Effects of digitalis on ventricular myocardial and His-Purkinje refractoriness and reentry in man

The effects of digitalis on retrograde conduction and refractoriness of the His-Purkinje system, ventricular myocardium and reentry within the His-Purkinje system were studied in 17 patients using the ventricular extrastimulus (V₂) technique. Studies were performed, before and 30 minutes after intravenous administration of ouabain, 0.01 mg/kg. After treatment with ouabain, there was a significant decrease in the functional refractory period (266 ± 19 to 254 ± 18 msec, P < 0.001), relative refractory period (253 ± 17 to 240 ± 16 msec, P < 0.001) and effective refractory period (242 ± 23 to 231 ± 24 msec, P < 0.005) of the ventricular muscle. In contrast, there was no significant change in retrograde His-Purkinje conduction and refractoriness. The phenomenon of reentry within the His-Purkinje system characterized by the reentrant beat (V₃) at critical retrograde conduction delays in the His-Purkinje system (V₂-H₂) within a narrow range of V₁-V₂ intervals was seen in 10 of 17 patients. Ouabain increased and shifted to the left the zone of reentry within the His-Purkinje system in 7 of 10 patients (36 ± 23 to 55 ± 23 msec, P < 0.001) and decreased it by 10 to 30 msec in the remaining 3 patients. The critical V₂-H₂ (186 ± 29 to 193 ± 27 msec, difference not significant [NS]) and V₁-V₂ (299 ± 30 to 294 ± 36 msec, NS) intervals for reentry did not significantly change after ouabain. However, the minimal V₁-V₂ intervals (266 ± 26 to 253 ± 25 msec, P < 0.025) decreased significantly, whereas the maximal V₂-H₂ intervals (266 ± 40 to 239 ± 37 msec, P < 0.01) increased significantly. Thus, in the intact human heart, digitalis (1) significantly decreased all measures of ventricular myocardial refractoriness, (2) had no significant effect on retrograde conduction and refractoriness of the His-Purkinje system, and (3) widened the zone of reentry within the His-Purkinje system due to shortening of the functional refractory period of the ventricular muscle with attainment of longer V₂-H₂ delays.