title: Left ventricular systolic performance in failing heart improved acutely by left ventricular reshaping.
abstract: OBJECTIVE
  If the geometric distortion during dilated heart failure could be corrected, the tension on the myocytes would be decreased, thereby leading to an improvement in left ventricular systolic function. We tested the effects of the CardioClasp (CardioClasp Inc, Pine Brook, NJ), a left ventricular reshaping device, on the failing heart, and our empirical data were compared with computationally derived data.
  
  
  METHODS
  Heart failure was induced by 4-week rapid cardiac pacing. At the terminal experiment, an isolated failing heart preparation (isovolumic contraction, n = 5) or an intact failing heart in vivo (n = 7) was used. The effects of the reshaping device on left ventricular performance were assessed by the slopes (Ees) of the left ventricular end-systolic pressure-volume relations, hemodynamics, and echocardiograph before and after placing the CardioClasp on the heart. The change in Ees as the result of left ventricular reshaping was also estimated from computed theoretical analysis and compared with empirical data.
  
  
  RESULTS
  There was a significant change in left ventricular dimension after placing the CardioClasp on the heart. In isolated heart preparation, Ees significantly increased from 1.40 +/- 0.44 mm Hg/mL to 2.42 +/- 0.63 mm Hg/mL after placing the device on the heart but returned to the baseline level (1.46 +/- 0.27 mm Hg) after removing it. Left ventricular developed pressure and left ventricular fractional area shortening were significantly increased as the result of left ventricular reshaping. Ees derived from computed theoretical analysis was highly correlated with confirming empirical data.
  
  
  CONCLUSIONS
  The CardioClasp can reshape the left ventricle and improve left ventricular systolic performance in failing hearts.
authors.affiliation: Division of Circulatory Physiology, Department of Medicine, Columbia University, New York, NY 10032, USA.
authors.forename: Kun-lun
authors.initials: KL
authors.lastname: He
authors.forename: Juichiro
authors.initials: J
authors.lastname: Shimizu
authors.forename: Geng-hua
authors.initials: GH
authors.lastname: Yi
authors.forename: Anguo
authors.initials: A
authors.lastname: Gu
authors.forename: M Abul
authors.initials: MA
authors.lastname: Kashem
authors.forename: Deborah L
authors.initials: DL
authors.lastname: Crabbe
authors.forename: Sulli
authors.initials: S
authors.lastname: Popilskis
authors.forename: Ed X
authors.initials: EX
authors.lastname: Wu
authors.forename: William P
authors.initials: WP
authors.lastname: Santamore
authors.forename: David
authors.initials: D
authors.lastname: Melvin
authors.forename: Jie
authors.initials: J
authors.lastname: Wang
mesh_terms: D000818:Animals; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects; D004195:Disease Models, Animal; D004285:Dogs; D004452:Echocardiography; D006333:Heart Failure / Q000209:etiology / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D008955:Models, Cardiovascular; D008962:Models, Theoretical; D009200:Myocardial Contraction / Q000502:physiology*; D011237:Predictive Value of Tests; D013223:Statistics as Topic; D013318:Stroke Volume / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology*