Effects of Myocardial Ischemia on Triggered Activity in Hamster Atrial Transplants

Effects of Ischemia on Triggered Activity. The effects of acute myocardial ischemia on delayed afterdepolarizations and triggered activity were determined in vascularized hamster atrial cheek pouch transplants. Triggered activity was initiated in eight normally perfused transplants by spontaneous or paced action potentials. During control, bursts of triggered activity lasted 14.4 ± 2.S sec (mean ± SEM), had an average cycle length of 456.6 ± 33.8 msec, and terminated following a subthreshold delayed afterdepolarization having an amplitude of 13.8 ± 0.5 mV. Interruption of blood flow to the transplants initially suppressed induction of triggered activity by spontaneous action potentials, shortened bursts of triggered activity initiated by pacing, and tended to prolong the cycle length during triggered bursts. Complete suppression of triggered activity occurred after 15–70 minutes of ischemia. Despite a reduction of delayed afterdepolarization amplitude during ischemia, the membrane potential at the peak of the afterdepolarization became less negative, secondary to ischemia‐induced reductions of resting membrane and takeoff potentials. Thus, suppression of triggered activity during ischemia appeared to be caused by a shift of the voltage threshold to less negative membrane potentials, rather than by a reduction in delayed afterdepolarization amplitude. (J Cardiovasc Electrophysiol, Vol. 1. pp. 139–144, April 1990)