Inhibition of demand pacemakers by myopotentials.

The inhibition of unipolar demand pacemakers by myopotentials was studied in 215 paced patients with or without symptoms and in steady pacing rhythm. ECG recordings were taken of all patients at rest and during effort in which maximal muscular strength from the pectoralis major (PM) and rectus abdominis (RA) muscles was required. In 75 patients (34.9%) transient pacing inhibition was observed. In these patients myopotentials from the PM and RA muscles were recorded simultaneously at rest and during special effort. The PM was the dominant source of inhibiting myopotentials in 50.7% of the total patients with oversensing and the RA was dominant in 28%. In the remaining 21.3%, neither of these muscle groups alone was able to cause inhibition and a clear synergy of both the PM and RA muscles was required. When oversensing occurred in a pacemaker implanted in the thoracic wall, the PM was the dominant cause in 54.4% of patients and the RA in 23.5%, while a synergy of both muscles was required in the remaining 22%. When the pacemaker was implanted in the abdominal wall, the RA was the dominant source of inhibiting myopotentials in all but two patients.