title: Hemodynamic effects of direct biventricular compression studied in isovolumic and ejecting isolated canine hearts.
abstract: BACKGROUND
  Biventricular direct cardiac compression (DCC) can potentially support the failing heart without the complications associated with a blood/device interface. The effect of uniform DCC on left and right ventricular performance was evaluated in 7 isolated canine heart preparations.
  
  
  RESULTS
  A computer-controlled afterload system either constrained the isolated heart to contract isovolumically or simulated hemodynamic properties of physiological ejection. Biventricular DCC was provided by a chamber surrounding the heart that allowed adjustment of the compression pressure, onset time, and duration. Through a series of ventricular preloads, the effect of DCC on the end-systolic pressure-volume relationship (ESPVR) was evaluated under isovolumic and ejecting conditions. Under both conditions, DCC shifted the ESPVR of the left and right ventricles upward by an amount approximately equal to the compression pressure. The augmentation of end-systolic pressure for each initial preload tested, however, was less under ejecting conditions, because reductions in end-systolic and end-diastolic volumes occurred with ejection. Nevertheless, the net effect was to increase stroke volume. Measurement of M&f1;O2 demonstrated that at a given ventricular volume, M&f1;O2 did not change with DCC; however, peak ventricular pressure increased substantially, so that the effective pressure-volume area increased.
  
  
  CONCLUSIONS
  Biventricular DCC can augment end-systolic pressure with no added costs of M&f1;O2. Under ejecting conditions, this augmentation of ventricular contracting ability manifests as increases in stroke volume. Thus, DCC represents a feasible alternative form of ventricular assist, and devices that support the heart in this manner should be further explored.
authors.affiliation: Department of Surgery, Division of Cardiothoracic Surgery, College of Physicians and Surgeons, Columbia University, New York, NY, USA. ja276@columbia.edu
authors.forename: J H
authors.initials: JH
authors.lastname: Artrip
authors.forename: J
authors.initials: J
authors.lastname: Wang
authors.forename: A R
authors.initials: AR
authors.lastname: Leventhal
authors.forename: J E
authors.initials: JE
authors.lastname: Tsitlik
authors.forename: H R
authors.initials: HR
authors.lastname: Levin
authors.forename: D
authors.initials: D
authors.lastname: Burkhoff
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004285:Dogs; D006321:Heart / Q000502:physiology*; D006439:Hemodynamics / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D012770:Shock, Cardiogenic / Q000503:physiopathology; D013318:Stroke Volume / Q000502:physiology*; D013599:Systole; D016276:Ventricular Function; D016278:Ventricular Function, Right / Q000502:physiology