title: Effects of therapeutic angiogenesis with plasmid VEGF165 on ventricular function in a canine model of chronic myocardial infarction.
abstract: OBJECTIVE
  Therapeutic angiogenesis is currently under investigation in ischemic heart disease. We examined the effect on left ventricular function induced by therapeutic angiogenesis by intramyocardial injection of plasmid VEGF(165), in a canine model of chronic myocardial infarction.
  
  
  METHODS
  Left thoracotomy was performed in 10 mongrel dogs, and myocardial infarction induced by ligation of the major diagonal coronary artery. At 7 postoperative (p.o.) day (pre-treatment), left ventricular ejection fraction was assessed by echocardiogram, and a second procedure was done: saline or plasmid VEGF(165) at 200 mg/mL was injected over 10 points of the ischemic areas of control or treated groups, respectively. Fourteen days later (post-treatment, day 21) a control echocardiogram was performed, the animals were sacrificed and histological examination was performed.
  
  
  RESULTS
  Ejection fraction was maintained in the treated group: 52.45 +/- 15.1% on day 7 and 48.53 +/-11.74% on day 21 (P=0.59), and tended to decrease in the control group, from 59.3 +/- 4% to 39.37 +/- 19.43% (P=0.04), although absolute values did not differ significantly between groups. Histological examination revealed a non significant increase in capillary vessels number in all areas in treated group. Paradoxically, arterioles were significantly less in number in all areas of treated dogs.
  
  
  CONCLUSIONS
  Intramyocardial injection of plasmid VEGF(165), in this canine model of chronic myocardial infarction, resulted in preservation of left ventricular ejection fraction, contrary to the control group where left ventricular ejection fraction showed continuous decline during the experiment. Histological examination, however, was unable to explain completely these results.
authors.affiliation: Instituto de Cardiologia do Rio Grande do Sul / Fundação Universitária de Cardiologia, Porto Alegre, RS, Brasil.
authors.forename: Ana Paula
authors.initials: AP
authors.lastname: Furlani
authors.forename: Renato A K
authors.initials: RA
authors.lastname: Kalil
authors.forename: Iran
authors.initials: I
authors.lastname: Castro
authors.forename: Andrés
authors.initials: A
authors.lastname: Cañedo-Delgado
authors.forename: Marinez
authors.initials: M
authors.lastname: Barra
authors.forename: Paulo Roberto
authors.initials: PR
authors.lastname: Prates
authors.forename: Roberto T
authors.initials: RT
authors.lastname: Sant'Anna
authors.forename: Ivo A
authors.initials: IA
authors.lastname: Nesralla
mesh_terms: D000818:Animals; D002196:Capillaries; D002908:Chronic Disease; D003331:Coronary Vessels; D004195:Disease Models, Animal; D004285:Dogs; D015316:Genetic Therapy / Q000379:methods*; D008297:Male; D009203:Myocardial Infarction / Q000503:physiopathology / Q000628:therapy*; D017202:Myocardial Ischemia / Q000628:therapy; D018919:Neovascularization, Physiologic / Q000235:genetics*; D010957:Plasmids / Q000627:therapeutic use; D011897:Random Allocation; D013318:Stroke Volume / Q000502:physiology; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000627:therapeutic use*; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A