Document Detail


Histopathological study of tissue reaction to pacemaker electrodes implanted in the endocardium.
MedLine Citation:
PMID:  15834208     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 However, cardiomyocytes under the tip had been replaced by fibrotic tissue in many other patients.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.
Authors:
Hiroshi Mase; Koichi Tamura; Atsushi Hiromoto; Masahiro Hotta; Saori Hotomi; Mayuko Togashi; Yuh Fukuda; Toshimi Yajima; Takashi Nitta; Shigeo Tanaka; Yuichi Sugisaki
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of Nippon Medical School = Nippon Ika Daigaku zasshi     Volume:  72     ISSN:  1345-4676     ISO Abbreviation:  J Nippon Med Sch     Publication Date:  2005 Feb 
Date Detail:
Created Date:  2005-04-18     Completed Date:  2005-07-19     Revised Date:  2012-09-25    
Medline Journal Info:
Nlm Unique ID:  100935589     Medline TA:  J Nippon Med Sch     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  52-9     Citation Subset:  IM    
Affiliation:
Nippon Medical School, Bunkyo-ku, Tokyo 113-8603, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Aged, 80 and over
Electrodes, Implanted / adverse effects*
Endocardium / pathology*
Female
Fibrosis
Heart Diseases / pathology,  therapy
Humans
Male
Middle Aged
Myocytes, Cardiac / pathology
Pacemaker, Artificial / adverse effects*
Stress, Mechanical

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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