Arrhythmogenic mechanisms in human atrial and ventricular muscle fibers.

Abstract

Mechanisms which may lead to cardiac arrhythmias were studied in atrial and ventricular tissues from human hearts. In human atrial fibers, diastolic depolarization (DD) was consistently present, but did not induce spontaneous discharge. Epinephrine enhanced DD, could induce delayed afterdepolarizations (DADs) and (in combination with strophanthidin) trigger repetitive activity. The presence of DD modified the recovery of premature action potentials. Human ventricular fibers did not exhibit DD and were more resistant to Ca overload. It is concluded that in atrial tissues the presence of DD may not induce automatic arrhythmias, but it may influence conduction and re-entry rhythms. Cardioactive drugs may induce DADs and repetitive activity in the atria and less easily in the ventricles. The attainment of a threshold may be facilitated when DADs are superimposed.