Abstract
In a series of 60 patients with Stokes-Adams disease treated by artificial pacing atrio-ventricular [A-V] conduction returned in about 25%. In the patients in whom A-V conduction returned, and who were treated by ventricular pacemaking, parasystole developed; hemodynamic function was then equal to, or better than, that achieved by ventricular pacing alone but the risk of sudden death was greatly increased. This was probably due to the development of ventricular fibrillation triggered by a high-energy pacemaking stimulus falling during the vulnerable period of the cardiac cycle, and the risk of this arrhythmia appeared to be at its maximum during the early post-operative period. With the patient at rest the sudden loss of atrial contribution to ventricular filling caused an immediate fall in cardiac output of about 25%. Subsequent changes in ventricular stroke volume returned the output to its initial level, despite a constant heart rate. The most effective timing of atrial systole as judged acutely by the systemic or R. V. pressure was that corresponding to a physiological P-R interval.