title: Impact of Afterload Increase on Left Ventricular Myocardial Deformation Indices.
abstract: Left ventricular (LV) afterload could be associated with reduced myocardial contractility. The aim of this study was to evaluate the relative impact of increased afterload on LV myocardial deformation indices in chronic aortic constriction, with regard to hypertrophy, myocardial fibrosis, and mitochondrial function, and to differentiate acute versus chronic afterload effect.
  
  
  
  Young pigs underwent aortic banding (n = 11) or sham (n = 7) operations. Nineteen weeks later, LV morphology and systolic function, including myocardial deformation, were assessed by echocardiography before and after banding release or acute aortic constriction (in the sham group). After the animals were euthanized, mitochondrial function and LV interstitial fibrosis were assessed.
  
  
  
  The chronic banding group (n = 8) presented with significant LV hypertrophy compared with the sham group (n = 7), and longitudinal strain (LS) was significantly altered (16.9 ± 0.7% vs 20.3 ± 0.7%, P = .001) while circumferential, radial strain, and ejection fraction were not. LS abnormalities were situated mostly on the basal and mid segments and on the septal wall. There was also significantly more myocardial fibrosis in the chronic banding group compared with the sham group, while mitochondrial function was preserved. The relative contributions of hypertrophic and fibrotic remodeling and of afterload to alter global LS were 62%, and 38%, respectively. Acute aortic banding also significantly altered LS. The ratio of LS to septal wall thickness enabled differentiation between chronic and acute afterload increase (1.9 ± 0.2 in the chronic group vs 2.9 ± 0.3 in the acute group, P = .001).
  
  
  
  LS is susceptible to both hypertrophic and fibrotic remodeling and afterload increase, particularly on the basal and mid LV segments of the septum. The ratio of LS to septal wall thickness enables differentiation of acute from chronic afterload LS alteration.
authors.affiliation: INSERM U1045, Pessac, France; Université de Bordeaux, Bordeaux, France; Cardiologic Hospital Haut-Leveque (Pessac), CHU de Bordeaux, Pessac, France; IHU Liryc, Pessac, France. Electronic address: patricia.reant@chu-bordeaux.fr.
authors.forename: Patricia
authors.initials: P
authors.lastname: Reant
authors.affiliation: Université de Bordeaux, Bordeaux, France; Cardiologic Hospital Haut-Leveque (Pessac), CHU de Bordeaux, Pessac, France; INSERM U1034, Adaptation Cardiovasculaire à l'Ischémie, Pessac, France.
authors.forename: Alexandre
authors.initials: A
authors.lastname: Metras
authors.affiliation: INSERM U1045, Pessac, France; IHU Liryc, Pessac, France.
authors.forename: Dominique
authors.initials: D
authors.lastname: Detaille
authors.affiliation: INSERM U1034, Adaptation Cardiovasculaire à l'Ischémie, Pessac, France.
authors.forename: Annabel
authors.initials: A
authors.lastname: Reynaud
authors.affiliation: INSERM U1045, Pessac, France; IHU Liryc, Pessac, France.
authors.forename: Philippe
authors.initials: P
authors.lastname: Diolez
authors.affiliation: Université de Bordeaux, Bordeaux, France; INSERM U1034, Adaptation Cardiovasculaire à l'Ischémie, Pessac, France.
authors.forename: Beatrice
authors.initials: B
authors.lastname: Jaspard-Vinassa
authors.affiliation: Université de Bordeaux, Bordeaux, France; Cardiologic Hospital Haut-Leveque (Pessac), CHU de Bordeaux, Pessac, France.
authors.forename: Raymond
authors.initials: R
authors.lastname: Roudaut
authors.affiliation: Université de Bordeaux, Bordeaux, France; INSERM U1034, Adaptation Cardiovasculaire à l'Ischémie, Pessac, France; Department of Anesthesia and Critical Care II, CHU de Bordeaux, Bordeaux, France.
authors.forename: Alexandre
authors.initials: A
authors.lastname: Ouattara
authors.affiliation: Université de Bordeaux, Bordeaux, France; Cardiologic Hospital Haut-Leveque (Pessac), CHU de Bordeaux, Pessac, France; INSERM U1034, Adaptation Cardiovasculaire à l'Ischémie, Pessac, France.
authors.forename: Laurent
authors.initials: L
authors.lastname: Barandon
authors.affiliation: INSERM U1045, Pessac, France; Université de Bordeaux, Bordeaux, France; Cardiologic Hospital Haut-Leveque (Pessac), CHU de Bordeaux, Pessac, France; IHU Liryc, Pessac, France.
authors.forename: Pierre
authors.initials: P
authors.lastname: Dos Santos
authors.affiliation: Université de Bordeaux, Bordeaux, France; Cardiologic Hospital Haut-Leveque (Pessac), CHU de Bordeaux, Pessac, France; IHU Liryc, Pessac, France; INSERM U1034, Adaptation Cardiovasculaire à l'Ischémie, Pessac, France.
authors.forename: Stephane
authors.initials: S
authors.lastname: Lafitte
mesh_terms: D000818:Animals; D001024:Aortic Valve Stenosis / Q000150:complications / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D001794:Blood Pressure; D004452:Echocardiography / Q000379:methods; D055119:Elastic Modulus; D054459:Elasticity Imaging Techniques / Q000379:methods; D008297:Male; D009200:Myocardial Contraction; D015203:Reproducibility of Results; D012680:Sensitivity and Specificity; D013314:Stress, Mechanical; D013318:Stroke Volume; D013552:Swine; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology*
keywords: Animal model; Aortic stenosis; Echocardiography; Left ventricular afterload; Left ventricular hypertrophy; Myocardial strain