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Atherosclerosis is increasingly considered as a low grade inflammatory response of the arterial wall to a variety of stimuli [FusterL Libby, 2001]. It is accepted that the adhesion of circulating leukocytes and monocytes to endothelial cells (EC) and subsequent transendothelial migration are an important step in the initiation and the development of atherosclerotic lesions [HillisF Jang, 1994]. This process is mediated by receptors expressed on the surface of vascular EC – cell adhesion molecules (CAM) under the action of an enhanced oxidative stress, lipopolysaccharide and proinflammatory cytokines. Vascular cell adhesion molecule (VCAM-1) and intercellular adhesion molecule (ICAM-1) are two members of the immunoglobulin gene superfamily that play important but different roles in the adhesion of blood cells to the vascular endothelium. The significance of these molecules in the course of atherogenesis is confirmed by their immunohistochemically established elevated expression in the atherosclerotic plaques [CybulskyG O’Brien et al., 1993] and by experimental models proving a delayed lesion development in case of their absence [Cybulsky et al., 2001]. Circulating forms of adhesion molecules that have been described are probably generated by cleavage to a site close to membrane insertion. The amount of ICAM-1 released has been demonstrated to be directly correlated with the surface expression of ICAM-1 in EC in culture and a correlation between plasma VCAM-1 and VCAM-1 mRNA has been reported in human atherosclerotic aorta [Leuwenberg et al., 1992; Pigott et al., 1992]. Levels of soluble cell adhesion molecules have been postulated to be useful risk predictor of cardiovascular events in healthy populations and various settings of ischemic heart disease [de Lemos et al., 2000; Hwang et al., 1997; Mulvihill et al., 2000, 2001; O’Malley et al., 2001; Ridker et al., 1998]. Nonetheless, the pathologic role of different soluble adhesion molecules in various stages of coronary artery disease is not fully defined. Two electrocardiographic markers ventricular arrhythmias (VA), [Bigger et al., 1981; Farrell et al., 1991; Kostis et al., 1987] and impaired cardiac autonomic function, as indicated by depressed heart rate variability (HRV), [Bigger at al., 1992; Farrell et all, 1991;

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Markers of Endothelial Activation and Impaired Autonomic Function in Patients with Acute Coronary Syndromes – Potential Prognostic and Therapeutic Implication