Subendocardial infarction produces epicardial parasympathetic denervation in canine left ventricle.

Forty dogs underwent anterior descending coronary artery dissection with most having occlusion that was either maintained or reperfused. Study was performed 1-4 days later. Multiple electrodes placed in normal and ischemic zones were used to determine the depth of the epicardial rim overlying a subendocardial infarction. This was done by comparing voltage differential with respect to time (dV/dt) measurements of sequential bipolar electrograms along each needle. By this means, test sites with a rim were documented, and depths of epicardial biopsies for choline acetyltransferase were chosen. Epicardial effective refractory period (ERP) responses to vagal nerve stimulation were measured. In sham-operated controls, vagal stimulation prolonged ERP, and choline acetyltransferase activity was equivalent in all sites. In contrast, dogs with all durations of coronary occlusion and various thicknesses of subendocardial infarction had no significant prolongation of ERP limited to rim sites overlying the infarct during vagal nerve stimulation. Corresponding choline acetyltransferase activity was decreased in rim sites compared with remote areas. In addition, dogs given norepinephrine or physostigmine (to potentiate parasympathetic responses) did not demonstrate significant ERP prolongation with vagal stimulation. Infusion of acetylcholine into the distal ligated coronary artery produced dose-dependent prolongation of ERP in sites overlying the infarct. These data taken together support the hypothesis that subendocardial infarction, regardless of its homogeneity or thickness, produces parasympathetic denervation of the overlying epicardial rim.