Electrotonic Remodeling Following Myocardial Infarction: A Link to Sudden Cardiac Death?

Abstract

A potential mechanism for ventricular fibrillation (VF) and sudden cardiac death following myocardial infarction (MI) is the remodeling of repolarization currents, leading to increased action potential duration and dispersion of repolarization. Recently, it has been shown in vitro that electrotoni c loading, resulting from heterogene ities in the ventricle, triggers the remodelin g of the Ito current. Thus, we studied electrotonic coupling in the post-MI heart, as measured by myocardial electrical impedance (MEI). Infarcts were induced in dogs by LAD coronary artery ligation. The dogs were instrumented with MEI electrodes in normal (LCX and LAD) and infarcted myocardium. After recovery, MEI was measured in awake-unsedated animals 1, 2, and 7 days after MI. Subsequently, VF-susceptibility was tested by a 2-min LCX occlusion during submaximal exercise; 11 animals developed VF (susceptible, S) and 10 did not (resistant, R). Healing myocardial infarct had significantly lower MEI than normal myocardium (see figure). This difference was steady by day 2 post-MI (287±8.5 vs. 425±16.7 Ω, ANOVA P<0.05). Furthermore, significant differences were observed between resistant and susceptible animals: One week after MI, susceptible dogs had a wider electrotonic disparity between remote myocardium and scar (R: 86.5±20.7 vs. S: 183.7±12.6Ω, P<0.05). These data suggest that electrotonic remodeling following MI may contribute to malignant ventricular arrhythmias.