INCREASED SERUM CONCENTRATIONS OF ADHESION MOLECULES AFTER CORONARY ANGIOPLASTY

1. Reocclusion is still a significant complication after percutaneous transluminal coronary angioplasty. The injury of coronary arteries res ulting from PTCA plays an important role in the pathophysiology of bot h abrupt closure and late restenosis after an initially successful pro cedure, Cytokines play a pivotal role in the accumulation of circulati ng blood cells at the endothelium and are known to regulate their inte raction with the vessel wall. 2. To obtain further information about t his interaction, serum concentrations of soluble endothelial leukocyte adhesion molecule 1 (sELAM-1), leucocyte endothelial cell adhesion mo lecule 1 (sL-selectin), intercellular adhesion molecule 1 (sICAM-1), i nterleukin 2 receptor (sIL-2R) and interleukin 8 (IL-8) detected by en zyme-linked immunosorbent assay were monitored in 30 consecutive patie nts referred for elective PTCA, Fifteen patients who underwent electiv e coronary angiography without PTCA served as controls. 3. All patient s underwent successful first PTCA. Within 24 h the serum concentration s of sELAM-1 increased gradually from 21.7 (SD 7.1) to 48.2 (SD 8.6) n g/ml (P<0.01); levels of sl-selectin rose from 982.1 (SD 128.7) to 154 1.3 (SD 104.6) ng/ml after 48 h (P<0.01). Serum levels of IL-8 remaine d stable initially, but peaked at the end of the observation time of 7 2 h (9.4, SD 3.8, versus 16.1, SD 4.9 ng/ml; P<0.05). A positive corre lation was found between the number of dilatations and the rise in the se parameters (P<0.01). No significant changes were found in the serum concentrations of sICAM-1 and sIL-2R after PTCA or in any of the para meters in patients after coronary angiography. 4. We conclude that PTC A induces a significant rise in the concentration of certain adhesion molecules in serum. Thus, we provide preliminary data on the potential role of cytokines for blood cell-endothelium interaction after PTCA. Further investigations and larger numbers of patients are needed to cl arify the role of circulating cytokines for endothelial injury and res tenosis after PTCA.