However, cytokines of the IL-6 family have been shown to play a role in all stages of the development
and progression of atherosclerosis, from early inflammatory lesions to destabilisation of the plaque [5]. Pro-inflammatory cytokines are thought to be involved in reperfusion injury, repair processes and scar tissue formation after myocardial infarction [3]. Circulating levels of IL-6 and C-reactive protein (CRP) have been shown to correlate with infarct size [6], whereas the knowledge of other novel members of DAPT cost the IL-6 family like soluble interleukin-6 receptor (sIL-6R) and soluble glycoprotein 130 (sgp130) is limited in patients with myocardial infarction. The IL-6 signalling is activated through two different ways and it has been a matter of discussion whether this results in both a pro- and anti-inflammatory effect of IL-6 [7]. In the classical IL-6 signalling pathway IL-6 binds to IL-6R, which is a membrane-bound receptor on the cell surface [8]. The receptor–ligand complex then associates with the common signal transducing receptor gp130, RGFP966 in vivo initiating activation of intracellular signalling pathways.
The membrane-bound IL-6R is present in cells like hepatocytes, monocytes, inactive B and T-lymphocytes [8] and cardiac myocytes [9] whereas gp130 is widely expressed in most cell types in the human body. In the second way of IL-6 signalling, which has been named the transsignalling system, IL-6 binds to a soluble form of IL-6R (sIL-6R), and this complex binds subsequently to gp130 on cells. The gp130/IL6/sIL-6R complex activates intracellular pathways, and exerts its function in cells not expressing the IL-6R [10]. This IL-6 transsignalling pathway may be more important for the pro-inflammatory effect of IL-6 than the classical receptor signalling [7]. The soluble form of gp130 (sgp130) is the natural inhibitor of this transsignalling system [11]. It inhibits the ability of the circulating IL-6/sIL-6R complex to bind to membrane bound gp130. These less studied members of the IL-6 signalling system, i.e. sgp130 and sIL-6R, might give additional mechanistic insights into the atherosclerotic process
associated with STEMI. The aims of the present study were to elucidate possible associations between members of the IL-6 transsignalling system including sIL-6R Thiamine-diphosphate kinase and sgp130 and (1) the degree of myocardial necrosis, (2) left ventricular (LV) impairment, and (3) dysglycemia as well as conventional risk factors in patients with ST-elevation myocardial infarction (STEMI). This study was a cross-sectional cohort study of STEMI patients admitted to Oslo University Hospital Ullevål, Norway and treated with primary PCI. From June 2007 to August 2011 a total of 1028 patients with diagnosed STEMI were included consecutively during weekdays after written informed consent was obtained. The study was approved by the Regional Ethics Committee.