title: Electrophysiological characterization of murine myocardial ischemia and infarction.
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.
authors.affiliation: Department of Cardiology, Children's Hospital, Boston, MA 02115, USA.
authors.forename: J
authors.initials: J
authors.lastname: Gehrmann
authors.forename: S
authors.initials: S
authors.lastname: Frantz
authors.forename: C T
authors.initials: CT
authors.lastname: Maguire
authors.forename: M
authors.initials: M
authors.lastname: Vargas
authors.forename: A
authors.initials: A
authors.lastname: Ducharme
authors.forename: H
authors.initials: H
authors.lastname: Wakimoto
authors.forename: R T
authors.initials: RT
authors.lastname: Lee
authors.forename: C I
authors.initials: CI
authors.lastname: Berul
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology; D013504:Cardiovascular Surgical Procedures; D004195:Disease Models, Animal; D004558:Electric Stimulation / Q000379:methods; D004562:Electrocardiography; D004594:Electrophysiology; D006329:Heart Conduction System / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D008297:Male; D051379:Mice; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000150:complications / Q000401:mortality* / Q000601:surgery; D016019:Survival Analysis; D020257:Ventricular Remodeling / Q000502:physiology