Studies have shown disparate results in relation to the role of plasma concentrations of cell adhesion molecules in atherosclerosis. Moreover, the differentiation of primary vs secondary alterations of these markers, in response to myocardial injury, has not been clear. We measured specific soluble cell adhesion molecules and inflammatory markers in men admitted acutely with chest pain and compared them to healthy controls.
We prospectively studied men (total n=241), admitted acutely with chest pain (7.4+/-9.4 h, 71% within 10 h), unstable angina (n=67), acute myocardial infarction (n=47) and chest pain without ischaemic heart disease (n=45) and compared them with a stratified sample of randomly selected healthy controls (n=82). Soluble intercellular adhesion molecule (sICAM-1), endothelial selectin, vascular cell adhesion molecule, interleukin-6 and C-reactive protein were measured by ELISA and P-selectin expression by flow cytometry. Multiple regression analysis was used to control for the impact of classical risk factors. At baseline ICAM-1, interleukin-6 and C-reactive protein were significantly elevated in patient groups whereas no difference in vascular cell adhesion molecule or endothelial selectin was found. At 3 month follow-up, ICAM-1 level was unchanged in ischaemic heart disease patients. In all groups C-reactive protein and interleukin-6 levels were lower at review. ICAM-1 levels at follow-up were higher in ischaemic heart disease groups (but not in chest pain without ischaemic heart disease) relative to controls and remained so only in the unstable angina group following regression. sICAM-1, interleukin-6 and C-reactive protein strongly correlated with smoking. In the acute phase, ICAM-1 was confounded by smoking following regression and C-reactive protein and interleukin-6 remained significant in both ischaemic heart disease groups after multiple regression. There was no relationship to events which occurred in 23% of ischaemic heart disease patients (further acute myocardial infarction 5.3%, sudden cardiac death 0.9% or recurrent angina 16.7%).
We found an inflammatory response with higher sICAM-1, interleukin-6 and C-reactive protein in patients presenting soon after developing an acute coronary syndrome. As sICAM-1 was not affected by the acute event this plasma marker may be an important risk factor for the development of the acute coronary syndrome, particularly unstable angina.