The expression of endothelial activation markers E-selectin and VCAM-1 on degenerative heart valves may explain why patients with fibrotic heart valves are susceptible to recurrent endocarditis.
Inflammatory cytokines such as interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-α), as well as shear stress, cause endothelial cells (ECs), to undergo not only functional alterations but also structural reorganizations, which contribute to vascular leakage. Like ECs of the human aorta, ECs on heart valves are exposed to extreme shear stress. However, while ECs expression of cell adhesion molecules (CAMs) in large vessels has been widely studied, it seems that there are no such studies on ECs of heart valves, although this knowledge might be important for our understanding of the aetiological aspects of local inflammatory responses. Using immunohistochemistry, this study characterized the CAM expression of ECs on degenerative, mostly calcified heart valves and on heart valves with florid endocarditis. As expected, the constitutively expressed molecules (ICAM-1, CD34, CD31) were found both on degenerative and on inflamed valves. Furthermore, marked expression of E-selectin and VCAM-1 was found not only on inflamed valves, but also on larger portions of the degenerative valves with no morphological evidence of inflammation. This striking finding might help to explain why patients with fibrotic heart valves are susceptible to recurrent endocarditis. Why the endothelial activation markers E-selectin and VCAM-1 are expressed on degenerative heart valves requires further investigation. Copyright © 2000 John Wiley & Sons, Ltd.
M�ller et al. (Mon,) studied this question.