In vitro characteristics of repolarization abnormality--a possible cause of arrhythmias

When membrane potential (Vm) remains at depolarized levels for prolonged intervals, quiescence and/or repetitive activations occur. In situ such events would be associated with arrhythmias. One way for such a state to occur is abnormal delay of repolarization leading to marked prolongation of action potential (AP) duration (APD). We studied canine Purkinje fibers in which abnormal AP prolongation had been induced by hypoxic, acidic Tyrode's with or without epinephrine, or by Ni++. AP's exhibited a prolonged secondary plateau with or without early afterdepolarizations (EAD's); they were up to ten minutes in duration. With programmed stimulation, APD's displayed a markedly exaggerated interval dependence with slight increases in diastolic interval causing transitions from normal to abnormal and very long AP's. Normalization of AP's occurred during prolonged rapid pacing trains and only gradually returned to abnormality after cessation of pacing. We also induced EAD's via programmed stimulation at plateau Vm levels. Repolarization could be brought on abruptly via these stimulus-induced EAD's; in certain instances trains of EAD's were required. The above characteristics of the state for which the term "repolarization failure" seems appropriate may have implications for in situ arrhythmias, e.g. in "Torsade de Pointes" ventricular tachycardia.