title: Adjustable, physiological ventricular restraint improves left ventricular mechanics and reduces dilatation in an ovine model of chronic heart failure.
abstract: BACKGROUND
  Ventricular restraint is a nontransplantation surgical treatment for heart failure. The effect of varying restraint level on left ventricular (LV) mechanics and remodeling is not known. We hypothesized that restraint level may affect therapy efficacy.
  
  
  RESULTS
  We studied the immediate effect of varying restraint levels in an ovine heart failure model. We then studied the long-term effect of restraint applied over a 2-month period. Restraint level was quantified by use of fluid-filled epicardial balloons placed around the ventricles and measurement of balloon luminal pressure at end diastole. At 4 different restraint levels (0, 3, 5, and 8 mm Hg), transmural myocardial pressure (P(tm)) and indices of myocardial oxygen consumption (MVO2) were determined in control (n=5) and ovine heart failure (n=5). Ventricular restraint therapy decreased P(tm) and MVO2, and improved mechanical efficiency. An optimal physiological restraint level of 3 mm Hg was identified to maximize improvement without an adverse affect on systemic hemodynamics. At this optimal level, end-diastolic P(tm) and MVO2 indices decreased by 27% and 20%, respectively. The serial longitudinal effects of optimized ventricular restraint were then evaluated in ovine heart failure with (n=3) and without (n=3) restraint over 2 months. Optimized ventricular restraint prevented and reversed pathological LV dilatation (130+/-22 mL to 91+/-18 mL) and improved LV ejection fraction (27+/-3% to 43+/-5%). Measured restraint level decreased over time as the LV became smaller, and reverse remodeling slowed.
  
  
  CONCLUSIONS
  Ventricular restraint level affects the degree of decrease in P(tm), the degree of decrease in MVO2, and the rate of LV reverse remodeling. Periodic physiological adjustments of restraint level may be required for optimal restraint therapy efficacy.
authors.affiliation: Division of Cardiac Surgery, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115, USA.
authors.forename: Ravi K
authors.initials: RK
authors.lastname: Ghanta
authors.forename: Aravind
authors.initials: A
authors.lastname: Rangaraj
authors.forename: Ramanan
authors.initials: R
authors.lastname: Umakanthan
authors.forename: Lawrence
authors.initials: L
authors.lastname: Lee
authors.forename: Rita G
authors.initials: RG
authors.lastname: Laurence
authors.forename: John A
authors.initials: JA
authors.lastname: Fox
authors.forename: R Morton
authors.initials: RM
authors.lastname: Bolman
authors.forename: Lawrence H
authors.initials: LH
authors.lastname: Cohn
authors.forename: Frederick Y
authors.initials: FY
authors.lastname: Chen
mesh_terms: D000818:Animals; D001794:Blood Pressure; D006348:Cardiac Surgical Procedures / Q000009:adverse effects / Q000295:instrumentation* / Q000379:methods; D003331:Coronary Vessels / Q000503:physiopathology / Q000601:surgery; D004195:Disease Models, Animal; D018450:Disease Progression; D004452:Echocardiography; D006333:Heart Failure / Q000503:physiopathology / Q000601:surgery* / Q000628:therapy*; D006334:Heart Function Tests; D006352:Heart Ventricles / Q000503:physiopathology* / Q000601:surgery*; D008026:Ligation; D008137:Longitudinal Studies; D008297:Male; D012756:Sheep; D013995:Time; D016896:Treatment Outcome; D016277:Ventricular Function, Left