Contribution of depolarized foci with variable conduction impairment to arrhythmogenesis in 1 day old infarcted canine cardiac tissue: an in vitro study

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 infarcted 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 entrance 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.