-Original-

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

Hiroshi Mase¹, Koichi Tamura^2,3, Atsushi Hiromoto¹, Masahiro Hotta¹, Saori Hotomi¹, Mayuko Togashi³, Yuh Fukuda³, Toshimi Yajima⁴, Takashi Nitta⁴, Shigeo Tanaka⁴ and Yuichi Sugisaki^2,3

¹Medical Student, Nippon Medical School
²Division of Surgical Pathology, Nippon Medical School Hospital
³Department of Pathology, Nippon Medical School
⁴Division of Cardiovascular Surgery, Nippon Medical School

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∼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 However, cardiomyocytes under the tip had been replaced by fibrotic tissue in many other patients.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.

J Nippon Med Sch 2005; 72: 52-59

Keywords
pacemaker, pacing electrode, PM implantation, pathology

Correspondence to
Koichi Tamura, MD, DMSc, Division of Surgical Pathology, Nippon Medical School Hospital, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan
tamura@nms.ac.jp

Received, October 22, 2004
Accepted, December 14, 2004