ACUTE AND CHRONIC CYCLE LENGTH DEPENDENT INCREASE IN VENTRICULAR PACING THRESHOLD

Several factors have been shown to influence ventricular pacing threshold in humans, including pacing lead location (endocardial vs epicardial), lead maturation, and antiarrhythmic agents. To determine whether ventricular pacing rate has a significant influence on acute and chronic pacing thresholds, we measured pacing thresholds in 16 patients receiving an implantable antitachycardia pacemaker cardioverter defibrillator (Cadence(TM)). Ventricular pacing thresholds were determined using the device programmer at cycle lengths of 600, 400, and 300 msec at the time of implantation; prior to hospital discharge at 3-14 days; and during follow-up outpatient visits at 6-8 weeks, 3 months, and 6 months to 1 year. Eleven patients had an epicardial lead system and five an endocardial lead system. Eleven patients were being treated with antiarrhythmic drug therapy. Device output ranged from 1-10 V and was adjustable in 1-V increments (pulse width was held constant at 1 msec). A cycle length dependent increase in pacing threshold (defined as a greater-than-or-equal-to 1-V increase in threshold at 400 or 300 msec relative to 600 msec) was observed in 10/16 patients during 12/72 pacing trials at 400 msec, and in 15/16 patients during 31/67 trials at 300 msec. In trials in which an increase in pacing threshold occurred, the magnitude of the increase at 400 msec relative to 600 msec was only 1 V in all 12 trials, but at 300 msec the increase ranged from 4-9 V in 7/31 (2.3%) trials. There was an equal percentage (67%) of patients demonstrating a cycle length dependent increase in threshold with measurements made at the time of device implantation and at the 6 month to 1 year follow-up period. Two-way analysis of variance showed a significant effect of cycle length and time from implantation on mean pacing thresholds at the three cycle lengths. In conclusion, a cycle length dependent increase in pacing threshold occurred in virtually all patients during follow-up of up to 12 months and, thus, its presence was independent of lead location, presence of antiarrhythmic agents, and the state of lead maturation. These findings suggest that pacing thresholds measured at rates just above the sinus rate may not always apply to the faster rates utilized for antitachycardia pacing and indicates the need for threshold measurement at the designed pacing rate.