title: Temporal evolution of left ventricular strain late after repair of coarctation of the aorta using 3D MR tissue tagging.
abstract: OBJECTIVE
  Following repair of coarctation of the aorta (CoA), LV mass is increased along with morbidity and mortality. Previous studies have reported increased shortening indices and impaired diastolic function. However, direct measurements of local material motion and temporal evolution of strain have been lacking.
  
  
  METHODS
  Magnetic resonance (MR) tissue tagging was used to quantify regional three-dimensional myocardial deformation throughout systole and much of diastole in 14 patients (aged 19-23) who had CoA repair 17-23 years previously, and 15 age-, sex- and BSA-matched normal volunteers (NV).
  
  
  RESULTS
  Mass to end-diastolic volume ratio was increased in the CoA group (1.23 +/- 0.12 g/mL CoA vs. 1.14 +/- 0.10 g/mL NV, p = 0.039), together with ejection fraction (65.3 +/- 4.4 vs. 60.8 +/-1.9%, p = 0.001) and systolic blood pressure (132.5 +/- 14.5 vs. 117.3 +/- 11.6 mmHg, p = 0.004). At end-systole, circumferential shortening was normal, but longitudinal shortening was decreased (14.9 +/- 1.3 vs. 16.8 +/- 1.4%, p < 0.001). Although systolic strain rates were not significantly different, early diastolic strain rate (EDSR) in the CoA group was increased in the circumferential direction (-71 +/- 23 vs. -52 +/- 20%/sec, p = 0.029), but decreased in the longitudinal direction (-27 +/- 12 vs. -39 +/- 11%/sec, p = 0.015). Longitudinal shortening and circumferential EDSR were related to right arm-leg pressure gradient (R2 = 0.20, p = 0.016 and R2 = 0.38, p < 0.001, respectively) and to mass index (R2 = 0.18, p = 0.024 and R2 = 014, p = 0.049, respectively).
  
  
  CONCLUSIONS
  MR tagging allows quantitative information on the temporal evolution of myocardial deformation. Directionally dependent changes in strain evolution are seen late after CoA repair. These changes are related to both persistent arm-leg pressure gradient and degree of hypertrophy and may be indicators of developing dysfunction.
authors.affiliation: Department of Anatomy with Radiology, University of Auckland, New Zealand. a.young@auckland.ac.nz
authors.forename: Alistair A
authors.initials: AA
authors.lastname: Young
authors.forename: Brett R
authors.initials: BR
authors.lastname: Cowan
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Occleshaw
authors.forename: Helen C
authors.initials: HC
authors.lastname: Oxenham
authors.forename: Thomas L
authors.initials: TL
authors.lastname: Gentles
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001017:Aortic Coarctation / Q000503:physiopathology* / Q000601:surgery; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D021621:Imaging, Three-Dimensional / Q000379:methods*; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*