title: Cardiac remodeling in a new pig model of chronic heart failure: Assessment of left ventricular functional, metabolic, and structural changes using PET, CT, and echocardiography.
abstract: OBJECTIVE
  Large animal models are needed to study disease mechanisms in heart failure (HF). In the present study we characterized the functional, metabolic, and structural changes of myocardium in a novel pig model of chronic myocardial infarction (MI) by using multimodality imaging and histology.
  
  
  RESULTS
  Male farm pigs underwent a two-step occlusion of the left anterior descending coronary artery with concurrent distal ligation and implantation of a proximal ameroid constrictor (HF group), or sham operation (control group). Three months after the operation, cardiac output and wall stress were measured by echocardiography. Left ventricle (LV) volumes and mass were measured by computed tomography (CT). Myocardial perfusion was evaluated by [(15)O]water and oxygen consumption using [(11)C]acetate positron emission tomography, and the efficiency of myocardial work was calculated. Histological examinations were conducted to detect MI, hypertrophy, and fibrosis. Animals in the HF group had a large anterior MI scar. CT showed larger LV diastolic volume and lower ejection fraction in HF pigs than in controls. Perfusion and oxygen consumption in the remote non-infarcted myocardium were preserved in HF pigs as compared to controls. Global LV work and efficiency were significantly lower in HF than control pigs and was associated with increased wall stress. Histology showed myocyte hypertrophy but not increased interstitial fibrosis in the remote segments in HF pigs.
  
  
  CONCLUSIONS
  The chronic post-infarction model of HF is suitable for studies aimed to evaluate LV remodeling and changes in oxidative metabolism and can be useful for testing new therapies for HF.
authors.affiliation: Turku PET Centre, University of Turku and Turku University Hospital, Kiinamyllynkatu 4-8, 20521, Turku, Finland, miikka.tarkia@tyks.fi.
authors.forename: Miikka
authors.initials: M
authors.lastname: Tarkia
authors.forename: Christoffer
authors.initials: C
authors.lastname: Stark
authors.forename: Matti
authors.initials: M
authors.lastname: Haavisto
authors.forename: Rasmus
authors.initials: R
authors.lastname: Kentala
authors.forename: Tommi
authors.initials: T
authors.lastname: Vähäsilta
authors.forename: Timo
authors.initials: T
authors.lastname: Savunen
authors.forename: Marjatta
authors.initials: M
authors.lastname: Strandberg
authors.forename: Ville-Veikko
authors.initials: VV
authors.lastname: Hynninen
authors.forename: Virva
authors.initials: V
authors.lastname: Saunavaara
authors.forename: Tuula
authors.initials: T
authors.lastname: Tolvanen
authors.forename: Mika
authors.initials: M
authors.lastname: Teräs
authors.forename: Johanna
authors.initials: J
authors.lastname: Rokka
authors.forename: Mikko
authors.initials: M
authors.lastname: Pietilä
authors.forename: Pekka
authors.initials: P
authors.lastname: Saukko
authors.forename: Anne
authors.initials: A
authors.lastname: Roivainen
authors.forename: Antti
authors.initials: A
authors.lastname: Saraste
authors.forename: Juhani
authors.initials: J
authors.lastname: Knuuti
mesh_terms: D000818:Animals; D002908:Chronic Disease; D004195:Disease Models, Animal; D004452:Echocardiography / Q000379:methods; D006333:Heart Failure / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology; D008297:Male; D055414:Myocardial Perfusion Imaging / Q000379:methods; D010101:Oxygen Consumption; D049268:Positron-Emission Tomography / Q000379:methods; D013552:Swine; D014057:Tomography, X-Ray Computed / Q000379:methods; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology*; D020257:Ventricular Remodeling