelle et fédération de cardiologie, Hôpital Henri Mondor, Créteil, France. 16. Service de médecine nucléaire, Hôpital Salengro CHRU de Lille, Lille, France. 17. UFR de Médecine, Université de Lille 2, Lille, France.
Abstract
PURPOSE: Few data are available regarding the relation of left ventricular (LV) mechanical dyssynchrony to remodelling after acute myocardial infarction (MI) and stem cell therapy. We evaluated the 1-year time course of both LV mechanical dyssynchrony and remodelling in patients enrolled in the BONAMI trial, a randomized, multicenter controlled trial assessing cell therapy in patients with reperfused MI. METHODS:Patients with acute MI and ejection fraction (EF) ≤ 45 % were randomized to cell therapy or to control and underwent thallium single-photon emission computed tomography (SPECT), radionuclide angiography, and echocardiography at baseline, 3 months, and 1 year. Eighty-three patients with a comprehensive 1-year follow-up were included. LV dyssynchrony was assessed by the standard deviation (SD) of the LV phase histogram using radionuclide angiography. Remodelling was defined as a 20 % increase in LV end-systolic volume index (LVESVI) at 1 year. RESULTS: At baseline, LVEF, wall motion score index, and perfusion defect size were significantly impaired in the 43 patients (52 %) with LV remodelling (all p < 0.001), without significant increase in LV mechanical dyssynchrony. During follow-up, there was a progressive increase in LV SD (p = 0.01). Baseline independent predictors of LV remodelling were perfusion SPECT defect size (p = 0.001), LVEF (p = 0.01) and a history of hypertension (p = 0.043). Bone marrow cell therapy did not affect the time-course of LV remodelling and dyssynchrony. CONCLUSIONS: LV remodelling 1 year after reperfused MI is associated with progressive LV dyssynchrony and is related to baseline infarct size and ejection fraction, without impact of cell therapy on this process.
RCT Entities:
PURPOSE: Few data are available regarding the relation of left ventricular (LV) mechanical dyssynchrony to remodelling after acute myocardial infarction (MI) and stem cell therapy. We evaluated the 1-year time course of both LV mechanical dyssynchrony and remodelling in patients enrolled in the BONAMI trial, a randomized, multicenter controlled trial assessing cell therapy in patients with reperfused MI. METHODS:Patients with acute MI and ejection fraction (EF) ≤ 45 % were randomized to cell therapy or to control and underwent thallium single-photon emission computed tomography (SPECT), radionuclide angiography, and echocardiography at baseline, 3 months, and 1 year. Eighty-three patients with a comprehensive 1-year follow-up were included. LV dyssynchrony was assessed by the standard deviation (SD) of the LV phase histogram using radionuclide angiography. Remodelling was defined as a 20 % increase in LV end-systolic volume index (LVESVI) at 1 year. RESULTS: At baseline, LVEF, wall motion score index, and perfusion defect size were significantly impaired in the 43 patients (52 %) with LV remodelling (all p < 0.001), without significant increase in LV mechanical dyssynchrony. During follow-up, there was a progressive increase in LV SD (p = 0.01). Baseline independent predictors of LV remodelling were perfusion SPECT defect size (p = 0.001), LVEF (p = 0.01) and a history of hypertension (p = 0.043). Bone marrow cell therapy did not affect the time-course of LV remodelling and dyssynchrony. CONCLUSIONS: LV remodelling 1 year after reperfused MI is associated with progressive LV dyssynchrony and is related to baseline infarct size and ejection fraction, without impact of cell therapy on this process.
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