title: Right latissimus dorsi cardiomyoplasty improves left ventricular energetics.
abstract: BACKGROUND
  The mechanism by which cardiomyoplasty appears to enhance left ventricular (LV) function is not well understood. We applied the time-varying elastance model to study the effect of cardiomyoplasty on LV function, ventriculovascular coupling, and LV energetics in an acute canine model.
  
  
  METHODS
  Right latissimus dorsi cardiomyoplasty was performed in 5 dogs. The end-systolic pressure-volume relation was generated by using brief caval occlusions. End-systolic elastance, effective arterial elastance, stroke work, internal work, total mechanical work, and stroke work efficiency (stroke work/total mechanical work) were calculated from these pressure-volume data. Myocardial oxygen consumption and overall mechanical efficiency (stroke work/myocardial oxygen consumption) were predicted using the myocardial oxygen consumption-total mechanical work relation.
  
  
  RESULTS
  Skeletal muscle contraction significantly increased end-systolic elastance, an index of contractility. Although stroke work did not change significantly, the increase in end-systolic elastance led to a 29% decrease in total mechanical work, a 50% decrease in internal work, and an increase in stroke work efficiency from 53% to 66%. This was consistent with the observed 29% decrease in effective arterial elastance/end-systolic elastance, an indicator of ventriculovascular coupling that is related inversely to stroke work efficiency. Predicted myocardial oxygen consumption decreased by at least 22%, and predicted overall mechanical efficiency increased at a minimum from 16.1% to 18.4%.
  
  
  CONCLUSIONS
  These results support the theory that cardiomyoplasty unloads the LV by decreasing LV volumes and increasing contractility. These effects appear to improve LV energetics by decreasing total mechanical work without significantly affecting stroke work, resulting in improved stroke work efficiency. The decrease in total mechanical work strongly suggests a decrease in myocardial oxygen consumption and an increase in overall mechanical efficiency.
authors.affiliation: Division of Cardiac Surgery, Brigham and Women's Hospital, Boston Massachusetts 02115, USA.
authors.forename: L
authors.initials: L
authors.lastname: Aklog
authors.forename: F Y
authors.initials: FY
authors.lastname: Chen
authors.forename: B J
authors.initials: BJ
authors.lastname: deGuzman
authors.forename: M P
authors.initials: MP
authors.lastname: Murphy
authors.forename: W J
authors.initials: WJ
authors.lastname: Smith
authors.forename: R G
authors.initials: RG
authors.lastname: Laurence
authors.forename: R F
authors.initials: RF
authors.lastname: Appleyard
authors.forename: L H
authors.initials: LH
authors.lastname: Cohn
mesh_terms: D000818:Animals; D001011:Aorta / Q000502:physiology; D001696:Biomechanical Phenomena; D001794:Blood Pressure / Q000502:physiology; D002306:Cardiac Volume / Q000502:physiology; D018421:Cardiomyoplasty / Q000379:methods*; D004195:Disease Models, Animal; D004285:Dogs; D004548:Elasticity; D005544:Forecasting; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics; D008297:Male; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000637:transplantation; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D013599:Systole; D018924:Vascular Capacitance / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*; D017725:Ventricular Pressure / Q000502:physiology