title: A percutaneous swine model of myocardial infarction.
abstract: BACKGROUND
  The aim of this study was to develop a percutaneous, low risk, and reproducible technique of MI that simulates human disease.
  
  
  METHODS
  MI was induced in 44 swine (32.8+/-7.2 kg) by percutaneous embolization coil deployment in the left anterior descending coronary artery. Hemodynamic measurements, left heart catheterization, and echocardiography were performed pre, post, and 30 days after MI. 3D NOGA viability mapping was performed at baseline and 30 days. Excised hearts were examined histologically.
  
  
  RESULTS
  Pre-MI mortality was 6.8% and 24 h mortality was 13.6%. All pigs that survived 24 h after MI remained alive at 30 days. The mean left ventricular ejection fraction decreased from 58.4% to 42.1% (p<0.001) at 30 days. The average thrombolysis in myocardial infarction score was 3, 0, and 1.5 at baseline, post-MI, and 30 days, respectively. At 30 days, the end diastolic diameter, end diastolic volume, end systolic volume, and wall motion index increased from 3.76 to 3.89 cm, 32.5 to 50.0 ml, 14.9 to 27.0 ml, and 1.01 to 1.38, respectively (all p<0.05), while the ejection fraction decreased from 56.5% to 49.4% (p<0.01). Additionally, at 30 days, statistically significant reductions in both unipolar and bipolar voltage in the mid and apical regions of the left ventricle were observed. Postmortem pathology showed a transmural scar in the apical anteroseptal regions with fibrosis in the MI region, which accounted for 14.8% and 14.2% of the total left and right ventricular myocardial area and volume, respectively.
  
  
  CONCLUSIONS
  This model of MI is reliable, reproducible, has a pathophysiology similar to humans, and a lower mortality and ventricular fibrillation rates compared to other models. This model may be used to evaluate the effects of pharmacologics, gene therapy, and stem cell transplantation for the treatment of cardiovascular disease as well as studying mechanisms of cardiac remodeling.
authors.affiliation: Arizona Heart Institute, 2632 N 20th St, Phoenix, AZ, 85006, USA; Arizona State University, Tempe, AZ, USA.
authors.forename: Nabil
authors.initials: N
authors.lastname: Dib
authors.forename: Edward B
authors.initials: EB
authors.lastname: Diethrich
authors.forename: Ann
authors.initials: A
authors.lastname: Campbell
authors.forename: Amir
authors.initials: A
authors.lastname: Gahremanpour
authors.forename: Michael
authors.initials: M
authors.lastname: McGarry
authors.forename: Shaun R
authors.initials: SR
authors.lastname: Opie
mesh_terms: D000792:Angiography; D000818:Animals; D004195:Disease Models, Animal; D004452:Echocardiography; D005069:Evaluation Studies as Topic; D005260:Female; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000473:pathology; D006439:Hemodynamics / Q000502:physiology; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000209:etiology / Q000473:pathology*; D015203:Reproducibility of Results; D013318:Stroke Volume / Q000502:physiology; D034421:Sus scrofa; D013997:Time Factors