IMMUNOHISTOCHEMISTRY IN DILATED CARDIOMYOPATHY

Citation
U. Kuhl et al., IMMUNOHISTOCHEMISTRY IN DILATED CARDIOMYOPATHY, European heart journal, 16, 1995, pp. 100-106
Citations number
37
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0195668X
Volume
16
Year of publication
1995
Supplement
O
Pages
100 - 106
Database
ISI
SICI code
0195-668X(1995)16:<100:IIDC>2.0.ZU;2-C
Abstract
The aetiology of dilated cardiomyopathy is unknown by definition. Vira l myocarditis is often viewed as an early stage in the progression of the disease leading to cardiomyopathy and heart failure in human. The chronic inflammatory process is manifested histologically as a sparse, diffuse lymphocytic infiltration of the myocardium, classified as bor derline or ongoing myocarditis according to the Dallas classification. Because of limitations of light microscopy, chronic myocarditis remai ns an enigmatic condition to diagnose and to treat. In contrast to rou tine histological staining procedures, immunohistochemical methods ena ble better identification and quantification of infiltrating cells and also provide further evidence that the activated immunological proces s within the myocardium is ongoing. In 176 patients with clinically su spected dilated cardiomyopathy, borderline myocarditis was diagnosed i n only 14 cases (8%) histologically. However; using immunohistological analysis of endomyocardial biopsies, pathologically increased lymphoc ytic infiltration was revealed in 67 biopsy specimens (38%), and activ ated lymphocytes or activated macrophages in all analysed inflamed car diac tissues. All positive biopsies showed an activated vascular endot helium, demonstrated by the enhanced expression of different adhesion molecules Various cytokines were locally released from activated infla mmatory cells. This may cause a cytokine-rich micro-environment which could be responsible for the enhanced expression of adhesion molecules and thereby contribute to the inflammatory traffic of immune cells in to inflamed myocardial areas. These observations underline the hypothe sis that the immune process is still active in a group of patients wit h clinically suspected dilated cardiomyopathy, causing progression of the disease.