title: Long-term monitoring of the changes in signal-averaged ECG after coronary artery occlusion and intracoronary endothelin-1 injection in dogs.
abstract: Myocardium undergoes functional changes in the infarcted region primarily due to ischemia. Following myocyte functional alterations of the noninfarcted myocardium are caused by remodelling and hypertrophy. We have monitored and compared changes in the electrocardiographical (ECG) image after coronary artery occlusion (CAO, n=5) and intracoronary endothelin-1 (ET-1, n=3) administration during a 6-month period. In 3 dogs, the CAO was repeated 6 months after the first occlusion. Signal-averaged ECG (SA ECG) was recorded before the operation and 10 days, 1 month, 3 months and 6 months after myocardial infarction (MI). The modified Wigner distribution was used for spectrotemporal analysis of the SA ECG. Eight-hour Holter monitoring was performed in each dog before and after experimental MI. Spectrotemporal representations of the QRS complex were stabilized after the first 1-month period in the group of dogs after CAO. The same results were also observed after the repeated CAO. No arrhythmias were recorded 9 days after CAO. The spectrotemporal representations of the QRS complex after intracoronary ET-1 administration were not stabilized during the whole observed period. Very few arrhythmic events were recorded by Holter monitoring already 3 days after intracoronary ET-1 injection. Experimental MI induced by CAO caused a changed ECG image, which was stable from 1 month after MI induction till the end of the monitoring. However, the ECG image after ET-1 administration was not stable during the whole observed period. No arrhythmic events were recorded in either group 3 months postoperatively that could be caused by healthy myocardial status before the experimental MI induction. In clinical practice, however, ischemic heart disease usually precedes the MI. Arrhythmogenic substrate could thus be a consequence of combination of healthy status of the myocardium before MI and MI itself.
authors.affiliation: Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava, Slovak Republic. peter.hubka@fmed.uniba.sk
authors.forename: P
authors.initials: P
authors.lastname: Hubka
authors.forename: M
authors.initials: M
authors.lastname: Bernadic
authors.forename: I
authors.initials: I
authors.lastname: Hulín
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D003327:Coronary Disease / Q000209:etiology; D004195:Disease Models, Animal; D004285:Dogs; D015716:Electrocardiography, Ambulatory; D019332:Endothelin-1; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D009203:Myocardial Infarction / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D012307:Risk Factors; D012815:Signal Processing, Computer-Assisted; D013997:Time Factors
chemical_list: D019332:Endothelin-1