title: Obesity reduces left ventricular strains, torsion, and synchrony in mouse models: a cine displacement encoding with stimulated echoes (DENSE) cardiovascular magnetic resonance study.
abstract: BACKGROUND
  Obesity affects a third of adults in the US and results in an increased risk of cardiovascular mortality. While the mechanisms underlying this increased risk are not well understood, animal models of obesity have shown direct effects on the heart such as steatosis and fibrosis, which may affect cardiac function. However, the effect of obesity on cardiac function in animal models is not well-defined. We hypothesized that diet-induced obesity in mice reduces strain, torsion, and synchrony in the left ventricle (LV).
  
  
  METHODS
  Ten 12-week-old C57BL/6 J mice were randomized to a high-fat or low-fat diet. After 5 months on the diet, mice were imaged with a 7 T ClinScan using a cine DENSE protocol. Three short-axis and two long-axis slices were acquired for quantification of strains, torsion and synchrony in the left ventricle.
  
  
  RESULTS
  Left ventricular mass was increased by 15% (p = 0.032) with no change in volumes or ejection fraction. Subepicardial strain was lower in the obese mice with a 40% reduction in circumferential strain (p = 0.008) a 53% reduction in radial strain (p = 0.032) and a trend towards a 19% reduction in longitudinal strain (p = 0.056). By contrast, subendocardial strain was modestly reduced in the obese mice in the circumferential direction by 12% (p = 0.028), and no different in the radial (p = 0.690) or longitudinal (p = 0.602) directions. Peak torsion was reduced by 34% (p = 0.028). Synchrony of contraction was also reduced (p = 0.032) with a time delay in the septal-to-lateral direction.
  
  
  CONCLUSIONS
  Diet-induced obesity reduces left ventricular strains and torsion in mice. Reductions in cardiac strain are mostly limited to the subepicardium, with relative preservation of function in the subendocardium. Diet-induced obesity also leads to reduced synchrony of contraction and hypertrophy in mouse models.
authors.forename: Sage P
authors.initials: SP
authors.lastname: Kramer
authors.forename: David K
authors.initials: DK
authors.lastname: Powell
authors.forename: Christopher M
authors.initials: CM
authors.lastname: Haggerty
authors.forename: Cassi M
authors.initials: CM
authors.lastname: Binkley
authors.forename: Andrea C
authors.initials: AC
authors.lastname: Mattingly
authors.forename: Lisa A
authors.initials: LA
authors.lastname: Cassis
authors.forename: Frederick H
authors.initials: FH
authors.lastname: Epstein
authors.affiliation: Departments of Pediatrics, Physiology and Medicine, University of Kentucky, 800 Rose St, MN-150, Lexington, KY 40536, USA. bkf@gatech.edu.
authors.forename: Brandon K
authors.initials: BK
authors.lastname: Fornwalt
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D059305:Diet, High-Fat; D004195:Disease Models, Animal; D017379:Hypertrophy, Left Ventricular / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D019028:Magnetic Resonance Imaging, Cine; D051379:Mice; D008810:Mice, Inbred C57BL; D009200:Myocardial Contraction; D009765:Obesity / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology; D011237:Predictive Value of Tests; D013314:Stress, Mechanical; D013318:Stroke Volume; D013997:Time Factors; D054159:Torsion, Mechanical; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D016277:Ventricular Function, Left