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Electrotonic remodeling following myocardial infarction in dogs susceptible and resistant to sudden cardiac death

Departments of ¹Physiology and Cell Biology, ²Electrical and Computer Engineering, ³Surgery, ⁴Anesthesiology, and ⁵Biomedical Engineering, and ⁶Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio

Submitted 15 October 2007 ; accepted in final form 26 November 2007

Passive electrical remodeling following myocardial infarction (MI) is well established. These changes can alter electrotonic loading and trigger the remodeling of repolarization currents, a potential mechanism for ventricular fibrillation (VF). However, little is known about the role of passive electrical markers as tools to identify VF susceptibility post-MI. This study investigated electrotonic remodeling in the post-MI ventricle, as measured by myocardial electrical impedance (MEI), in animals prone to and resistant to VF. MI was induced in dogs by a two-stage left anterior descending (LAD) coronary artery ligation. Before infarction, MEI electrodes were placed in remote (left circumflex, LCX) and infarcted (LAD) myocardium. MEI was measured in awake animals 1, 2, 7, and 21 days post-MI. Subsequently, VF susceptibility was tested by a 2-min LCX occlusion during exercise; 12 animals developed VF (susceptible, S) and 12 did not (resistant, R). The healing infarct had lower MEI than the normal myocardium. This difference was stable by day 2 post-MI (287 ± 32 vs. 425 ± 62 , P < 0.05). Significant differences were observed between resistant and susceptible animals 7 days post-MI; susceptible dogs had a wider electrotonic gradient between remote and infarcted myocardium (R: 89 ± 60 vs. S: 180 ± 37 ). This difference increased over time in susceptible animals (252 ± 53 at 21 days) due to post-MI impedance changes on the remote myocardium. These data suggest that early electrotonic changes post-MI could be used to assess later arrhythmia susceptibility. In addition, passive-electrical changes could be a mechanism driving active-electrical remodeling post-MI, thereby facilitating the induction of arrhythmias.

myocardial ischemia; myocardial electrical impedance; ventricular fibrillation

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