Pathogen Burden, Inflammation, Proliferation and Apoptosis in Human In-Stent Restenosis

Abstract

Pathogenic events leading to in-stent restenosis (ISR) are still incompletely understood. Among others, inflammation, immune reactions, deregulated cell death and growth have been suggested. Therefore, atherectomy probes from 21 patients with symptomatic ISR were analyzed by immunohistochemistry for pathogen burden and compared to primary target lesions from 20 stable angina patients. While cytomegalovirus, herpes simplex virus, Epstein-Barr virus and Helicobacter pylori were not found in ISR, acute and/or persistent chlamydial infection were present in 6/21 of these lesions (29%). Expression of human heat shock protein 60 was found in 8/21 of probes (38%). Indicated by distinct signals of CD68, CD40 and CRP, inflammation was present in 5/21 (24%), 3/21 (14%) and 2/21 (10%) of ISR cases. Cell density of ISR was significantly higher than that of primary lesions (977 ± 315 vs. 431 ± 148 cells/mm²; p < 0.001). There was no replicating cell as shown by Ki67 or PCNA. TUNEL⁺ cells indicating apoptosis were seen in 6/21 of ISR specimens (29%). Quantitative analysis revealed lower expression levels for each intimal determinant in ISR compared to primary atheroma (all p < 0.05). In summary, human ISR at the time of clinical presentation is characterized by low frequency of pathogen burden and inflammation, but pronounced hypercellularity, low apoptosis and absence of proliferation.

Journal

Journal ID (publisher-id): JVR

Journal ID (nlm-ta): J Vasc Res

Journal ID (doi): 10.1159/issn.1018-1172

Title: Journal of Vascular Research

Publisher: S. Karger AG

ISSN (Print): 1018-1172

ISSN (Electronic): 1423-0135

Publication date Subscription-year: 2004

Publication date (Print): December 2004

Publication date (Electronic): 03 December 2004

Volume: 41

Issue: 6

Pages: 525-534

Affiliations

^aDepartment of Cardiology, University of Bonn, Bonn; ^bCardiology Division, University of Munich, Munich, and ^cInstitute of Pathology, University of Bonn, Bonn, Germany

Article

Publisher ID: 81809 Other ID: J Vasc Res 2004;41:525–534

DOI: 10.1159/000081809

PubMed ID: 15528935

Copyright statement: © 2004 S. Karger AG, Basel

License:

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Page count

Figures: 4, Tables: 2, References: 38, Pages: 10

Product

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Categories

Subject: Research Paper