Association between apelin-12 and N-terminal pro-brain natriuretic peptide depending no- reflow phenomenon in STEMI patients

Background In acute myocardial infarction, hypoxia, through the hypoxia inducible factor pathway, increases the level of apelin, protecting the myocardium from ischemia-reperfusion injury. In the absence of apelin, Ca2+ desensitization of the actin-myosin system, excess Ca2+ concentrations, calpain I activation, troponin degradation, ventricular dysfunction, and BNP secretion are observed. Purpose To evaluate association between apelin-12 and N-terminal pro-brain natriuretic peptide in STEMI patients depending on reperfusion injury. Methods In this study we included hundred patients with following criteria: chest pain lasting for more than 30 minutes, a 12-lead ECG characterized with ST-segment elevation in at least two contiguous leads ≥2.5 mm in men <40 years, ≥2mm in men ≥40 years, or ≥1.5 mm in women in leads V2-V3 and/or ≥1 mm in other leads, rise of cardiac troponin I, and patients who have undergone primary percutaneous coronary intervention (PCI) within period of 12h. The levels of apelin-12, creatine kinase (CK), the MB fraction of creatine kinase (CKMB), troponin I, NT-proBNP, CRP, and other routine laboratory parameters were measured. Results In patients with TIMI flow ≤2 the median of apelin-12 level was 1.94 (0.26-8.88), and with TIMI flow 3, it was 2.42 (0.49-10.90). Variability was observed in the apelin values (Mann-Whitney test) based on TIMI flow grade (p<0.010), and in the the N-terminal pro-brain natriuretic peptide (p<0.031) (Table 1). The degree of association between apelin-12 and NT-proBNP was analyzed with Pearson’s correlation resulting in patients without reperfusion injury (TIMI flow 3). p= -0.042, while in those with reperfusion injury (TIMI flow ≤2) p= -0.25. Figure 1 shows the association of apelin-12 and NT-proBNP in patients with TIMI flow grade 3, while Figure 2 this association shows in patients with TIMI flow grade ≤2.Conclusions: Apelin-12 levels inversely correlated with N-terminal pro-brain natriuretic peptide levels depending reperfusion injury. This confirms the predictive value of Apelin for reperfusion injury which may lead to contractile myocardial dysfunction increasing level of NT-proBNP.