Fractionated heart activation can be detected as late potentials from surface recordings of signal-averaged electrocardiograms (SA ECG) which are considered as a marker of sustained ventricular tachycardia. For animal studies, reference values in time and frequency domain analyses are essentially missing. In the present study, we have established reference values in SA ECG time domain analysis and time-frequency representation of heart activation in healthy dogs. A group of 25 healthy mongrel dogs (body weight 12-15 kg) was investigated. Wigner distribution and our modification of Fast Fourier transform (FFT), gliding window FFT, was applied in SA ECG frequency domain analysis. Reference values in time domain SA ECG were established. Time and voltage criteria were adapted to short duration of heart cycle and fast voltage decrement of the QRS complex in dogs. Wigner distribution and gliding window FFT were applied in order to describe mean heart activation in the frequency domain. Contribution of higher frequencies (30-80 Hz) was detected by both frequency analysis methods in the second third of ventricular activation in healthy animals. Presented results could offer a basis for further experimental arrhythmologic studies.
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 repres
entations 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.