Author + information
- Received November 12, 1985
- Revision received March 26, 1986
- Accepted April 4, 1986
- Published online September 1, 1986.
- ↵*Address for reprints:James E. Rosenthal, MD, Reingold Electrocardiography Center, Northwestern University Medical School, 310 East Superior Street, Chicago, Illinois 60611.
To assess the roles of entrance and exit block after canine myocardial infarction, single stage coronary artery ligations of canine circumflex coronary arteries were performed. After 1 day, atria and ventricles were paced using single stimuli and trains. After isolation, simultaneous microelectrode impalements were made in in-farcted and uninfarcted tissue. Spontaneous foci, when identifiable, were always located in infarcted tissue. They could frequently be triggered by one or more driven beats, and their activity could often be terminated (“annihilated”) by a properly timed beat. Foci with varying combinations of extrance and exit conduction impairment were observed.
Variations in conduction characteristics altered the manifest arrhythmic pattern. With partial entrance block and intact exit conduction, foci could be electrotonically modulated and entrained into regular patterns. Activity that emerged from a focus with sufficient conduction delay could modulate the focus, and entrain it to discharge at a slower rate (“autoentrainment”). The results suggest that modulated parasystole may contribute to arrhythmogenesis after canine myocardial infarction and that variations in entrance and exit characteristics of depolarized foci may result in variable and complex arrhythmic patterns.
- Received November 12, 1985.
- Revision received March 26, 1986.
- Accepted April 4, 1986.
- American College of Cardiology Foundation