Influence of apelin-12 on troponin levels and the rate of MACE in STEMI patients

Abstract

BackgroundDuring acute myocardial infarction, phosphorylated TnI levels, Ca2+ sensitivity and ATPase activity are decreased in the myocardium, and the subsequent elevation in Ca2+ levels activates protease I (caplain I), leading to the proteolytic degradation of troponins. Concurrently, the levels of apelin and APJ expression are increased by limiting myocardial injury.MethodsIn this prospective observational study, 100 consecutive patients with ST-elevation acute myocardial infarction were included. Patients meeting the following criteria were included in our study: (1) continuous chest pain lasting for >30 min, (2) observation of ST-segment elevation of more than 2 mm in two adjacent leads by electrocardiography (ECG), (3) increased cardiac troponin I levels, and (4) patients who underwent reperfusion therapy. We evaluated the levels of apelin-12 and troponin I on the first and seventh days after reperfusion therapy in all patients.ResultsApelin-12 was inversely correlated with troponin I levels (Spearman’s correlation = −0.40) with a p value <0.001. There was variability in the apelin values on the seventh day (Kruskal-Wallis test) based on major adverse cardiac events (MACE) (p = 0.012). Using ROC curve analyses, a cut-off value of >2.2 for the association of apelin with MACE was determined, and the AUC was 0.71 (95% CI, 0.58–0.84). Survival analysis using the Kaplan-Meier method showed a lower rate of MACE among patients with apelin levels >2.2 (p = 0.002), and the ROC curve analysis showed a statistically significant difference in the area under the curve (p = 0.004).ConclusionThe influence of apelin levels on troponin levels in the acute phase of STEMI is inversely correlated, whereas in the non-acute phase, low apelin values were associated with a high rate of MACE.

APJ as Promising Therapeutic Target of Peptide Analogues in Myocardial Infarction- and Hypertension-Induced Heart Failure

“…The increase in apelin levels in the early period after MI has also been recently confirmed in a clinical study, reporting a significant six-fold increase in apelin in MI patients at hospital admission compared to the control group [ 35 ]. These data are in line with Krasniqi and collaborators who reported that high apelin levels within seven days post-MI were correlated to low rates of developing major adverse cardiac events (MACE) in a clinical study [ 129 ]. It should be kept in mind, however, that the spontaneous increase in apelin levels in the first days after MI was not sufficient to fully protect the hearts.…”

Prognostic Value of Combining Apelin-12 and Estimated Glomerular Filtration Rate in Patients with ST-Segment Elevation Myocardial Infarction

“…It has been reported that the plasma concentration of apelin-12 after acute myocardial infarction (AMI) is significantly lower than that in the control population [ 15 , 16 ]. Apelin-12 is negatively associated with troponin I levels, high-sensitivity C-reactive protein, neutrophil/lymphocyte ratio, and the rate of MACE, indicating that apelin-12 can serve as a prognostic biomarker for STEMI patients [ 9 , 17 ]. This is consistent with the results of our study.…”

“…The authors found that the incidence of MACE was significantly higher in patients with low apelin-12 levels than in those with high apelin-12 ( p < 0.001) [ 8 ]. Another observational study suggested that the MACE rate was much lower in patients with an apelin-12 level >2.2 ng/mL [ 9 ]. The underlying cardioprotective mechanisms may be that the apelin system promotes vasodilation, reduces blood pressure in a nitric oxide-dependent way, increases cardiac contractility, and improves angiogenesis after myocardial infarction [ 10 ].…”