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Increased endothelial cell expression of a3ß1 integrin in cardiac valvulopathy in the primary (Hughes) and secondary antiphospholipid syndrome

Institute of Pathology, Department of Medicine ‘B’; Sheba Medical Center, Tel-Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Israel

Y Shoenfeld

R Manor

Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Israel

I Goldberg

Institute of Pathology, Department of Medicine ‘B’; Sheba Medical Center, Tel-Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Israel

L Ziporen

J George

Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Israel

S Polak-Charcon

Institute of Pathology, Department of Medicine ‘B’; Sheba Medical Center, Tel-Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Israel

M C Amigo

Departments of Rheumatology; Instituto Nacional de Cardiologia ‘Ignacio Chavez’, Mexico

R Garcia-Torres

Department of Pathology, Instituto Nacional de Cardiologia ‘Ignacio Chavez’, Mexico

R Segal

Department of Rehabilitation, Shmuel Harofeh, Beer Jacob, Israel

J Kopolovic

Institute of Pathology, Department of Medicine ‘B’; Sheba Medical Center, Tel-Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Israel

The objective of this work was to determine markers of endothelial cell activation in valves from patients with antiphospholipid syndrome (APS) and heart valve involvement, in order to establish a role for endothelial cells in the pathogenesis of the valvular disease.

Sixteen valves from ten patients with APS, obtained from autopsies or removed during valve replacement, were studied. Two groups of valves were used as controls. One group included seven normal valves from patients who died from non-cardiac diseases. The other group of valves were obtained from patients with bacterial endocarditis during autopsies or valve replacement operations.

Immunoperoxidase and immunofluorescence stainings with antibodies to human immunoglobulins, endothelial cells, a₃ß₁ integrin, collagen IV, laminin and fibronectin were employed.

Three histopathological patterns were apparent: normal valves, valves with verrucous endocarditis and valves with fibrocalcific changes. In all the valves with verrucous endocarditis the following findings were observed: (1) increased expression of the a₃ß₁ integrin on the endothelial cells, (2) increased amount of collagen IV, laminin and fibronectin, (3) proliferation of blood vessels and (4) linear subendothelial deposition of immunoglobulins and complement. The valves with fibrocalcific changes were deformed and showed a thick layer of collagen IV, laminin and fibronectin, yet in two valves the indothelial cells showed an expression of the a₃ß₁ integrin. The control valves did not express the integrin and had only a thin subendothelial band of collagen IV.

In valves from patients with APS,¹ markers of endothelial cell activation are upregulated while the inflammatory exudate is scant. There is also a prominent deposition of immunoglobulins in the valves from patients with APS, suggesting a possible association between the deposition of the antibodies and the activation of the endothelial cells in APS.

Key Words: Libman–Sacks endocarditis • antiphospholipid syndrome • systemic lupus syndrome • systemic lupus erythematosus • basement membrane • anti-cardiolipin antibodies • integrins

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