This ex vivo study demonstrates that delayed after depolarizations and resultant triggered activity can occur in human ventricular and Purkinje fibers, particularly under the influence of epinephrine and ouabain.
We studied the electrophysiologic characteristics of ventricular muscle and Purkinje fibers from the hearts of five patients undergoing cardiac transplantation. All five patients had congestive failure and coronary artery disease before surgery and were receiving digitalis therapy. Ventricular muscle had a maximal diastolic potential (MDP) of -78 +/- 1 mV (mean +/- SEM), an action potential (AP) amplitude of 104 +/- 2 mV, a phase 0 upstroke velocity (Vmax) of 297 +/- 19 V/sec and an AP duration at 50% repolarization (APD50) of 190 +/- 4 msec. Purkinje fibers had an MDP of -80 +/- 2 mV, an AP amplitude of 107 +/- 2 mV, a Vmax of 388 +/- 25 V/sec and an APD50 of 195 +/- 9 msec. Fibers from infarcted sections of the heart had significantly longer APD than those from noninfarcted, which resulted in marked dispersion of APD in infarcted and adjacent zones. Both epinephrine and ouabain induced delayed after depolarizations in Purkinje fiber. This suggest that delayed after depolarizations and resultant triggered activity can occur in the human ventricle.
Dangman et al. (Mon,) studied this question.
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