Electrotonic remodeling following myocardial infarction in dogs susceptible and resistant to sudden cardiac death.
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 Omega vs. 425 +/- 62 Omega, 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 Omega vs. S: 180 +/- 37 Omega). This difference increased over time in susceptible animals (252 +/- 53 Omega 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.
Dept. of Physiology and Cell Biology, The Ohio State Univ., 1645 Neil Ave., 305 Hamilton Hall, Columbus, OH 43210, USA.
Carlos L
CL
Del Rio
Patrick I
PI
McConnell
Monica
M
Kukielka
Roger
R
Dzwonczyk
Bradley D
BD
Clymer
Michael B
MB
Howie
George E
GE
Billman
D000818:Animals; D003331:Coronary Vessels / Q000601:surgery; D016757:Death, Sudden, Cardiac / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control; D004195:Disease Models, Animal; D004285:Dogs; D017097:Electric Impedance; D006329:Heart Conduction System / Q000503:physiopathology*; D008026:Ligation; D009203:Myocardial Infarction / Q000150:complications* / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology*; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000150:complications* / Q000209:etiology / Q000473:pathology / Q000503:physiopathology