<b>Levels of Soluble E-selectin and ICAM-1 in the Coronary Circulation of Patients with Stable Coronary Artery Disease</b>

Abstract

SUMMARYThe recruitment of circulating leukocytes to atherosclerotic sites is mediated by a family of adhesion molecules.The objective of the present study was to evaluate the relationship between circulating adhesion molecule levels in the coronary circulation and the severity of coronary atherosclerosis in patients with stable coronary artery disease.The subjects were 79 patients undergoing coronary angiography. According to the severity of coronary atherosclerosis as assessed by the Gensini Score (GS) of the left coronary artery, they were classified into three groups: group C (no organic stenosis, score 0, n=14), group M (mild organic stenosis, score 1-13, n=39) and group S (severe organic stenosis, score ≥14, n=26). Blood samples were taken from the aorta (Ao) and coronary sinus (CS), and plasma levels of soluble E-selectin (sE-selectin) and soluble intercellular adhesion molecule-1 (sICAM-1) were measured by enzyme-linked immunosorbent assay. These levels were then compared between groups.There were no significant differences in plasma sICAM-1 levels in the Ao or CS between the three groups. The difference in sICAM-1 levels between the CS and Ao (CSAo) also showed no significant difference. Plasma sE-selectin levels in both the Ao and CS were significantly higher in group S than in groups C and M (p<0.05), but there were no significant differences in CS-Ao. There was a weak but significant correlation between the plasma levels of these adhesion molecules and the number of coronary risk factors present. Multivariate analysis showed that the number of coronary risk factors was the only positive predictor (p=0.0048) of the GS; there was no association between the plasma level of either adhesion molecule and the GS.In patients with stable coronary artery disease, sICAM-1 plasma levels do not indicate the severity of coronary atherosclerosis, while sE-selectin plasma levels appear to reflect the severity of systemic rather than coronary atherosclerosis. (Jpn Heart J 2002; 43: 93-101) From the

Endothelial microparticles correlate with high-risk angiographic lesions in acute coronary syndromes

“…However, only a few studies have addressed a possible correlation of such markers with degree of stenosis or types of lesions seen in angiography. Oishi et al [4] reported that E-selectin is elevated in early stages of stenosis but not in advanced stenosis while conversely ICAM-1 was elevated in advanced stenosis; but Nasuno et al [5] could not confirm the findings on ICAM-1 and suggested that elevated E-selectin reflected systemic rather than coronary atherosclerosis.…”

“…However, the clinical significance and specificity of those methods remain controversial and no consensus has been reached on which should be adopted for routine clinical assessment of endothelial status in CAD. Oishi et al [4] reported a weak but significant correlation between elevated E-selectin or ICAM and the degree of stenosis of coronary lesions, but this was not confirmed in another study [5]. Katristsis et al [6] reported that elevated C-reactive protein (CRP) was associated with high-risk angiographic lesions (such as irregular lesions, eccentric location, or presence of thrombus), whereas others failed to find such a correlation.…”

Intracellular Proatherogenic Events and Cell Adhesion Modulated by Extracellular Thiol/Disulfide Redox State

“…Critical events in the initiation of the vascular inflammatory disease are the adhesion of leukocytes to the dysfunctional and injured endothelium and the penetration of these cells into the vessel wall to generate foam cells. Mechanistic studies show that transcriptional activation of adhesion molecules, including P-selectin, E-selectin, vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and platelet endothelial cell adhesion molecule (PECAM), [5][6][7] by nuclear factor-B (NF-B) 8,9 plays a pivotal role in the process of cell-cell adhesion. NF-B is activated by oxidative stress, which can be caused by reactive oxygen species (ROS) and reactive nitrogen species generated in free radical reactions from products of enzymes (NADPH oxidases and nitric oxide [NO] synthases [NOSs]) present in the vascular endothelium and smooth muscle.…”

The effects of exercise stress testing on soluble E‐selectin, von Willebrand factor, and circulating endothelial cells as indices of endothelial damage/dysfunction

“…In patients with stable CAD, plasma sEsel levels appear to reflect the severity and cumulative nature of systemic risk factors rather than coronary atherosclerosis per se (27). Moreover, the exact origins of CECs (arterial versus venous, coronary versus peripheral release), their mechanisms of detachment, and potential transcapillary passage have not been fully established.…”