Title of article :
Adhesion molecule expression and ventricular remodeling in chronic rheumatic heart disease: a cause or effect in the disease progression — a pilot study
Author/Authors :
Saikia، نويسنده , , Uma Nahar and Kumar، نويسنده , , Rohit Manoj and Pandian، نويسنده , , V.K.G. Rajasekara Pal and Gupta، نويسنده , , Shivali and Dhaliwal، نويسنده , , R.S. and Talwar، نويسنده , , K.K.، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2012
Abstract :
Background
tic fever and chronic rheumatic heart disease (RHD) remains one of the most important causes of cardiovascular morbidity leading to a major public health problem, especially in developing countries. This was a pilot study to assess the presence of inflammation and expression of adhesion molecules by immunohistochemistry (IHC) in endomyocardial biopsy specimens of patients with chronic RHD.
s
ocardial biopsy was obtained from 14 patients of chronic RHD with no features of activity clinically. Biopsies were processed for histology and IHC. IHC was carried using monoclonal antibodies against CD3, CD4, CD8, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1.
s
orphologically, varying degree of interstitial and perivascular fibrosis was seen in all the 13 patients (100%). Mild fibrosis (1+) was seen in five patients (38.5%); moderate interstitial fibrosis (2+) was present in four patients (30.8%).There was no Aschoff nodule or evidence of active myocarditis in any of the biopsy specimens.
histochemistry
te positivity of (2+) and intense positivity of (3+) for intercellular adhesion molecule-1 was seen in 11 and 2 patients, respectively. With vascular cell adhesion molecule-1, four showed mild positivity (1+), and three showed intense positivity (3+). The phenotypic analysis of the inflammatory cells in our study revealed CD8+ cells in 77%, CD4+ in 23.1%, and CD3+ in 38.5% of total patients, which suggests chronicity.
sion
nspecific histomorphological changes and increased adhesion molecules expression could be a part of the ventricular remodeling due to the hemodynamic stress by the stenotic or regurgitant lesions of RHD itself.
Keywords :
RhD , Adhesion Molecules , inflammation
Journal title :
Cardiovascular Pathology
Journal title :
Cardiovascular Pathology