Abstract
Demand failures during permanent cardiac pacing were studied in four patients with coronary heart disease and cardiomyopathies, by means of in vivo and in vitro analyses of the pacemaker system. A common feature of the electrogram analyses (except during a second replacement in one patient), was extremely low values of amplitudes (0.77-4.36 mV) and maximum derivatives (0.16-1.06 V/sec). In spite of low electrogram amplitudes, the myocardial threshold values were low in all patients. An attempt in one patient at unipolarizing a bipolar system made the adaptation between electrogram and pulse generator more difficult. Autopsy showed that the tip of the bipolar electrode was positioned in a fibrotic area of the myocardium. The signal available for the sensing circuit will also be reduced because of voltage division between the electrode/tissue interface impedance and the input impedance of the pulse generator. Although the pulse generators used had a high input impedance (10-50 K omega), the tissue interface impedance may have caused a further reduction in the electrogram amplitude of 10-30%. This may have contributed to demand failure. In vitro studies confirmed that test pulses with characteristics similar to those of the electrograms found in this investigation, were inadequate for pacemaker inhibition. Special care should be taken during electrogram recordings in patients with severe myocardial disease. One should consider the implantation of a high sensitivity pulse generator or the recently introduced sensitivity programmable pulse generators as first choice for this group of patients.