Electromechanical properties of Purkinje fiber strands isolated from human ventricular endocardium

Abnormalities in the regulation of intracellular Ca2+ were observed in cardiac cells obtained from failing human hearts. However, the electromechanical properties and pharmacologic responses of human ventricular Purkinje fibers have not been well characterized.

Strands of free-running Purkinje fibers and/or trabecular muscle fibers with a diameter of around 1.5 mm were removed from the endocardial surface of ventricles obtained from 16 transplant recipient hearts. Action potential (AP) was detected by conventional microelectrode techniques and twitch force by a force-displacement transducer.

The human Purkinje fiber strands as revealed by histologic examination were composed of Purkinje cells and the surrounding ventricular muscle cells. In well-polarized Purkinje fibers (mean +/- SE of maximum diastolic potential [MDP] = -85 +/- 1 mV) showing fast-response AP (Phase 0 Vmax >100 V/sec), the cardiotonic agents isoproterenol and strophanthidin (1 to 2 micromol/liter) accelerated the slope of diastolic depolarization and induced delayed afterdepolarization but not spontaneous APs. Steady-state contraction and the post-rest potentiation of contraction (PRPC) were similar in both Purkinje fibers and ventricular muscles, but inotropic agents induced tachyarrhythmia only in Purkinje fibers. In partially depolarized Purkinje fibers (MDP <-70 mV) with slow-response AP, isoproterenol and/or strophanthidin readily induced automatic and triggered rhythms.

Accumulation of excessive cytosolic Ca2+ in the presence of cardiotonic agents could lead to tachyarrhythmias in Purkinje fibers, but rarely in ventricular muscles of failing human hearts.