title: Ventricular geometry, strain, and rotational mechanics in pulmonary hypertension.
abstract: BACKGROUND
  We tested the hypothesis that right ventricular (RV) pressure overload affects RV function and further influences left ventricular (LV) geometry, which adversely affects LV twist mechanics and segmental function.
  
  
  RESULTS
  Echocardiographic images were prospectively acquired in 44 patients (age, 46+/-12 years; 82% women) with evidence of pulmonary hypertension (estimated pulmonary artery systolic pressure, 71+/-23 mm Hg) and in 44 age- and gender-matched healthy subjects. Patients with intrinsic LV diseases were excluded. RV lateral wall longitudinal strain (LS) and interventricular septal (IVS) LS were reduced in the pulmonary hypertension group compared with control subjects (-15.9+/-7.6% versus -25.5+/-6.1%, P<0.001; and -17.3+/-4.4% versus -20.2+/-3.9%, P=0.002, respectively), whereas LV lateral wall LS was preserved. RV lateral wall LS and IVS LS, but not LV lateral wall LS, correlated with pulmonary artery systolic pressure (r=0.56, P<0.01; r=0.32, P<0.01) and LV eccentricity index (r=0.57, P<0.01; r=0.57, P<0.01). IVS and LV lateral wall circumferential strain (CS) were both reduced in the pulmonary hypertension group. Although IVS CS and LV lateral wall CS correlated with pulmonary artery systolic pressure and LV eccentricity index, after adjustment of CS for LV eccentricity index, differences between groups persisted for IVS CS (P<0.01) but not LV lateral wall CS (P=0.09). LV torsion was decreased in patients with pulmonary hypertension compared with control subjects (9.6+/-4.9 degrees versus 14.7+/-4.9 degrees , P<0.001). LV torsion inversely correlated with pulmonary artery systolic pressure (r=-0.39, P<0.01) and LV eccentricity index (r=-0.3, P<0.01). LV untwisting rates were similar in both groups (P=0.7).
  
  
  CONCLUSIONS
  Chronic RV pressure overload directly affects RV longitudinal systolic deformation. RV pressure overload further influences IVS and LV geometry, which impairs LV torsion and segmental LS and CS, more for the IVS than for the free wall of the LV.
authors.affiliation: Department of Cardiovascular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.
authors.forename: Sarinya
authors.initials: S
authors.lastname: Puwanant
authors.forename: Margaret
authors.initials: M
authors.lastname: Park
authors.forename: Zoran B
authors.initials: ZB
authors.lastname: Popović
authors.forename: W H Wilson
authors.initials: WH
authors.lastname: Tang
authors.forename: Samar
authors.initials: S
authors.lastname: Farha
authors.forename: Deepa
authors.initials: D
authors.lastname: George
authors.forename: Jacqueline
authors.initials: J
authors.lastname: Sharp
authors.forename: Jirapa
authors.initials: J
authors.lastname: Puntawangkoon
authors.forename: James E
authors.initials: JE
authors.lastname: Loyd
authors.forename: Serpil C
authors.initials: SC
authors.lastname: Erzurum
authors.forename: James D
authors.initials: JD
authors.lastname: Thomas
mesh_terms: D000328:Adult; D001696:Biomechanical Phenomena; D016022:Case-Control Studies; D004562:Electrocardiography; D005260:Female; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011651:Pulmonary Artery / Q000503:physiopathology; D018487:Ventricular Dysfunction, Left / Q000473:pathology / Q000503:physiopathology; D018497:Ventricular Dysfunction, Right / Q000473:pathology / Q000503:physiopathology