Inflammatory endothelial activation was present in 67% of dilated cardiomyopathy patients compared to 0% of controls, correlating with intramyocardial infiltrates.
Cross-Sectional (n=166)
Is the expression of cell adhesion molecules increased and correlated with inflammatory infiltrates in endomyocardial biopsies of patients with dilated cardiomyopathy?
Endothelial cell adhesion molecule expression is significantly elevated in dilated cardiomyopathy and correlates with inflammatory infiltrates, suggesting diagnostic utility for inflammatory cardiomyopathy.
Absolute Event Rate: 67% vs 0%
BACKGROUND: Dilated cardiomyopathy (DCM) is pathogenically linked to inflammatory cardiomyopathy (InfCM), which is characterized by intramyocardial infiltration. The transendothelial migration of immunocompetent cells is mediated by cell adhesion molecules (CAMs). METHODS AND RESULTS: We investigated the expression pattern of CAMs (immunoglobulin superfamily, 32 selectins, and beta1- and beta2-integrins) in endomyocardial biopsies from DCM patients (n=152; left ventricular ejection fraction 3 CAMs (inflammatory endothelial activation), nor did any control tissue prove positive for InfCM (>7.0 CD3+ lymphocytes per 1 mm2). In comparison, 64% (n=97) of the DCM biopsies were evaluated positive for InfCM and 67% (n=101) for inflammatory endothelial activation, respectively. Whereas expression of HLA class I, HLA-DR, intercellular cell adhesion molecule-1, and CD29 was distributed homogeneously within a patient's serial sections, immunoreactivity of vascular cell adhesion molecule-1, lymphocyte function antigen-3, and the selectins was accentuated on single vascular endothelia. Sixty-six percent of the DCM biopsies presented CD29 abundance also within the extracellular matrix and the sarcolemma. CD62P and CD62E were present in 16% and 40% of the DCM patients, respectively. Endothelial CAM representatives correlated with one another (P<0.05), except for CD62P with HLA. Endothelial CAM expression correlated with intramyocardial infiltrates phenotyped by the corresponding counterreceptors. CONCLUSIONS: Inflammatory endothelial activation is present in 67% of DCM patients. Because CAM expression correlates with the immunohistological diagnosis of InfCM and counterreceptor-bearing intramyocardial infiltrates, evaluation of endothelial CAMs might be of diagnostic significance in InfCM.
Noutsias et al. (Tue,) conducted a cross-sectional in Dilated cardiomyopathy (n=166). Evaluation of endothelial cell adhesion molecules (CAMs) vs. Autopsy controls was evaluated on Inflammatory endothelial activation (concurrent abundance of >3 CAMs). Inflammatory endothelial activation was present in 67% of dilated cardiomyopathy patients compared to 0% of controls, correlating with intramyocardial infiltrates.