Electrophysiological characterization of murine myocardial ischemia and infarction

Citation
J. Gehrmann et al., Electrophysiological characterization of murine myocardial ischemia and infarction, BAS R CARD, 96(3), 2001, pp. 237-250
Citations number
83
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
BASIC RESEARCH IN CARDIOLOGY
ISSN journal
03008428 → ACNP
Volume
96
Issue
3
Year of publication
2001
Pages
237 - 250
Database
ISI
SICI code
0300-8428(200105/06)96:3<237:ECOMMI>2.0.ZU;2-F
Abstract
Background Genetically altered mice will provide important insights into a wide variety of processes in cardiovascular physiology underlying myocardia l 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, who le-animal techniques and experimental protocols for detailed electrophysiol ogical characterization in a mouse model of myocardial ischemia and infarct ion. Methods FVB mice underwent open-chest surgery for ligation of the left anterior descending coronary artery or sham operation. By means of echocar diographic imaging, electrocardiography, intracardiac: electrophysiology st udy, and conscious telemetric ECG recording for heart rate variability (HRV ) analysis, we evaluated ischemic and postinfarct cardiovascular morphology and function in mice. Results Coronary artery ligation resulted in antero- apical infarction of the left ventricular wall. MI mice showed decreased ca rdiac function by echocardiography, infarct-typical pattern on EGG, and inc reased arrhythmia vulnerability during: electrophysiological study. Electro physiological properties were determined comprehensively, hut were not alte red significantly as a consequence of MI. Autonomic nervous system function , measured by indices of HRV, did not appear altered in mice during ischemi a 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 compa rison with mutant murine models necessitating ischemia or scar to elicit an identifiable phenotype. The limitations of directly extrapolating murine c ardiac electrophysiology data to conditions in humans need to be considered .