Abstract 14071: In-vivo Assessment of the Peri-infarcted Region by a Novel Micro-electrode Array System in a Large Animal Model of Myocardial Infarction
Introduction: Ventricular arrhythmias are life threatening complications in ischemic cardiomyopathy associated with significant mortality. Inhomogeneity in conduction and dispersion of refractoriness are substrates for reentry tachycardias. Micro-electrode array (MEA) systems are currently used to study extracellular field potentials of myocytes in vitro.
Hypothesis: Aim of this study was to validate and apply for the first time a novel epicardial MEA 128-channel electrode in a large animal model of myocardial infarction (MI).
Methods: We induced MI by percutaneous coil occlusion of the proximal LAD in swine (body weight: 20±1.5 kg, n=6). Epicardial mapping in-vivo was performed by a lateral mini thoracotomy (length 5 cm) with placement of a flexible 128-channel-MEA (32x32 mm, 100 μm electrodes with 2.7 mm distance) on (a) healthy, (b) infarcted and (c) peri-infarcted areas of the left ventricle. Animals were stimulated with predefined pacing protocols.
Results: We assed global as well as regional function after MI confirming its efficacy and impact. Application of the MEA - electrode was safe and feasible, showing reproducible results in all animals. Analyzing different ventricular regions in 2D- reconstruction maps we found the inhomogeneity of conduction velocity to be significantly increased creating a characteristic pattern in the peri-infarcted region (Figure A). At each electrode the local ECG was registered to calculate differences in activation time. In comparison to recordings prior to the MI the peri-infarct tissue exhibited significant aberrations in spontaneous impulse propagation (Figure B) as well as in pacing protocol measurements.
Conclusions: We applied and demonstrated the feasibility of in-vivo epicardial MEA - mapping in a swine large animal model of MI. We believe this tool holds great potential for evaluating conduction velocity and impulse propagation for testing regenerative and anti-arrhythmic therapeutic strategies.
Author Disclosures: T. Plenge: None. M. Guschlbauer: None. A. Maul: None. M. Halbach: None. B. Krausgrill: None. A. Sterner-Kock: None. D. Stevens: None. S. Baldus: None. D. Ladage: None.
- © 2015 by American Heart Association, Inc.