title: Interventricular mechanical asynchrony in pulmonary arterial hypertension: left-to-right delay in peak shortening is related to right ventricular overload and left ventricular underfilling.
abstract: OBJECTIVE
  The purpose of this study was to explore in pulmonary arterial hypertension (PAH) whether the cause of interventricular asynchrony lies in onset of shortening or duration of shortening.
  
  
  BACKGROUND
  In PAH, leftward ventricular septal bowing (LVSB) is probably caused by a left-to-right (L-R) delay in myocardial shortening.
  
  
  METHODS
  In 21 PAH patients (mean pulmonary arterial pressure 55 +/- 13 mm Hg and electrocardiogram-QRS width 100 +/- 16 ms), magnetic resonance imaging myocardial tagging (14 ms temporal resolution) was applied. For the left ventricular (LV) free wall, septum, and right ventricular (RV) free wall, the onset time (T(onset)) and peak time (T(peak)) of circumferential shortening were calculated. The RV wall tension was estimated by the Laplace law.
  
  
  RESULTS
  The T(onset) was 51 +/- 23 ms, 65 +/- 4 ms, and 52 +/- 22 ms for LV, septum, and RV, respectively. The T(peak) was 293 +/- 58 ms, 267 +/- 22 ms, and 387 +/- 50 ms for LV, septum, and RV, respectively. Maximum LVSB was at 395 +/- 45 ms, coinciding with septal overstretch and RV T(peak). The L-R delay in T(onset) was -1 +/- 16 ms (p = 0.84), and the L-R delay in T(peak) was 94 +/- 41 ms (p < 0.001). The L-R delay in T(peak) was not related to the QRS width but was associated with RV wall tension (p < 0.05). The L-R delay in T(peak) correlated with leftward septal curvature (p < 0.05) and correlated negatively with LV end-diastolic volume (p < 0.05) and stroke volume (p < 0.05).
  
  
  CONCLUSIONS
  In PAH, the L-R delay in myocardial peak shortening is caused by lengthening of the duration of RV shortening. This L-R delay is related to LVSB, decreased LV filling, and decreased stroke volume.
authors.affiliation: Department of Physics and Medical Technology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, the Netherlands. jt.marcus@vumc.nl
authors.forename: J Tim
authors.initials: JT
authors.lastname: Marcus
authors.forename: C Tji-Joong
authors.initials: CT
authors.lastname: Gan
authors.forename: Jaco J M
authors.initials: JJ
authors.lastname: Zwanenburg
authors.forename: Anco
authors.initials: A
authors.lastname: Boonstra
authors.forename: Cor P
authors.initials: CP
authors.lastname: Allaart
authors.forename: Marco J W
authors.initials: MJ
authors.lastname: Götte
authors.forename: Anton
authors.initials: A
authors.lastname: Vonk-Noordegraaf
mesh_terms: D000328:Adult; D003971:Diastole / Q000502:physiology; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D012044:Regression Analysis; D013599:Systole / Q000502:physiology; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*; D018497:Ventricular Dysfunction, Right / Q000503:physiopathology*; D017725:Ventricular Pressure / Q000502:physiology