Electrophysiological characterization of murine myocardial ischemia and infarction

被引:62
作者
Gehrmann, J
Frantz, S
Maguire, CT
Vargas, M
Ducharme, A
Wakimoto, H
Lee, RT
Berul, CI
机构
[1] Childrens Hosp, Dept Cardiol, Boston, MA 02115 USA
[2] Brigham & Womens Hosp, Dept Cardiol, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA
关键词
myocardial infarction; mice; echocardiography; electrophysiology; heart rate variability;
D O I
10.1007/s003950170054
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 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 cardiac function by echocardiography, infarct-typical pattern on EGG, and increased arrhythmia vulnerability during: electrophysiological study. Electrophysiological properties were determined comprehensively, hut 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.
引用
收藏
页码:237 / 250
页数:14
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