Expression of endothelial cell adhesion molecules on heart valves: up-regulation in degeneration as well as acute endocarditis

✍ Scribed by M�ller, Annette M.; Cronen, Claus; Kupferwasser, Leon Iri; Oelert, Hellmut; M�ller, Klaus-Michael; Kirkpatrick, C. James

• Publisher: John Wiley and Sons
• Year: 2000
• Tongue: English
• Weight: 176 KB
• Volume: 191
• Category: Article
• ISSN: 0022-3417
• DOI: 10.1002/(sici)1096-9896(200005)191:1<54::aid-path568>3.0.co;2-y

✦ Synopsis

In¯ammatory cytokines such as interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-a), 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 in¯ammatory responses. Using immunohistochemistry, this study characterized the CAM expression of ECs on degenerative, mostly calci®ed heart valves and on heart valves with ¯orid endocarditis. As expected, the constitutively expressed molecules (ICAM-1, CD34, CD31) were found both on degenerative and on in¯amed valves. Furthermore, marked expression of E-selectin and VCAM-1 was found not only on in¯amed valves, but also on larger portions of the degenerative valves with no morphological evidence of in¯ammation. This striking ®nding might help to explain why patients with ®brotic 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.