Open Access The Adult Göttingen Minipig as a Model for Chronic Heart Failure After Myocardial Infarction: Focus on Cardiovascular Imaging and Regenerative Therapies

Authors: Schuleri, Karl H.1; Boyle, Andrew J.2; Centola, Marco1; Amado, Luciano C.3; Evers, Robert3; Zimmet, Jeffrey M.3; Evers, Kristine S.3; Ostbye, Katherine M.3; Scorpio, Diana G.4; Hare, Joshua M.5; Lardo, Albert C.1

Source: Comparative Medicine, Volume 58, Number 6, December 2008 , pp. 568-579(12)

Publisher: American Association for Laboratory Animal Science

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Abstract:

Porcine models have become increasingly popular in cardiovascular research. The standard farm pig rapidly increases in body weight and size, potentially confounding serial measurements of cardiac function and morphology. We developed an adult porcine model that does not show physiologic increases in heart mass during the study period and is suitable for long-term study. We compared adult minipigs with the commonly used adolescent Yorkshire swine. Myocardial infarction was induced in adult Göttingen minipigs and adolescent Yorkshire swine by occlusion of the left anterior descending coronary artery followed by reperfusion. At 8 wk after infarction, the left ventricular ejection fraction was 34.1 ± 2.3% in minipigs and 30.7 ± 2.0% in Yorkshire swine. The left ventricular end-diastolic mass in Yorkshire pigs assessed by magnetic resonance imaging increased 17 ± 5 g, from 42.6 ± 4.3 g at week 1 after infarction to 52.8 ± 6.6 g at week 8, whereas it remained unchanged in minipigs. Cardiac anatomy and physiology in adult minipigs were evaluated invasively by angiography and noninvasively by Multidetector Computed Tomography and by Magnetic Resonance Imaging at 1.5 T and 3 T prior to myocardial infarction and during folow-up. This porcine heart failure model is reproducible, mimics the pathophysiology in patients who have experienced myocardial infarction, and is suitable for imaging studies. New heart failure therapies and devices can be tested preclinically in this adult animal model of chronic heart failure.

Document Type: Research article

Affiliations: 1: Department of Medicine, Division of Cardiology, Johns Hopkins University, Baltimore, Maryland; Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland 2: Department of Medicine, Division of Cardiology, University of California-San Francisco, San Francisco, California 3: Department of Medicine, Division of Cardiology, Johns Hopkins University, Baltimore, Maryland 4: Department of Molecular and Comparative Pathobiology, Johns Hopkins Medical Institutions, Baltimore, Maryland 5: Department of Medicine, Division of Cardiology, University of Miami, Miami, Florida

Publication date: 2008-12-01

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