title: Left ventricular reshaping: effects on the pressure-volume relationship.
abstract: OBJECTIVE
  We tested whether the CardioClasp device (CardioClasp, Inc, Cincinnati, Ohio), a non-blood contact device, would improve left ventricular contractility by acutely reshaping the left ventricle and reducing left ventricular wall stress.
  
  
  METHODS
  In dogs (n = 6) 4 weeks of ventricular pacing (210-240 ppm) induced severe heart failure. Left ventricular function was evaluated before and after placement of the CardioClasp device, which uses 2 indenting bars to reshape the left ventricle. Hemodynamics, echocardiography, and Sonometrics crystals dimension (Sonometrics Corporation, London, Ontario, Canada) were measured at steady state and during inferior vena caval occlusion.
  
  
  RESULTS
  The CardioClasp device decreased the left ventricular end-diastolic anterior-posterior dimension by 22.8% +/- 1.9%, decreased left ventricular wall stress from 97.3 +/- 22.8 to 67.2 +/- 7.7 g/cm(2) (P =.003), and increased the fractional area of contraction from 21.3% +/- 10.5% to 31.3% +/- 18.1% (P =.002). The clasp did not alter left ventricular end-diastolic pressure, left ventricular pressure, left ventricular dP/dt, or cardiac output. With the CardioClasp device, the slope of the end-systolic pressure-volume relationship was increased from 1.87 +/- 0.47 to 3.22 +/- 1.55 mm Hg/mL (P =.02), the slope of preload recruitable stroke work versus end-diastolic volume was increased from 28.4 +/- 11.0 to 44.1 +/- 23.5 mm Hg (P =.02), and the slope of maximum dP/dt versus end-diastolic volume was increased from 10.6 +/- 4.6 to 18.6 +/- 7.4 mm Hg x s(-1) x mL(-1) (P =.01). The CardioClasp device increased the slope of the end-systolic pressure-volume relationship by 68.0% +/- 21.7%, the slope of preload recruitable stroke work versus end-diastolic volume by 50.7% +/- 18.1%, and the slope of maximum dP/dt versus end-diastolic volume by 85.7% +/- 28.9%.
  
  
  CONCLUSIONS
  The CardioClasp device decreased left ventricular wall stress and increased the fractional area of contraction by reshaping the left ventricle. The CardioClasp device was able to maintain cardiac output and arterial pressure. The clasp increased global left ventricular contractility by increasing the slope of the end-systolic pressure-volume relationship, the slope of preload recruitable stroke work versus end-diastolic volume, and the slope of maximum dP/dt versus end-diastolic volume. In patients with heart failure, the CardioClasp device might be effective for clinical application.
authors.affiliation: Cardiovascular Research, Temple University, Philadelphia, PA 19140, USA. mkashem@temple.edu
authors.forename: Abul
authors.initials: A
authors.lastname: Kashem
authors.forename: Sarmina
authors.initials: S
authors.lastname: Hassan
authors.forename: Deborah L
authors.initials: DL
authors.lastname: Crabbe
authors.forename: David B
authors.initials: DB
authors.lastname: Melvin
authors.forename: William P
authors.initials: WP
authors.lastname: Santamore
mesh_terms: D000818:Animals; D002304:Cardiac Pacing, Artificial; D002311:Cardiomyopathy, Dilated / Q000150:complications*; D003250:Constriction; D004195:Disease Models, Animal; D004285:Dogs; D004452:Echocardiography; D006333:Heart Failure / Q000150:complications*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology / Q000601:surgery*; D008422:Materials Testing; D013318:Stroke Volume; D016277:Ventricular Function, Left; D017725:Ventricular Pressure; D020257:Ventricular Remodeling