Laura Ernande1, Cyrille Bergerot2, Nicolas Girerd3, Hélène Thibault4, Einar Skulstad Davidsen5, Pierre Gautier Pignon-Blanc2, Camille Amaz2, Pierre Croisille6, Marc L De Buyzere7, Ernst R Rietzschel7, Thierry C Gillebert7, Philippe Moulin8, Mikhael Altman9, Geneviève Derumeaux10. 1. Service des Explorations Fonctionnelles Cardiovasculaires & Centre d'Investigation Clinique, Louis Pradel Hospital, Lyon, France; INSERM U955, Team 8, Faculté de Médecine de Créteil, Institut Mondor de Recherche Biomédicale, Université Paris-Est Créteil, Créteil, France. 2. Service des Explorations Fonctionnelles Cardiovasculaires & Centre d'Investigation Clinique, Louis Pradel Hospital, Lyon, France. 3. INSERM, Centre d'Investigations Cliniques 9501, Université de Lorraine, CHU de Nancy, Institut Lorrain du Cœur et des Vaisseaux, Nancy, France. 4. Service des Explorations Fonctionnelles Cardiovasculaires & Centre d'Investigation Clinique, Louis Pradel Hospital, Lyon, France; CarMeN INSERM Unit 1060, Claude Bernard Lyon 1 University, Lyon, France. 5. Department of Heart Disease, Haukeland University Hospital, Bergen, Norway. 6. CREATIS, UMR CNRS 5220, INSERM U1044, Université Jean Monnet Saint-Etienne, CHU Saint-Etienne, Université de Lyon, Lyon, France. 7. Department of Cardiology, Ghent University, Ghent, Belgium. 8. CarMeN INSERM Unit 1060, Claude Bernard Lyon 1 University, Lyon, France; Department of Endocrinology, Louis Pradel Hospital, Lyon, France. 9. INSERM U955, Team 8, Faculté de Médecine de Créteil, Institut Mondor de Recherche Biomédicale, Université Paris-Est Créteil, Créteil, France. 10. Service des Explorations Fonctionnelles Cardiovasculaires & Centre d'Investigation Clinique, Louis Pradel Hospital, Lyon, France; INSERM U955, Team 8, Faculté de Médecine de Créteil, Institut Mondor de Recherche Biomédicale, Université Paris-Est Créteil, Créteil, France. Electronic address: gderumeaux@gmail.com.
Abstract
BACKGROUND: In normal subjects, left ventricular (LV) dimensions have been shown to decrease over time, while wall thickness is increasing. The aim of this study was to investigate LV remodeling in a cohort of patients with type 2 diabetes mellitus during a 3-year follow-up period and its potential association with decreased longitudinal systolic strain (εL). METHODS: One hundred seventy-two patients with type 2 diabetes without overt heart disease were prospectively enrolled and underwent echocardiography with speckle-tracking imaging to assess global LV εL at baseline and at 3 years. The associations between alteration in εL (defined as |εL| < 18%), LV geometry at baseline, and LV remodeling over time were evaluated. RESULTS: Among the 172 enrolled patients, 154 completed 3-year follow-up. At baseline, patients with εL alteration had higher LV end-systolic volumes (28 ± 11 vs 23 ± 9 mL, P < .001) and relative wall thicknesses (RWT; 0.44 ± 0.06 vs 0.40 ± 0.07, P = .008) compared with those with normal εL. At 3-year follow-up, RWTs remained stable in both groups. LV volumes significantly decreased in patients with normal εL but not in patients with εL alteration. Multivariate analysis showed that εL alteration was independently associated with LV end-systolic volume (β = 5.0, P = .006) and RWT (β = 0.03, P = .03) at baseline and with changes in both LV end-diastolic volume (β = 19.1, P = .001) and LV end-systolic volume (β = 2.6, P = .047) over 3 years. CONCLUSIONS: In patients with type 2 diabetes, εL alteration was associated with higher RWT and LV volumes and with the absence of decreases in LV volumes over time, which might be an early sign of adverse LV remodeling.
BACKGROUND: In normal subjects, left ventricular (LV) dimensions have been shown to decrease over time, while wall thickness is increasing. The aim of this study was to investigate LV remodeling in a cohort of patients with type 2 diabetes mellitus during a 3-year follow-up period and its potential association with decreased longitudinal systolic strain (εL). METHODS: One hundred seventy-two patients with type 2 diabetes without overt heart disease were prospectively enrolled and underwent echocardiography with speckle-tracking imaging to assess global LV εL at baseline and at 3 years. The associations between alteration in εL (defined as |εL| < 18%), LV geometry at baseline, and LV remodeling over time were evaluated. RESULTS: Among the 172 enrolled patients, 154 completed 3-year follow-up. At baseline, patients with εL alteration had higher LV end-systolic volumes (28 ± 11 vs 23 ± 9 mL, P < .001) and relative wall thicknesses (RWT; 0.44 ± 0.06 vs 0.40 ± 0.07, P = .008) compared with those with normal εL. At 3-year follow-up, RWTs remained stable in both groups. LV volumes significantly decreased in patients with normal εL but not in patients with εL alteration. Multivariate analysis showed that εL alteration was independently associated with LV end-systolic volume (β = 5.0, P = .006) and RWT (β = 0.03, P = .03) at baseline and with changes in both LV end-diastolic volume (β = 19.1, P = .001) and LV end-systolic volume (β = 2.6, P = .047) over 3 years. CONCLUSIONS: In patients with type 2 diabetes, εL alteration was associated with higher RWT and LV volumes and with the absence of decreases in LV volumes over time, which might be an early sign of adverse LV remodeling.
Authors: Danielle L Shepherd; Cody E Nichols; Tara L Croston; Sarah L McLaughlin; Ashley B Petrone; Sara E Lewis; Dharendra Thapa; Dustin M Long; Gregory M Dick; John M Hollander Journal: J Mol Cell Cardiol Date: 2015-12-03 Impact factor: 5.000