Background: Adhesion molecules are expressed on vascular endothelium and on immune and inflammatory cells. Recently increased levels of adhesion molecules have been shown in patients with rheumatic mitral stenosis. This study examined the serum levels of the adhesion molecules intercellular adhesion molecule I (ICAM-1), vascular cell adhesion molecule I (VCAM-1), and E-selectin in patients with rheumatic mitral stenosis and the effects of percutaneous mitral balloon valvuloplasty (PMBV) on these adhesion molecules. Materials and methods: Thirty five patients (3 men, 32 women, mean age 39 5 years) with severe rheumatic mitral stenosis who underwent percutaneous balloon mitral valvuloplasty, and 35 age and sex matched healthy control subjects were included in the study. Serum levels of ICAM-1, VCAM-I, and E-selectin were measured in all patients who underwent PMBV and in all control subjects. Blood samples were taken for measurement of adhesion molecules immediately before and 24 h after the mitral balloon valvuloplasty. Results: The plasma levels of soluble adhesion molecules E-selectin, ICAM-I and VCAM-I were significantly elevated in patients with mitral stenosis compared to control subjects: E-selectin, 97 +/- 59 vs. 45 +/- 24 ng/ml (P=.001), sICAM-1, 874 +/- 301 ng/ml vs. 238 82 ng/ml (P<.0001); sVCAM-1, 3056 +/- 763 ng/ml vs. 985 +/- 298 ng/ml (P<.0001). Plasma levels of VCAM-1 significantly increased 24 h after the valvuloplasty procedure (3056 +/- 763 ng/ml vs. 3570 +/- 1225 ng/ml P=.013). Plasma levels of E-selectin showed a significant decrease after PMBV (97 +/- 59 vs. 70 +/- 58 ng/ml, P=.043) and plasma levels of ICAM-I did not show any change after PMBV (874 +/- 301 vs. 944 +/- 3 77 ng/ml, P=.356). Conclusion: Cellular adhesion molecules, sICAM-1, E-selectin, sVCAM-1 have shown changes in different directions in response to PMBV These results necessitate further studies to clarify the mechanism underlying the association between adhesion molecules and PMBV as well as rheumatic mitral stenosis. (C) 2004 Elsevier Inc. All rights reserved.