title: A new model of ventricular plication: a suturing technique to decrease left ventricular dimensions, improve contractility, and attenuate ventricular remodeling after myocardial infarction in the rat heart.
abstract: BACKGROUND
  The Batista procedure (cardio-reduction) is a surgical technique in patients with dilated cardiomyopathy that results in improvement of ventricular function. The purpose of this study was to test a new suturing technique without resection for cardio-reduction of myocardial infarct scars in rats.
  
  
  RESULTS
  Myocardial infarction (MI) was induced by occluding the left coronary artery 4 weeks before enrollment. Animals then were randomized to a control (n = 11) or treatment group (n = 11). A pursestring suture was placed within the border zones of the infarcted area and was either tightened (treated) or not (controls). Echocardiography was used to measure left ventricular diameters before, 1 hour, and 6 to 7 weeks after plication. Acutely after plication, end-diastolic length (EDL) decreased from 0.70 +/- 0.03 cm to 0.53 +/- 0.02 cm, P < .001; end-systolic length (ESL) decreased from 0.51 +/- 0.03 cm to 0.23 +/- 0.02 cm, P < .001; and fractional shortening (FS) increased from 27.6 +/- 1.5% to 57.6 +/- 2.3%, P < .001, whereas controls were unchanged. In control rats EDL increased from baseline at 0.73 +/- 0.02 cm to 0.82 +/- 0.04 cm at 6 weeks postsurgery, P < .05; ESL increased from 0.54 +/- 0.02 cm to 0.66 +/- 0.04 cm, P < .005; and FS decreased from 26.9 +/- 1.1% to 19.2 +/- 1.2% at 6 weeks, P < .05. In contrast, at 6 weeks in plicated animals, EDL was significantly less than controls at 0.64 +/- 0.02 cm, P < .005; ESL was significantly less than controls at 0.39 +/- 0.03 cm, P < .005, and FS was significantly better than controls at 40.5 +/- 2.2%, P < .005.
  
  
  CONCLUSIONS
  The progressive LV enlargement between 4 and 10 weeks after MI reflects late ventricular remodeling. Plication by suturing infarcted tissue acutely decreases diameters and improves function. At 6 weeks, function remains improved over untreated animals.
authors.affiliation: Heart Institute Research, Good Samaritan Hospital, Division of Cardiology, University of Southern California, Los Angeles, CA 90017-2395, USA.
authors.forename: E R
authors.initials: ER
authors.lastname: Schwarz
authors.forename: M T
authors.initials: MT
authors.lastname: Speakman
authors.forename: R A
authors.initials: RA
authors.lastname: Kloner
mesh_terms: D000818:Animals; D005260:Female; D006352:Heart Ventricles / Q000601:surgery*; D017379:Hypertrophy, Left Ventricular / Q000601:surgery*; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000503:physiopathology / Q000601:surgery*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013536:Suture Techniques