Electrophysiological characterization of murine myocardial ischemia and infarction |
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Authors: | Josef Gehrmann Stefan Frantz Colin T Maguire Marcel Vargas Anique Ducharme Hiroko Wakimoto Richard T Lee Charles I Berul |
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Institution: | (1) Department of Cardiology, Children's Hospital · Boston, 300 Longwood Avenue, Boston, MA 02115, USA, E-mail: berul@cardio.tch.harvard.edu, US;(2) Department of Cardiology, Brigham & Women's Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA, US |
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Abstract: | Background Genetically altered mice will provide important insights into a wide variety of processes in cardiovascular physiology underlying
myocardial infarction (MI). Comprehensive and accurate analyses of cardiac function in murine models require implementation
of the most appropriate techniques and experimental protocols. Objective In this study we present in vivo, whole-animal techniques and experimental protocols for detailed electrophysiological characterization
in a mouse model of myocardial ischemia and infarction. Methods FVB mice underwent open-chest surgery for ligation of the left anterior descending coronary artery or sham-operation. By
means of echocardiographic imaging, electrocardiography, intracardiac electrophysiology study, and conscious telemetric ECG
recording for heart rate variability (HRV) analysis, we evaluated ischemic and post-infarct cardiovascular morphology and
function in mice. Results Coronary artery ligation resulted in antero-apical infarction of the left ventricular wall. MI mice showed decreased cardiac
function by echocardiography, infarct-typical pattern on ECG, and increased arrhythmia vulnerability during electrophysiological
study. Electrophysiological properties were determined comprehensively, but were not altered significantly as a consequence
of MI. Autonomic nervous system function, measured by indices of HRV, did not appear altered in mice during ischemia or infarction.
Conclusions Cardiac conduction, refractoriness, and heart rate variability appear to remain preserved in a murine model of myocardial
ischemia and infarction. Myocardial infarction may increase vulnerability to inducible ventricular tachycardia and atrial
fibrillation, similarly to EPS findings in humans. These data may be of value as a reference for comparison with mutant murine
models necessitating ischemia or scar to elicit an identifiable phenotype. The limitations of directly extrapolating murine
cardiac electrophysiology data to conditions in humans need to be considered.
Received: 5 October 2000, Returned for 1. revision: 2 November 2000, 1. Revision received: 24 November 2000, Returned for
2. revision: 28 November 2000, 2. Revision received: 13 December 2000, Accepted: 14 December 2000 |
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Keywords: | Myocardial infarction – mice – echocardiography – electrophysiology – heart rate variability |
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