No abstract

The electrode-tissue interface is that area lying between the cathode of a low-voltage implantable pacemaker or cardioverter-defibrillator (ICD) lead and the endocardium or epi-myocardium of the cardiac chamber being paced. The electrical stimulus that is delivered to this interface is responsible for myocyte depolarization with consequent cardiac contraction. The process by which this occurs is reasonably well understood and any explanation requires a basic understanding of the physics and cellular electrophysiology of pacing. The effective and efficient delivery of electrical energy to the myocardium via the lead is dependent on many factors to be discussed in this review. However, despite numerous evolutionary changes occurring in the cathode's material, design, and surface configuration, it was not until the incorporation of steroid-elution to the electrode-tissue interface that reliable and significantly low stimulation threshold cardiac pacing became possible.

Animal testing results were reproducible in the acute human test setting. The lead reduced the paced FFRW signal amplitudes significantly, allowing for high atrial sensitivity settings but without sensing the FFRW. A robust P-wave signal could be retained.

A transvenous pacing lead with a porous electrode which slowly elutes the steroid, dexamethasone sodium phosphate, has been developed. Previous investigations show low and constant stimulation thresholds persisting over at least the first two years post-implantation. As it is not known whether this low threshold results from the steroid or electrode configuration, a double blind study was designed to compare the same electrode configuration with and without steroid over a 2-year follow-up period. There were ten patients in each group with similar age, sex, indications for pacing and implantation data. Regular measurements of postoperative pulse duration thresholds were performed using a customized VVIM pulse generator programmed to 1.5 V output. For the first two days post-implantation, there were no statistical differences in the pulse duration thresholds between the two pacing leads. From 2 weeks to 2 years the pulse duration thresholds for the steroid leads remained almost constant, whereas the leads without steroid showed a typical rise. The difference in pulse duration thresholds between the two groups of leads from two weeks onwards confirmed that it was the steroid rather than the electrode configuration which prevented the rise in chronic stimulation threshold.