Histopathological Study of Tissue Reaction to Pacemaker Electrodes Implanted in the Endocardium

Abstract

Limited information is available about histopathological reactions to the implanted endocardial electrodes of pacemakers (PM). Gross anatomic and histologic studies of tissue reactions to PM electrodes were made in thirteen autopsy cases (nine men and four women, ages 25 approximately 89 years, mean age 71.8) who died two months to twenty-one years after PM implantation. Nine of them had complete atrioventricular (AV) block, three had sick sinus syndrome, and one had bradycardia-tachycardia syndrome. The direct causes of death were not related to their PM. The tip with projecting tines was implanted in the right ventricle in all patients. At the contact area between the electrode and the endocardium, no tissue reaction was observed in one patient with a history of over sixteen years of PM implantation. However, cardiomyocytes under the tip had been replaced by fibrotic tissue in many other patients. In two patients in particular where the electrode had been implanted at the apex of each right ventricle, all cardiomyocytes had disappeared and only fibrotic tissue and adipose tissue were observed under the tip. These findings suggest that mechanical stress caused by attaching the tip tightly damages cardiomyocytes and brings about changes in the pacing thresholds. In three patients, a space was seen between the tip and the endocardium. A fibrous sheath covering the electrode extended to the tip and formed a thick fibrous cap. This non-excitable fibrous cap acted as a virtual electrode and possibly affected the elevation of the threshold in these patients. In four patients, extensive myocardial fibrosis due to disease, e. g. previous myocardial infarction, dilated cardiomyopathy, amyloidosis, or sarcoidosis, was found in the area surrounding the tip and also might affect the elevation of the threshold. We concluded that elevation of pacing thresholds after PM implantation is not due to reactive endocardial thickening. The space between the tip and the endocardium is occupied by a fibrous sheath, and an overly tight attachment damages cardiomyocytes causing replacement fibrosis. Thus, it is not desirable in some patients to insert the electrodes into the apex, where the myocardium is thin. To avoid the elevation of thresholds, development of further devices is necessary to allow electrode fixation to the endocardium with a more suitable pressure level.

Histological properties of oscillating intracardiac masses associated with cardiac implantable electric devices

“…After the implantation of the leads, fibrin deposits around the leads. This fibrin ultimately forms into connective tissue resulting in full coverage of the leads 10,12‐14 . It might be highly likely that the so‐called “ghosts” are the same histological strain as the EN type ICM 15 .…”

Acetylation mediates Cx43 reduction caused by electrical stimulation

“…However, the application of abnormal external electrical pulses is widely used in clinical settings such as defibrillator and pace-maker implantation and is known to cause significant deterioration of the myocardial substrate. Importantly, the cardiac tissue damage caused by current flow has not only a fibrotic component [51,52], but also a junctional component, as demonstrated by different reports showing that ventricular tachypacing, either induced by direct ventricular activation [28] or by rapid atrial pacing [29], can cause gap junctional remodeling and cardiomyocyte uncoupling [53]. …”

Investigation of the use of three electroencephalographic electrodes for long-term electroencephalographic recording in awake and sedated dogs

“…There is extensive information on the reaction of brain tissue to implanted electrodes of various metals, including consequences of intracerebral hematomas as well as the development of fibrous tissue reactions to long-term cardiac pacemaker and cochlear implant electrodes. 18,19 Future studies conducted with the SWE may involve recording of the location, size, and duration of subcutaneous or surface hemorrhage as a result of SWE placement to better elucidate the effects of hemorrhage on SWE function.…”