It has been shown that decreasing BNP levels are correlated with a decrease in wedge pressure [ 35].
Thus it was hard to assess the effects of SM in improving LVEF, respiratory function and decreasing BNP.
Subgroup analyses were performed to evaluate the effects of SM plus conventional treatment in improving NYHA classification, LVEF or PaO2, and decreasing BNP or PaCO2.
Only two trials with 206 patients [ 13, 39] assessed the effect of SM plus conventional treatment in decreasing BNP in patients with chronic cor pulmonale heart failure.
So, angiotensin II seems to bring about increased expression of BNP, and this is paralleled with decreased BNP levels after institution of ACE-I and/or angiotensin receptor blockade [ 1, 8].
In the placebo control study carried out by Parissis et al. serial levosimendan infusion of adult patients with decompensated heart failure significantly improved the left ventricular performance and decreased BNP and immune activation [ 17].
Due to a limited number of trials, poor methodological quality and significant heterogeneity among these trials, it was hard to assess the effects of SM as an adjuvant treatment in improving LVEF, PaO2 and decreasing BNP, PaCO2.
Indeed, a combination of high-dose furosemide with bolus hypertonic saline infusion in patients with New York Heart Association class IV HF resulted in improved diuresis, shortened hospital stay, decreased BNP levels and reduced readmissions compared with i.v. diuretic therapy alone [ 86].
Cheng and colleagues demonstrated that patients with a significant decrease of BNP at discharge compared with admission BNP levels had better outcomes, whereas BNP levels dropped minimally during hospitalization in patients that were re-hospitalized within 30 days [ 24].
These data indicate that the magnitude of the decrease in BNP and the absolute level of BNP at hospital discharge are predictors of adverse events.
