These regions are usually in the solvent exposed turns of the protein structure. These are also the regions where insertions and deletions of amino acids frequently occur, since they can be accommodated without major disruption of the fold or function of the protein. Amino acids in these regions should not be described as equivalent and comparisons between sub-types has little biological relevance. Many studies attempt to compare, and sometimes replicate, mutations seen in one subtype, such as H5, to those in another subtype. Careful consideration of the level of structural and functional conservation of that region, however, is crucial. This is especially important when inferring analogous mutations from subtypes belonging to a different phylogenetic group. We feel that the use of this set of residue numbering and analysis of structural conservation will facilitate cross-subtype comparisons and reduce confusion in reporting amino acid numbering. The present substudy of the LEAF trial is the first to explore possible associations between inflammatory markers and LV function and Ginsenoside-F5 myocardial injury in patients developing acute HF following PCI-treated STEMI. The main finding of the study was that circulating levels of IL-8, measured at the time of inclusion, were highly associated with improvement in LV function during the first 6 weeks after STEMI. High levels of IL-8 have recently been shown to be associated with adverse clinical outcome in patients with chronic HF. We found that high levels of IL-8 were associated with less improvement in LV function during the first 6 weeks after STEMI. Interestingly, this association between IL-8 and recovery of LV function was present without any association to peak TnT or final infarct size after 6 weeks suggesting that IL-8 levels may reflect other aspects of myocardial injury than necrosis. IL-8 plays a fundamental role in regulating neutrophil infiltration in ischemic and reperfused myocardium. Activated neutrophils release several factors which can cause tissue and endothelial damage. Additionally, neutrophils can form aggregates that plug capillaries, contributing to microvascular obstruction. MVO was in an experimental animal model of reperfused infarcted myocardium found to be associated with adverse LV remodelling and segmental function, beyond and independent of infarct size. MVO has been shown to be associated with reduced myocardial salvage after primary PCI in STEMI patients, and MVO was a stronger predictor of LV remodelling than peak creatine kinase and infarct size. It therefore seems that MVO may be associated with LV remodelling and impaired function also by mechanisms not related to myocardial necrosis and infarct size alone. Hypothetically, IL-8 may, by its effects on neutrophils, be part of an inflammatory cascade that contributes to such injury of the reperfused myocardium. Although there were trends in differences in baseline characteristics between patients with high vs. low Il-8 levels, the data suggest that differences in IL-8 levels probably are more related to the acute MI and the accompanying degree of heart failure than the patients’ medical Dimesna history before the index MI. Although mainly non-significant trends, due to the relatively low number of patients, more patients in the group with high levels of IL-8 were in cardiogenic shock or had an IABP inserted, and patients with high IL-8 levels had higher peak TnT levels and lower systolic blood pressure. The time courses of different markers like IL-6, CRP and TNFa were consistent with previous studies on patients with either acute decompensated HF or acute MI. Our data, however, is from a STEMI population with very large MIs and severe HF, including cardiogenic shock.