As severe MOF, with postoperative tSOFA score death in ICU, independently from IL-8 and neopterin levels, as well as from the amount of the pre-implant multi-organ dysfunction. Indeed, in critically ill patients, differences in mortality have been previously reported to be better predicted by the maximal t-SOFA score in the first days of ICU stay; tSOFA score higher than 10 has been associated with elevated mortality rates. Moreover, in our series, patients with elevated IL-6 levels were also characterised by a longer ICU stay, hospitalisation and higher tSOFA score after 1 week, reflecting a greater disarrangement of multi-organ function than in those with lower IL-6 levels. Altogether, these data suggest a more BYL719 critical clinical course in patients with preoperative elevated IL-6 levels than in patients with lower IL-6 levels. The concentration range of IL-6 levels has been found extremely broad in our LVAD-candidates, ranging from negligible to extremely pathological values, greater than the highest value found in CHF patients. These data suggest that in a few ESHF patients, the hemodynamic collapse requiring LVAD implantation is associated with increased activation of systemic inflammation, linked to the IL-6 signals; among preoperative variables, IL-6 levels are associated only with the total leukocyte count, regardless of the hemodynamic status, as defined by INTERMACS profiles. Therefore, the evaluation of IL-6 levels in LVAD-candidates may provide additional information on patient’s risk profile, in addition to the prognostic information provided by the INTERMACS profiles, and could allow to highlight patients more susceptible of poorer outcome in the early phase of LVAD support, although not strictly associated to the risk of death. Indeed, in our series of patients, the pre-implant cut-off-point for IL-6 at 8.3 pg/ml did not allow to predict survival in the short-time of LVAD support. Postoperatively, elevated IL-6 levels were reported in patients who died because of MOF in the early phase of LVAD support, and the activation of monocytes was proposed as a crucial mechanism involved in the development of MOF. In a previous study we reported that, after LVAD implantation, neopterin levels progressively increased mainly in non-survivors. In the present cohort, postoperative Neo/Cr and IL-8 levels increased mainly in patients who showed preoperative IL-6 levels higher than 8.3 pg/ml, reflecting, postoperatively, a more marked monocyte activation and adverse inflammatory milieu. Moreover, postoperative IL-6 levels showed similar profiles in both groups, with a peak level in the first postoperative days. This finding supports the hypothesis that only IL-6-dependent inflammatory signals, present at pre-implant, may be responsible for triggering stimuli that favor a more marked monocyte activation and adverse inflammatory milieu after LVAD implantation, as evidenced by the greater release of IL-8 and neopterin.