title: The right ventricular response to high afterload: comparison between healthy persons and patients with transposition of the great arteries: a 2D strain study.
abstract: OBJECTIVE
  To evaluate the contraction pattern of the systemic right ventricle (RV) in comparison to healthy controls.
  
  
  METHODS
  31 patients (14 female, mean age 21.5 ± 3.3 years) with congenital corrected (ccTGA) and surgical corrected (D-TGA) TGA and 31 age-matched healthy controls (17 female, mean age 23.1 ± 2.6 years) were included in the study. We compared the contraction pattern of the systemic RV with findings in the right and left ventricle (LV) of healthy controls. Echocardiograms were performed for all patients (19.3 ± 2.5 years after the operation) and all healthy controls. Using a novel computer software (GE Ultrasound, Horton, Norway) that allows automatic frame-by-frame tracking of accoustic markers during the heart cycle longitudinal and circumferential strain and strain rate were defined as parameters of myocardial deformation.
  
  
  RESULTS
  In the systemic free RV wall, circumferential strain was greater than longitudinal strain (-25.6 ± 4.2% vs. -15.2 ± 3.9%, P < 0.001), opposite to the contraction pattern of the subpulmonary free RV wall (-17.7 ± 4.1% vs. -28.3 ± 3.3%, P < 0.001). Compared with controls, segmental analysis of the free RV wall resulted in lower systolic longitudinal and higher systolic circumferential strain and strain rate values. In the free LV wall, circumferential strain was lower than longitudinal strain (-19.1 ± 2.7% vs. -26.8 ± 4.5%, P < 0.001) in contrast to the data in the systemic free LV wall (-24.5 ± 3.1% vs. -16.7 ± 3.5%, P < 0.001).
  
  
  CONCLUSIONS
  Myocardial deformation parameters were significantly different in systemic and normal RV indicating a dependency of myocardial deformation parameters on right ventricular afterload. The use of myocardial deformation imaging identified a shift from longitudinal to circumferential contraction pattern in the systemic RV in comparison to the LV. This might demonstrate a response to the systemic load creating a myocardial hypertrophy.
authors.affiliation: Department of Cardiology, University Hospital RWTH Aachen, Aachen, Germany. mibecker@ukaachen.de
authors.forename: Michael
authors.initials: M
authors.lastname: Becker
authors.forename: Carmen
authors.initials: C
authors.lastname: Hümpel
authors.forename: Christina
authors.initials: C
authors.lastname: Ocklenburg
authors.forename: Eberhard
authors.initials: E
authors.lastname: Muehler
authors.forename: Joerg
authors.initials: J
authors.lastname: Schroeder
authors.forename: Christian
authors.initials: C
authors.lastname: Eickholt
authors.forename: Rainer
authors.initials: R
authors.lastname: Hoffmann
authors.forename: Nikolaus
authors.initials: N
authors.lastname: Marx
authors.forename: Andreas
authors.initials: A
authors.lastname: Franke
mesh_terms: D000328:Adult; D001794:Blood Pressure; D055119:Elastic Modulus; D054459:Elasticity Imaging Techniques / Q000379:methods*; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D006801:Humans; D008297:Male; D009200:Myocardial Contraction; D014188:Transposition of Great Vessels / Q000000981:diagnostic imaging* / Q000503:physiopathology*