Using His bundle recording techniques, the direct and autonomically mediated conduction system effects of quinidine were examined in 5 cardiac transplant recipients who had anatomically denervated hearts. Control conduction interval and refractory period measurements were made, and then 10 mg/kg quinidine gluconate was infused over a 20-min period. At 30 min. the electrophysiologic changes induced by quinidine were determined. Quinidine significantly increased the atrial-His (AH) interval (from 97±9[SEM] to 108±7 ms, P<0.001), the His-ventricular (HV) interval (from 43.9±1 to 52.8±3 ms, P<0.01), the donor heart sinus cycle length (from 599±38 to 630±56 ms, P<0.08), and the atrial effective refractory period (from 214±14 to 241±11 ms, P<0.01). Quinidine significantly decreased the innervated, remnant atrial sinus cycle length (from 847±104 to 660±96 ms, P<0.01) as well as the blood pressure. The mean plasma concentration of quinidine at the time that electrophysiologic measurements were repeated was 4.37±0.449 μg/ml. It is concluded that quinidine's predominant sinus nodal and atrioventricular nodal effects in man are autonomically mediated and opposite to its direct actions upon these structures. On the other hand, quinidine's prevailing effect on atrial refractoriness and His-Purkinje conduction in man is direct.
CITATION STYLE
Mason, J. W., Winkle, R. A., Rider, A. K., Stinson, E. B., & Harrison, D. C. (1977). The electrophysiologic effects of quinidine in the transplanted human heart. Journal of Clinical Investigation, 59(3), 481–489. https://doi.org/10.1172/JCI108663
Mendeley helps you to discover research relevant for your work.