title: Effect of transmyocardial laser revascularization on myocardial perfusion and left ventricular remodeling after myocardial infarction in rats.
abstract: OBJECTIVE
  To monitor perfusion changes in remote myocardium caused by transmyocardial laser revascularization (TMLR) and to investigate the influence of TMLR on left ventricular morphology and function.
  
  
  METHODS
  The coronary arteries were ligated in 32 Wistar rats. Eight weeks later, cine magnetic resonance (MR) imaging was performed in both the treatment (n = 12) and control group (n = 8). TMLR was then performed in the remote myocardium in the treated group. Twelve weeks after myocardial infarction, cine MR imaging, including dobutamine-induced (10 micro g per kilogram of body weight per minute via the tail vein) stress, was repeated and followed with hemodynamic measurements in both groups and with perfusion MR imaging (in-plane resolution, 140 x 140 micro m) of the isolated heart at rest and during nitroglycerin-induced stress in the TMLR group (n = 10).
  
  
  RESULTS
  Left ventricular dilatation and hypertrophy were enhanced in the TMLR group (change in end-diastolic volume at 8-12 weeks: control group, 24.6 micro L +/- 16.7 and TMLR group, 81.7 micro L +/- 15.7; change in left ventricular mass: control group, 54.5 mg +/- 19.2 and TMLR group, 124.1 mg +/- 30.7; P <.03 for both). Ejection fractions at rest were approximately equal (control group, 40% +/- 2; TMLR group, 38% +/- 2; P value not significant), but during dobutamine-induced stress, the ejection fraction was higher in the TMLR group (54.4% +/- 4.9; control group, 47.4% +/- 4.8; P <.05). TMLR-treated areas were better perfused than was untreated myocardium (difference in perfusion: TMLR-treated vs control region, 3.89 mL/min/g +/- 0.83 at rest vs 2.29 mL/min/g +/- 1.06 during nitroglycerin-induced stress; P <.05 for both). Hemodynamic measurements revealed no differences between groups.
  
  
  CONCLUSIONS
  High-spatial-resolution perfusion MR imaging depicted a significant perfusion improvement after TMLR. Post-myocardial infarction remodeling of the left ventricle was found to be enhanced.
authors.affiliation: Physikalisches Institut (EP5), Universität Würzburg, Josef Schneider-Strasse 2, 97080 Würzburg, Germany.
authors.forename: Matthias
authors.initials: M
authors.lastname: Nahrendorf
authors.forename: Karl-Heinz
authors.initials: KH
authors.lastname: Hiller
authors.forename: Dirk
authors.initials: D
authors.lastname: Theisen
authors.forename: Kai
authors.initials: K
authors.lastname: Hu
authors.forename: Christiane
authors.initials: C
authors.lastname: Waller
authors.forename: Ralf
authors.initials: R
authors.lastname: Kaiser
authors.forename: Axel
authors.initials: A
authors.lastname: Haase
authors.forename: Georg
authors.initials: G
authors.lastname: Ertl
authors.forename: Ralf
authors.initials: R
authors.lastname: Brinkmann
authors.forename: Wolfgang R
authors.initials: WR
authors.lastname: Bauer
mesh_terms: D000818:Animals; D003326:Coronary Circulation / Q000502:physiology*; D005260:Female; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology / Q000601:surgery; D053685:Laser Therapy / Q000295:instrumentation*; D018810:Magnetic Resonance Angiography; D019028:Magnetic Resonance Imaging, Cine; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000601:surgery*; D009204:Myocardial Revascularization / Q000295:instrumentation*; D009206:Myocardium / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013318:Stroke Volume / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology*